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of monetary units, and effectiveness is expressed in units such as the number of lives saved, the years of life saved, the days of disability avoided, and so on. [48] To analyze difficult and complex clinical problems for which no clear consensus exists among experts, a clinical decision model may be constructed to outline explicitly various diagnostic or therapeutic options, and the possible clinical events and outcomes. Probabilities for various clinical events and outcomes can be estimated on the basis of the best available current evidence from the medical literature or, if this is not available, from the physicians' clinical judgment. Each possible outcome is assigned a cost and a utility. By convention, perfect health is assigned a utility value of 1, and death is assigned a value of 0. Various schemes have been devised to assign utility values to different degrees of disease or symptom severity. Thus, cost and health benefit can be calculated for the various options under consideration. The conclusions drawn from any type of clinical decision analysis can only be as accurate as the assumptions on which the model is based. In cases in which the TABLE 11-2 -- Key Terms in Cost-Effectiveness Analysis Cost: amount of resource required, usually expressed in monetary units. Effectiveness: health benefit achieved, commonly expressed in units such as the number of lives saved, the days of disability avoided, the years of mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 4 life saved, and so on. Clinical decision model: a model of the clinical problem, usually constructed in the form of a decision tree, in which various diagnostic or therapeutic options are outlined, and the possible clinical events and outcomes are enumerated and assigned probabilities and utilities. This can be used to analyze the cost or health benefit of various options. Utility: the benefit associated with a specific outcome. By convention, perfect health is assigned a value of 1, and death is assigned a value of 0. Sensitivity analysis: an analysis in which certain parameters in the clinical decision model are systematically varied over reasonable ranges, so as to determine whether the results of the model are significantly affected. This is especially important if there is significant uncertainty or variability in the values of certain parameters. QALY: quality-adjusted life-year. Incremental cost-effectiveness: additional cost-effectiveness of a new strategy compared with the baseline strategy. parameters in the model can vary over a certain range or in which there is uncertainty regarding their values, it is critical to determine whether variation of parameter values over reasonable ranges significantly affects the results of the analysis. This process is referred to as sensitivity analysis. Given the results of a cost-effectiveness analysis, the decision about whether it is worthwhile to spend a certain additional amount to achieve an incremental benefit will depend on the society's values and socioeconomic conditions. In many analyses of health care delivery in the United States, the cost of renal dialysis (approximately $35,000 to $40,000 per patient per year in 1995) is often used as the benchmark for the cost that the American public is willing to bear to prolong life by 1 year. Data on the cost-effectiveness of echocardiography in patients presenting to the emergency department with acute chest pain are scarce. In more general cost-effectiveness analyses of diagnostic strategies for patients with chest pain, most studies have found the preferred initial strategy to be noninvasive testing for patients with low to intermediate pretest probability of coronary artery disease, and coronary angiography for those with high pretest probability. In a study by Kuntz et al,[49] exercise echocardiography cost $41,900 per quality-adjusted life-year (QALY) saved compared with exercise electrocardiography for 55-year-old men with atypical angina. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 4 Exercise SPECT cost $54,800 per QALY saved compared with exercise electrocardiography for these patients. The incremental cost-effectiveness ratio of routine coronary angiography compared with exercise echocardiography was $36,400 per QALY saved for 55-year-old men with typical angina. For 55-year-old men with nonspecific chest pain, the incremental cost-effectiveness ratio of exercise electrocardiography compared with no testing was $57,700 per QALY saved. The authors concluded that exercise electrocardiography or exercise echocardiography resulted in reasonable cost-effectiveness ratios for patients 245 at mild to moderate risk for coronary artery disease in terms of age, sex, and type of chest pain. Garber and Solomon analyzed the cost-effectiveness of five test strategies for patients with a history of chest pain and intermediate pretest probability (25% to 75%) of coronary artery disease.[50] These strategies involved a noninvasive test (treadmill exercise testing, planar nuclear imaging, SPECT, stress echocardiography, or positron emission tomography) followed by coronary angiography if the noninvasive test was positive. Using information from published literature on the sensitivity and specificity of each test, disease prevalence, and treatment efficacy, and basing cost calculations on Medicare payments, the authors developed a decision analytic model to assess the health outcomes and costs of the different strategies. They found that stress echocardiography improved health outcomes and reduced costs relative to exercise stress testing and planar nuclear imaging. The incremental cost-effectiveness ratio was $75,000 per QALY for SPECT relative to echocardiography, more than $640,000 per QALY for positron emission tomography relative to SPECT, and $94,000 per QALY for immediate coronary angiography relative to SPECT. The authors concluded that stress echocardiography, stress SPECT, and immediate coronary angiography are cost-effective alternatives to positron emission tomography and other strategies. Exercise treadmill testing for assessment of chest pain or risk stratification has been found to be cost-efficient even if greater expense is incurred when such tests are performed outside of regular laboratory hours. Krasuski et al [51] studied 195 patients scheduled for exercise stress testing during weekends or holidays for assessment of chest pain (75%) and other indications; the study population was not limited to chest pain patients from mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 4 the emergency department. The authors found the approach to be safe and effective for risk stratification and to shorten hospital stay. Although a formal cost-effectiveness analysis was not performed in this study, this approach was found to result in cost savings even when the greater expenses associated with testing during weekends or holidays were taken into consideration. For a general discussion of cost-effectiveness analysis for noninvasive diagnostic testing for coronary artery disease, refer to the paper by Hunink et al.[52] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/94.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Limitations Limitations in the Use of Regional Contractile Function to Evaluate Ischemia Evaluation of acute coronary syndrome with echocardiography has several limitations. Between episodes of cardiac ischemia, the patient's wall motion may be completely normal. Therefore, a normal resting echocardiogram performed in such a patient cannot rule out cardiac ischemia as the cause of the patient's symptoms. Stress testing should be considered after myocardial infarction is ruled out. The presence of pre-existing left ventricular dysfunction secondary to nonischemic cardiomyopathy or valvular heart disease makes the evaluation of new regional wall motion abnormalities more difficult and may cause the specificity of this technique to be lower for this population of patients. Image Quality The detection of regional wall motion abnormalities requires adequate visualization of endocardial borders. In patients with morbid obesity, chest wall deformity, chest trauma, or recent thoracic surgery, views with good image quality may be difficult to acquire, especially given the time constraints imposed by the need for rapid diagnosis and institution of therapy. The use of newer echocardiographic modalities, such as second harmonic imaging with echocardiographic contrast administration, may improve endocardial border delineation in such patients and make echocardiographic evaluation in the emergency department more practical. Personnel Availability Ready availability of sonographers to perform echocardiographic examinations and echocardiographers to interpret them is essential if mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 echocardiography is to enjoy more widespread use in the evaluation of patients with chest pain in the emergency department. This is not a problem during usual working hours in most hospitals. However, it may not be economically practical to have the personnel physically "on call" in the hospital 24 hours a day for most community hospitals or even tertiary medical centers. Contacting sonographers and echocardiographers on call outside of the hospital inevitably causes a delay in the management of such patients. One approach to deal with this problem is to train emergency department personnel to perform echocardiograms. An obstacle to successful implementation of this approach is the difficulty in gaining and maintaining sufficient experience in performing echocardiographic studies in the context of the rotating shift system in most emergency departments. This logistical problem may be at least partially solved with the advent of digital tele-echocardiography systems. Acquired images can be transmitted over a high-speed network to an experienced echocardiographer outside the hospital for immediate interpretation. Future systems may incorporate the capability for greater real-time interaction between the off-site interpreting physician and the on-site sonographer to ensure the acquisition of all requisite images for any particular clinical situation. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/95.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Future Developments Tele-echocardiography The accurate interpretation of stress echocardiographic images requires experienced echocardiographers, who may not be immediately available in the hospital during off-hours. Having an experienced echocardiographer available in the hospital 24 hours a day or to come into 246 the hospital when such cases occur may not be practical in many hospitals. In addition, the latter option may further delay definitive treatment. Electronic transmission of echocardiographic images has been used as part of telemedicine projects in a number of centers. In nonemergency settings, successful use has been reported in the difficult diagnostic cases requiring expert interpretation, such as patients with congenital heart disease.[53] [54] [55] In the clinical trial by Trippi et al[28] using dobutamine stress echocardiography to determine which patients presenting with chest pain to the emergency room may be safely discharged, the echocardiograms were digitized into a quad-screen systolic eight-frame cineloop format with resolution of 320 by 240 pixels, and transmitted to the interpreting physician over the standard telephone line using a proprietary "lossless" format developed before DICOM standards.[56] [57] The test was completed within an average of 5.4 hours after presentation to the emergency room. It was found to have very good sensitivity and specificity and could potentially result in significant cost savings, as discussed previously in the section on Clinical Applications. Rapid technologic developments since that time, including faster processor speed, availability of higher capacity random access memory, and faster network connections via the Internet or dedicated lines may result in more mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 widespread use of this technology. Of course, the transmission of patient- specific data over publicly accessible networks will require proper encryption to ensure patient privacy. Myocardial Contrast Echocardiography The use of echocardiographic contrast with second harmonic imaging to evaluate myocardial perfusion is one of the most exciting developing areas of echocardiography. Ultrasonographic imaging for this purpose needs to be intermittent so as to minimize the destruction of micro-bubbles in the contrast agent. This technique, when perfected, has potential uses in the diagnosis of acute myocardial infarction, determination of ischemic and infarcted areas in conjunction with stress testing, evaluation of reperfusion status, detection of no reflow in the microvascular coronary circulation after restoration of flow in the epicardial coronary arteries, and evaluation of myocardial viability. Although promising, this echocardiographic technique needs to be further refined before its utility in the examination of patients with acute chest pain |
syndrome can be evaluated. Other Modalities Doppler tissue imaging[58] [59] [60] and color kinesis[61] [62] (Fig. 11-8) are two of the promising new imaging modalities, although further studies are needed to determine their utility in routine assessment of regional wall motion. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/96.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Chest Pain Centers Centers dedicated to diagnostic evaluation of patients presenting with chest pain suggestive of acute coronary syndrome have been set up in a number of medical centers in the United States, with the goal of improving the efficiency of evaluation while preserving or improving outcomes.[2] [34] [63] Most chest pain centers are based within the emergency department or in an adjacent observation unit. Others are located in a part of an inpatient telemetry unit. Patients presenting to the emergency department with chest pain are first stratified into several risk groups on the basis of their history, physical examination, and initial 12-lead ECG. High-risk patients, including those with significant acute ST-segment changes, hemodynamic instability, and known history of coronary artery disease, are admitted directly, usually to the coronary care unit. Those with acute ST-segment elevation or new LBBB will receive reperfusion therapy with thrombolytic agents or cardiac catheterization. Patients with low to moderate pretest probability of acute coronary syndrome, who have no contraindications to diagnostic testing according to the chest pain center protocol and no serious comorbid conditions that may interfere with discharge from the emergency department, are evaluated further in the chest pain center. Other low- to moderate-risk patients may be admitted to a step-down telemetry unit for further evaluation. Patients with noncardiac chest pain are treated and triaged according to their diagnosis. Although individual protocols vary, patients in the chest pain center often undergo serial cardiac enzyme marker determinations (e.g., at 0, 3, and 6 hours after presentation). Serial 12-lead ECGs or continuous ST-segment monitoring is also performed. The monitoring period generally ranges from 6 to 12 hours, although an experience with immediate stress testing in low- risk patients has also been reported. [64] [65] Patients who develop evidence of acute coronary syndrome during the period of monitoring are admitted. The mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 rest will undergo further diagnostic testing after the monitoring period for diagnosis of coronary artery disease and for risk stratification. A number of studies address possible choices for diagnostic testing in emergency department patients presenting with chest pain.[27] [28] [35] , [41] [66] [67] [68] [69] Graded exercise ECG testing is often obtained for those patients who can exercise to an adequate level, have no contraindications to exercise testing, and have no baseline ECG abnormalities that may interfere with the interpretation of stress ECGs. Exercise or pharmacologic stress imaging can be utilized in other patients. The incremental value and cost- effectiveness of imaging for patients being evaluated in chest pain centers who can exercise requires further study, as suggested by the American Heart Association.[70] Stress testing is usually supervised by an appropriately trained physician and performed in a dedicated area with resuscitative equipment available and should conform to American Heart Association guidelines for exercise ECG laboratories.[70] [71] As mentioned in an earlier section, accurate acquisition and interpretation of stress echocardiograms requires an experienced sonographer and echocardiographer. Thus, the chest pain center performing stress echocardiography will need a physician experienced in echocardiography to be available on call in or near the hospital, unless tele-echocardiography equipment is available to transmit images to the interpreting physician. Patients 247 Figure 11-8 (color plate.) Tissue Doppler imaging (TDI; top) and myocardial velocity gradient (MVG; bottom) images of the left ventricle in the parasternal short-axis view from a patient with left anterior descending coronary artery obstruction: at baseline (left), with low-dose (10 µg/kg/min) dobutamine (middle), and with high-dose (30 µg/kg/min) dobutamine (right). In the TDI images, the anteroseptal wall is color-coded blue because it is moving away from the transducer during systole. Similarly, the posterior wall is color-coded red because it is moving toward the transducer. MVG is derived from TDI, and it is defined as the slope of the regression line of the intramyocardial velocity profile across the myocardium. It reflects regional wall thickening and has been shown to be independent of the translational motion of the heart. In the MVG images, thickening of the myocardium is color-coded red, and thinning of the myocardium is color-coded blue. Calculated segmental MVGs are shown beside the corresponding segments. In this patient, MVG undergoes a dose-responsive increase in the posterior segment and no significant change in the anteroseptal segment supplied by the diseased coronary artery. (From Tsutsui H, Uematsu M, Shimizu H, et mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 al: J Am Coll Cardiol 1998;31:89–93. Reprinted with permission from the American College of Cardiology.) with positive stress tests will usually be admitted for further evaluation; those with negative evaluations will generally be discharged from the chest pain center with careful attention to adequate outpatient follow-up. An important part of the work of a successful chest pain center involves community outreach to increase public awareness of the importance of seeking prompt medical attention for chest pain. This will further improve the clinical outcome of patients presenting to the emergency department with acute coronary syndrome. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/97.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Summary Transthoracic, transesophageal, and stress echocardiography may all be useful in the evaluation of patients with acute chest pain presenting to the emergency department. Echocardiography can aid in the diagnosis of cardiac ischemia and myocardial infarction, help assess for other important causes of chest pain, and provide incremental prognostic information on both short- and long-term outcomes. New developments to enhance imaging and endocardial border definition, digital acquisition of images, tele-echocardiography, and the possibility of perfusion-based imaging using echocardiographic contrast promise to increase its utility even further in the future. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/98.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company 251 Chapter 12 - Echocardiography in the Coronary Care Unit Management of Acute Myocardial Infarction, Detection of Complications, and Prognostic Implications Elyse Foster MD Zian H. Tseng MD The earliest experimental models of myocardial infarction demonstrated that regional wall motion abnormalities ensue shortly after cessation of coronary flow.[1] When a coronary artery is ligated, the first abnormality is an impairment in relaxation of the affected wall. The diastolic abnormalities are followed within seconds by the development of systolic contraction abnormalities. These systolic abnormalities can be readily detected by conventional echocardiographic methods and form much of the basis for the echocardiographic evaluation of ischemia. Although segmental abnormalities in diastolic function are not readily measured by conventional echocardiography, the available information regarding global diastolic dysfunction has recently been found to have important prognostic significance. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/100.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Historical Perspective The use of echocardiography in patients with myocardial infarction occurred with the introduction of the first echocardiographic imaging techniques. [2] [3] [4] [5] M-mode echocardiography, with its high frame rate, permitted precise assessment of the reduction in wall thickening, but it was limited by its narrow view of the left ventricle. For example, fractional shortening, measured from the ventricular dimensions at the level of the basal septum and posterior wall, inaccurately represented global left ventricular function in patients with mid and apical wall motion abnormalities. Two-dimensional (2D) sector scanning, developed in the late 1970s, provided the necessary tomographic views for a complete evaluation of regional ventricular function. This bedside imaging method was soon employed widely for the early identification of apical aneurysms and thrombus formation[6] , [7] in patients with anterior myocardial infarction. Two-dimensional quantitative techniques also were developed that could accurately measure left ventricular ejection fraction in the presence of regional wall motion abnormalities. The role of right ventricular infarction in low output syndromes was appreciated,[8] [9] [10] and the high prevalence of post-myocardial infarction pericardial effusions was recognized. 252 The introduction of spectral and color Doppler echocardiography in the mid-1980s further enhanced the role of echocardiography by providing essential hemodynamic information. In addition, timely noninvasive diagnosis of complications of acute myocardial infarction, such as mitral regurgitation and ventricular septal defects, was possible. Newer methods, such as tissue Doppler imaging and mitral flow propagation velocities,[11] have enhanced our capacity to define left ventricular diastolic function mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 Transesophageal echocardiography allows better definition of the anatomic alterations responsible for the complications of acute myocardial infarction (e.g., papillary muscle rupture). Finally, the advances in digital imaging techniques since the 1980s have enabled the dissemination of stress echocardiography, which has assumed a major role in evaluation of patients with ischemic heart disease, as discussed in Chapter 13 and Chapter 14 . The portability of echocardiography and the extent of hemodynamic and anatomic information it provides ensure its place in the coronary care unit (CCU). Although its ability to provide direct information regarding coronary anatomy and myocardial perfusion have been limited to date, there is continued progress in these areas. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/101.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Applicable Modes of Echocardiography Transthoracic echocardiography (TTE) provides a rapid bedside assessment of wall motion and global left ventricular function, and it excludes the presence of complications.[12] [13] In the patient presenting with chest pain who has a nondiagnostic electrocardiogram, identification of a segmental wall motion abnormality assists in the determination of definitive therapy. In the patient with an established myocardial infarction, early noninvasive evaluation of ejection fraction indicates therapy with beta blockers, angiotensin converting enzyme inhibitors, or both. When recurrent pain complicates reperfusion therapy, electrocardiographic changes may be nonspecific. In this situation, echocardiography helps differentiate between recurrent ischemia and pericarditis. Importantly, the cause of hemodynamic instability in patients with myocardial infarction often can be established without invasive monitoring. In patients with severe hemodynamic compromise, TTE may be limited by mechanical ventilation and an inability to adequately position the patient. In this group, transesophageal echocardiography (TEE) has proven to be efficacious, especially in ruling out complications related to cardiac |
rupture.[14] [15] [16] [17] [18] [19] [20] [21] [22] Although large numbers of patients with acute myocardial infarction have not been studied, with careful sedation and close monitoring, TEE can be performed safely.[23] [24] [25] Stress echocardiography has assumed an increasingly important role in assessing the postinfarction patient for evidence of myocardial viability and for assessing the risk for recurrent ischemia. Dobutamine echocardiography, using low doses that do not significantly alter hemodynamics, has been shown to improve function in viable myocardial segments. Higher doses of dobutamine as well as exercise echocardiography can be used to detect residual ischemia, but they should be used with caution early after myocardial infarction.[26] Although one study showed no increase in cardiac enzymes after dobutamine stress, [27] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 there are isolated case reports of free wall rupture in association with high- dose dobutamine stress testing within the first week following myocardial infarction.[28] [29] Contrast echocardiography remains investigational for the evaluation of myocardial perfusion. Only one intravenous left-sided contrast agent is commercially available in the United States. Although this agent crosses the pulmonary circulation and opacifies the left ventricular cavity, in the approved dose ranges it does not routinely offer adequate assessment of myocardial perfusion. In a study using an investigational agent, a comparison between single photon emission computed tomography (SPECT) and myocardial contrast echocardiography (MCE) revealed limited sensitivity and high specificity for MCE detection of moderate or severe perfusion defects. MCE also underestimated the extent of SPECT defects. [30] The accuracy of MCE was enhanced by the combination of MCE and wall motion assessment.[30] [31] Rapid technologic developments in this field are under way. Saline contrast may be indicated for enhancement of tricuspid regurgitant jets in order to estimate pulmonary artery pressures and to exclude a patent foramen ovale in patients with cerebral embolization or hypoxemia in the setting of right ventricular infarction.[32] [33] Although three-dimensional (3D) echocardiography has proved to be an important research tool, it has not yet been widely adopted in the clinical setting. Studies in canine models suggest that accurate quantitation of infarct size with and without the use of myocardial contrast may be possible in the future.[34] [35] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/102.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Advantages and Limitations of Echocardiography in the Coronary Care Unit The major advantages to echocardiography in the CCU include its portability, noninvasive nature, and the wealth of anatomic and hemodynamic information provided. TEE, a semi-invasive technique, has an extremely low complication rate even among the most seriously ill.[36] [37] The limitations of echocardiographic evaluation include the limited transthoracic windows often encountered in the acutely ill coronary care patient, frustrating identification of important complications. Newer technologies such as tissue harmonics have enhanced endocardial border definition even in the most difficult patients. Another limitation is the largely qualitative analysis of regional wall motion abnormalities; quantitative techniques are cumbersome, require manual tracing, and, for the most part, have not been widely employed in the clinical setting.[38] [39] Nevertheless, surface echocardiography remains a mainstay of noninvasive diagnosis in the CCU. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/103.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 8 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Pathophysiology and Echocardiographic Correlations Timing and Evolution of Infarction The effects of acute coronary ligation in animal models of experimental myocardial infarction have been studied by echocardiography, leading to several observations: 253 1. Acute coronary ligation results in diminished systolic wall thickening and outward motion of the affected myocardial segment (dyskinesis) with close correlation between echocardiography and sonomicrometry. [40] [41] [42] [43] 2. The degree of dyskinesis produced was directly related to the severity of the perfusion deficit.[40] 3. Interventions during ischemia that increase afterload worsen wall motion, whereas afterload-reducing and inotropic agents improve wall motion.[40] [44] 4. The extent of wall motion abnormalities correlates with infarct size to a variable degree. In one study the wall motion abnormalities present at 2 hours following coronary ligation tended to overestimate infarct size because function had improved over the subsequent 48 hours. Although in this dog model echocardiographic infarct size even as predicted by late (48 hours) wall motion abnormalities correlated poorly with pathologic infarct size,[45] subsequent studies demonstrated that the extent of regional contraction abnormalities on 2D echocardiography with early (20 minutes) or late (2 days) echocardiography after permanent coronary occlusion correlated well with infarct size.[46] Despite these seemingly disparate results, these early studies provided a mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 8 basis for clinical studies using echocardiography to measure the beneficial effects of pharmacologic interventions on infarct size.[47] [48] [49] [50] [51] Reperfusion Therapy, Myocardial Stunning, and Infarct Size Experimental studies have demonstrated that approximately 30 minutes following an acute coronary occlusion, a wavefront of myocardial necrosis begins to proceed from endocardium to epicardium, resulting in a transmural myocardial infarction over a period of 4 to 6 hours.[52] This observation, coupled with the work of DeWood et al,[53] who demonstrated that an acute coronary thrombosis was responsible for most acute myocardial infarctions, led to what is probably the major therapeutic advance in cardiology: the use of thrombolytic therapy or primary angioplasty for acute myocardial infarction. The theoretical basis for the use of early reperfusion is grounded in the work of early investigators in this field who showed that timely restoration of coronary flow (i.e., coronary reperfusion) salvages myocardium. However, improvement in flow had variable immediate effects on wall motion abnormalities, with most animals showing improvement but others showing no improvement or even worsening.[40] After reperfusion there is no significant correlation between infarct size and extent of regional dyskinesis or area of systolic wall thinning by 2D echocardiography after reperfusion performed up to 10 days after reperfusion.[46] [54] Thus, echocardiographic wall motion abnormalities as a predictor of infarct extent appeared to be more accurate following permanent occlusion than after occlusion with reperfusion. There are several plausible explanations for the lack of correlation between infarct size and regional wall motion abnormalities in reperfused myocardium. Most often echocardiographic assessment results in an overestimation of infarct size. After restoration of flow, there may be persistent postischemic dysfunction in viable myocardial segments, known as myocardial stunning. The pathophysiologic basis for this phenomenon is covered in several excellent reviews.[55] [56] [57] Wall motion abnormalities 2 weeks after reperfusion correlate better with infarct size, [54] which suggests that return of function of stunned myocardium may be significantly delayed. The rate at which reperfusion occurs also affects function, and it may be relevant in terms of the type of therapy chosen in the acute postinfarction period. In a canine model of infarction, sudden complete reperfusion resulted in increased wall thickness and slow return of function over a 7-day period, which is consistent with cell swelling and reperfusion injury (albeit reversible). In contrast, staged partial reperfusion (followed mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 8 by complete reperfusion) did not lead to an immediate increase in wall thickness, with functional recovery being seen as early as 30 minutes.[58] Thus, echocardiography early after a reperfused myocardial infarction (i.e., within 2 weeks) may overestimate the eventual area of necrosis because of stunning, reperfusion injury, or both. Infarct size also may be overestimated if the abnormal motion of infarcted myocardium impairs endocardial motion of adjacent normal myocardium owing to a "tethering" effect. [59] Alternately, the area of necrosis may be underestimated in the presence of a nontransmural infarction that subtends less than 25% of the wall thickness, with the salvaged normal subepicardial region resulting in overall normal segmental function.[60] In patients with old infarctions (>6 months), echocardiographic infarct size tends to underestimate the volume of necrosis when measured at autopsy.[61] In some cases, the ventricular remodeling process may be responsible for the change in the tendency from early (<2 weeks) overestimation to late (>6 months) underestimation of infarct size.[62] To identify postischemic ventricular dysfunction or "stunned myocardium," investigators have examined the effect of inotropic stimulation on the function of reperfused, noninfarcted myocardium and compared it with the effect on infarcted tissue. Serial 2D echocardiography during dopamine infusion demonstrates an increase in the contractility of the reperfused myocardium, with improvements in systolic wall thickening and fractional area change. This improvement in regional function is associated with an improvement in regional myocardial blood flow.[63] This study and others provided the experimental basis for the clinical use of dobutamine in detecting myocardial viability.[64] [65] [66] [67] [68] [69] Another echocardiographic method under investigation for determining myocardial viability is ultrasonic tissue characterization.[70] [71] [72] Nonischemic myocardium shows cyclic variation in the integrated backscatter, whereas in ischemic myocardium this variation is diminished or lost. MCE using sonicated iodinated contrast media identifies segments with persistent flow deficits despite reperfusion of the epicardial vessel. The areas of no reflow are believed to be due to microvascular damage and correspond to nonviable segments as identified by positron emission tomography and thallium scintigraphy.[73] MCE also can measure the extent of microvascular occlusion, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 8 254 which occurs after prolonged ischemia and prevents adequate reperfusion. [74] Infarct Localization Infarcts are localized both with respect to the transmural extent of the infarction (i.e., subendocardial versus transmural) and to the anatomic location as related to the coronary distribution of the infarct related artery. Small nontransmural (i.e., subendocardial) myocardial infarctions may not be detected as an abnormality in contractile function. The transmural extent of infarction and regional systolic function is inversely related to fractional radial shortening in both acute (6 hours after occlusion) and subacute (72 hours after occlusion) infarctions.[60] [75] [76] Fractional shortening continues to deteriorate as the percent of total wall (transmurally) involved increases from 75% to 100%, contradicting the work of others who suggested the subepicardial third of the myocardium contributed little to systolic wall thickening.[77] The circumferential extent of the infarction and, to a lesser extent, its longitudinal extent (i.e., base to apex) correlate with the distribution of the affected coronary artery.[78] [79] The anterior, anterolateral, anteroseptal, and apical (anterior and septal) segments correspond roughly to the left anterior descending artery (LAD) distribution. The lateral wall and lateral apex are in the distribution of the left circumflex. The inferolateral wall is supplied by the posterior descending artery. In 80% of the population, the posterior descending artery arises from the right coronary artery (RCA) and supplies the inferolateral wall as well as the inferior free wall and inferior septum (right dominant). In the other 20% of patients, the posterior descending artery arises from the circumflex artery (left dominant system). The right ventricle is supplied by the RCA via its acute marginal branches. In general, infarctions in the LAD distribution tend to be more apically situated, whereas those in the RCA and the circumflex distribution are more basal in their location. Moreover, the extent of apical involvement and its distribution depends, to a degree, on the relative supply from the left anterior and posterior descending arteries. Of course, the presence of collaterals and previous bypass surgery alters the distribution of ischemia and infarction relative to the involved arterial supply. The most commonly accepted method for analyzing wall motion uses the 16-segment model recommended by the American Society of Echocardiography[38] (Fig. 12- mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 8 1) , with the approximate and most common native coronary arterial distribution in relation to these segments depicted in Figure 12-2 . Experimental Models of Mitral Regurgitation Mitral regurgitation is common in the setting of acute myocardial infarction. Only |
recently have experimental studies elucidated the mechanism. These studies have demonstrated incomplete coaptation of the mitral valve leaflets owing to alteration of systolic left ventricular geometry Figure 12-1 The 16-segment model for segmental wall motion analysis recommended by the American Society of Echocardiography.[29] A, anterior; AL, anterolateral; AS, anteroseptal; I, inferior; IL, inferolateral; IS, inferoseptal; L, lateral; PSAX, parasternal short axis; S, septal; SAX, short axis. during ischemia.[80] [81] Infarction of a papillary muscle and the underlying ventricular myocardium results in incomplete leaflet coaptation owing to an increase in the distance from the point of mitral leaflet coaptation to the mitral annulus.[81] [82] Although the extent of the underlying wall motion abnormality may be small and left ventricular function may be globally preserved, papillary muscle ischemia alone is insufficient to cause mitral regurgitation. These studies are supported by the clinical observation that mitral regurgitation occurs in patients with ischemia or infarction of the inferolateral or posteromedial papillary muscle and a small area of underlying myocardium with otherwise well-preserved left ventricular function.[15] Incomplete leaflet coaptation also may occur as a result of severe global left ventricular dysfunction rather than localized papillary muscle dysfunction. [80] The proposed mechanisms contributing to malcoaptation of the leaflets in the setting of global ventricular dysfunction include a prolonged rate of rise of left ventricular pressure (i.e., Figure 12-2 Arterial distribution of blood flow superimposed on a parasternal short-axis view. LAD, left anterior descending; LCx, left circumflex; RCA, right coronary artery. 255 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 8 decreased dP/dt), with less force exerted on the mitral leaflets; poor systolic approximation of the left ventricular walls; mitral annular dilation; and malalignment of the papillary muscles owing to increased left ventricular end-diastolic volume. More recent data from a canine model using 3D echo-cardiography suggest that functional mitral regurgitation associated with left ventricular systolic dysfunction occurs only in the presence of left ventricular dilation.[83] Hemodynamically significant mitral regurgitation relates strongly to the 3D geometry of the mitral valve attachments at the papillary muscle and annular in the presence of left ventricular dilation (i.e., postpericardiectomy). Likewise, in vitro modeling studies demonstrated an integrated mechanism of regurgitation in which an altered balance between abnormal leaflet tethering and decreased coapting forces results in mitral incompetence.[84] Thus, hemodynamically significant mitral regurgitation is seen both in patients with small inferior myocardial infarctions and posteromedial papillary muscle involvement and in patients with large anterior infarctions, left ventricular dilation, and globally reduced systolic function. Infarct Healing and Remodeling Echocardiographic studies have contributed significantly to the understanding of infarct healing and the ventricular remodeling that takes place in the hours and days following an acute myocardial infarction. The importance of these phenomena are recognized in relation to the beneficial effects of delayed reperfusion and afterload reduction with angiotensin converting enzyme inhibitors that reduce infarct expansion and ventricular dilation. The concept of infarct expansion originated with the observation that the infarcted segment of myocardium thins and stretches with an increase in the circumferential extent of the necrotic zone (Fig. 12-3) (Figure Not Available) . The clinical observation that infarct expansion is associated with higher mortality, both early (in-hospital) and late after myocardial infarction, [85] [86] , [72] led to the postulate that the change in the topography of the infarcted zone increases the hemodynamic burden on the remaining normal walls, Figure 12-3 (Figure Not Available) Concept of infarct expansion. In the initial phase of the infarction (left), there is regional dilation and thinning limited to the infarcted region. Over time, in addition to further expansion of the area of infarct, there may be mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 8 compensatory dilation of the remaining ventricle (right). (Redrawn from Eaton LW, Weiss JL, Bulkley BH, et al: N Engl J Med 1979;300:57–62. Copyright 1979 Massachusetts Medical Society. All rights reserved.) resulting in ventricular dilation and hypertrophy.[85] [87] [88] Both clinical and experimental data suggest the following: 1. Expansion of the endocardial segment occurs as early as 10 minutes after occlusion.[89] 2. Infarct thinning and expansion are progressive over a period of 7 days. [88] 3. A critical mass of infarction (approximately 20% of total left ventricular mass) was required for expansion.[90] 4. Infarct expansion in the dog is more likely after LAD than after left circumflex occlusion.[89] 5. Infarct expansion led to aneurysm formation.[88] 6. The segment lengths of normal myocardium increase in the presence of infarct expansion, leading to ventricular dilation.[91] 7. Microvascular obstruction in infarcted tissue plays a role in remodeling by reducing local myocardial function, which contributes to the dysfunction of adjacent noninfarcted myocardium.[92] The clinical significance of infarct expansion is further emphasized by the demonstration of the beneficial effects of a patent infarct-related artery. [87] Histologic studies in a rat model of infarction demonstrated that reperfusion too late to salvage myocardium (no reduction in infarct size or transmurality) inhibits infarct expansion[93] and was associated with increased scar thickness.[94] Echocardiographic studies in dogs showed that delayed reperfusion of an infarct (as late as 5 to 6 hours after occlusion) acutely decreases the degree of infarct thinning and ventricular dilation.[95] [96] Although delayed reperfusion may convert a bland infarct into a hemorrhagic infarct and may increase the risk of myocardial rupture slightly, many clinical studies support the concept that an open artery provides substantial benefit, possibly through decreased left ventricular dilation and aneurysm formation and, as a corollary, a decreased incidence of arrhythmias and a lower mortality.[87] [97] The time course of left ventricular remodeling following successful reperfusion in acute myocardial infarction is suggested by a 2D echocardiographic study that showed progressive infarct thinning for up to 1 month and left ventricular dilation for up to 14 days. The degree of remodeling as reflected in left ventricular volume was greatest in the patients with the largest infarcts (peak creatine kinase > 8000 U/L). Despite the progressive remodeling, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 8 wall motion score improved rapidly by 14 days, and it continued to improve gradually to 1 year. [98] Vasodilator therapy, theoretically through a reduction of left ventricular wall stress, influences post–myocardial infarction remodeling and improves prognosis. The salutary effects of treatment with angiotensin converting enzyme inhibitors, first shown in a rat model by Pfeffer et al,[99] [100] include attenuation of left ventricular dilation, improved left ventricular performance with a downward shift of the pressure-volume curve and higher ejection fraction, and improved long-term survival. These findings were subsequently confirmed in post–myocardial infarction patients with left ventricular dysfunction in the Survival and Ventricular Enlargement (SAVE) trial. Two canine studies using echocardiographic measurements have shown that nitrates and enalapril had similar beneficial effects on the remodeling process.[101] [102] The Carvedilol Heart Attack Pilot Study (CHAPS) demonstrated 256 attenuation of left ventricular remodeling with postinfarction administration of carvedilol. Echocardiography at baseline and after 3 months of treatment showed reduced left ventricular volumes and sphericity (long-axis–to– short-axis ratio).[103] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/104.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 10 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Echocardiography in the Diagnosis and Early Risk Stratification of Acute Myocardial Infarction Transferring the experience from the animal laboratory into the CCU, clinical investigators have confirmed the usefulness of echocardiography in diagnosis, localization, prognostic staging, and detecting of complications of myocardial infarction. Diagnostic Role of Echocardiography For an imaging modality to be useful in the diagnosis of myocardial infarction, it must be feasible in the majority of patients. Images of the left ventricle adequate for segmental analysis of wall motion can be obtained in greater than 90% of patients by skilled sonographers.[104] [105] [106] Tissue harmonic imaging and left-sided contrast agents have increased the percentage of patients in whom technically adequate images can be obtained.[107] [108] [109] In one study of segmental and global function in 70 critically ill patients, the number of uninterpretable segments fell from 5.4 with fundamental (standard) imaging to 4.4 with harmonic imaging and finally to 1.1 with a left-sided contrast agent. In addition, the usefulness of the modality is directly related to its sensitivity and specificity and to the prevalence of the disease in the population studied. The accuracy of an echocardiographic diagnosis of a myocardial infarction is dependent on echocardiography's ability to detect wall motion abnormalities in the involved segment. As shown in the animal laboratory, the severity of the wall motion abnormality depends on the transmural extent of the infarction and the circumferential limits depend on the arterial distribution and collateral blood supply. In considering the specificity of wall motion abnormalities for diagnosis of acute myocardial infarction, other causes of segmental dysfunction must be recognized. A false-positive diagnosis can often be avoided if wall mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 10 thickening is examined in addition to endocardial motion. The inward motion of the endocardial surface may be delayed or paradoxical owing to abnormal conduction in the presence of Wolff-Parkinson-White syndrome, [110] a left bundle branch block,[111] or right ventricular pacing. [112] Paradoxical septal motion also is present in right ventricular volume overload and following open heart surgery.[113] [114] In these conditions, the systolic thickening of the septum or other involved segment (e.g., posterolateral wall in Wolff-Parkinson-White syndrome, type A) should be preserved.[115] Nonischemic causes of segmental dysfunction that result in reduced systolic thickening and endocardial motion include focal myocarditis[116] and idiopathic cardiomyopathy. Several studies that have examined the specificity of echocardiographic wall motion abnormalities for diagnosis of acute myocardial infarction are worth noting. Among 65 patients presenting to the emergency room with chest pain, there were 5 false-positive echocardiograms, demonstrating regional asynergy in patients without infarction for a specificity of 85%.[117] In a more recent study by Peels et al[118] of 43 patients with chest pain and normal or nondiagnostic electrocardiogram, the specificity of echocardiographic wall motion abnormalities was 78% for ischemia and only 53% for infarction. The apparent discrepancy between the two studies is probably due to differences in prevalence of disease in the population studied. Sabia et al[105] used echocardiography to study 202 patients presenting to the emergency room with acute shortness of breath or chest pain. Of the 140 patients who were ruled out for myocardial infarction, 60 had regional wall motion abnormalities detected by echocardiography. Of those patients, 52% (31 of 60) had had a prior infarction and 53% (32 of 60) were found to have evidence of coronary artery disease on subsequent testing. Although the development of electrocardiographic Q waves is usually associated with a transmural infarction, the absence of Q waves does not always signify a nontransmural or subendocardial infarction.[119] Non–Q- wave infarctions are usually smaller, are associated with smaller enzyme leaks,[120] and more often are in the distribution of the left circumflex artery. [121] Two-dimensional echocardiographic evidence of a wall motion abnormality is present in 90% to 100% of patients with Q-wave infarctions [117] [122] [123] [124] compared with 75% to 85% in patients with non–Q-wave infarctions.[104] [114] [117] , [123] [124] [125] The most widely used scoring system for grading the severity of a wall mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 10 motion abnormality is that recommended by the American Society of Echocardiography, in which normal = 1, hypokinesis = 2, akinesis = 3, dyskinesis = 4, and aneurysm = 5[38] (Table 12-1) . Unlike other published scales,[106] hyperkinesis is not distinguished from normal contraction. Weiss et al[124] demonstrated that the finding of akinesis or dyskinesis is most common in the setting of transmural infarction, with milder degrees of wall motion abnormalities (i.e., hypokinesis) most likely representing nontransmural infarction or ischemia. Localization of Infarction Clinical studies have documented the accuracy of echocardiography in identifying the site of coronary occlusion. Echocardiographic localization has significant advantages TABLE 12-1 -- Scoring System for Grading Wall Motion[38] Score Wall Motion Endocardial Motion * Wall Thickening * 1 Normal Normal Normal (>30%) 2 Hypokinesis Reduced Reduced (<30%) 3 Akinesis Absent Absent 4 Dyskinesis Outward Thinning 5 Aneurysmal Diastolic deformity Absent or thinning *In |
systole. 257 over electrocardiographic localization, particularly for apical and lateral wall myocardial infarctions. Pierard et al[126] correlated echocardiographic infarct location with the site of coronary obstruction by coronary angiography in 45 patients and by necropsy in 4 patients. They assigned specific segments to the major coronary branches and found the following sensitivities: basal anterior = first diagonal (LAD, 71%) basal anteroseptal = first septal perforator (LAD, 83 middle anterior = second diagonal (LAD, 100%) mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 10 middle anteroseptal = second septal (LAD, 89%) basal posteroseptal = dominant RCA (89%) right ventricular anterolateral segment = right ventr ular marginal branch (83%) Ogawa et al[127] analyzed the location of echocardiographic wall motion abnormalities, electrocardiographic Q wave, and angiographic site of coronary artery occlusion in 26 patients with single-vessel disease. Inferior Q waves (II, III, and aVF) were associated with mid-inferior wall motion abnormalities. Furthermore, extension to the inferior septum correlated with RCA disease, whereas extension to the inferolateral wall correlated with circumflex coronary disease. A tall R wave in V was associated with 1 posterolateral wall motion abnormalities and a coronary lesion of the proximal circumflex artery. Electrocardiographic evidence of lateral infarction (Q in lead I or aVL) correlated with wall motion abnormalities of the inferolateral and anterolateral walls and disease in the circumflex system involving a large obtuse marginal branch. Circumflex disease also was associated with the presence of a Q wave in V and dyssynergy of the 6 lateral and inferior apical walls.[127] These studies did not compare echocardiographic to electrocardiographic localization of infarction. However, a study by Otto et al[106] suggested that imaging may be more precise, with an 81% concordance between echocardiography and angiography compared with 76% for electrocardiography.[106] Thus, the use of echocardiography to identify the region of segmental dyssynergy in the patient presenting with a myocardial infarction is clinically accurate in determining the site of coronary occlusion (Table 12-2) . One caveat is that the presence of pre-existing wall motion abnormalities and surgical grafts or collateral circulation altering the distribution of flow must be taken into account. Right Ventricular Infarction Right ventricular infarction (Table 12-3) occurs in up to one third of patients with inferior wall infarction and is seen rarely in patients with anterior infarction. The right ventricle is predominantly supplied by acute marginal branches of the RCA that arise in the middle third of its anatomic course. Occlusion of the RCA proximal to the origin of these branches results in ischemia and usually infarction of the right ventricle. Much less frequently, the right ventricle receives blood supply from a dominant left circumflex artery. In addition, the anterior apex of the right ventricle may mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 10 be supplied by the LAD "wrapping" around the apex of the heart. TABLE 12-2 -- Coronary Distribution Associated with Echocardiographic Segments Echocardiographic Segment Coronary Artery Supply * Base Anterior septum Proximal LAD Anterior Proximal LAD Anterolateral Proximal LAD (LCx) Inferolateral LCx Inferior RCA Inferior septum RCA Mid Anterior septum Mid LAD Anterior Mid LAD Anterolateral Mid LAD (LCx) Inferolateral LCx Inferior RCA Inferior septum RCA Apex Anterior Distal LAD Lateral Distal LAD Septum Distal LAD Inferior PDA (LAD) LAD, left anterior descending artery; LCx, left circumflex artery; PDA, posterior descending artery; RCA, right coronary artery. *Coronary distribution is variable in the presence of revascularization. The hemodynamic consequences of right ventricular infarction were first recognized in the mid-1970s with several descriptions of the associated mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 10 clinical syndrome appearing simultaneously in the literature.[128] [129] Using gated scintigraphy, detectable right ventricular dyssynergy was reported by other investigators shortly thereafter.[130] [131] In one of these reports, Sharpe et al[112] also described the M-mode echocardiographic finding of right ventricular infarction. In 6 patients, they found evidence of right ventricular enlargement and paradoxical septal motion correlating with the scintigraphic and hemodynamic findings. Isner and Roberts[132] reported the incidence of right ventricular infarction in 236 necropsy specimens of acute and chronic infarctions. In their series, none of the 97 patients with pathologic evidence of an isolated anterior wall myocardial infarction had right ventricular involvement. In contrast, the incidence of right ventricular involvement in patients with infarction involving the posterior wall was 24% (33 of 139). Specifically, all of the right ventricular infarcts, which were confined to the posterior portion of the right ventricular free wall, TABLE 12-3 -- Echocardiographic Signs of Right Ventricular Infarction PRIMARY Right ventricular dilation Segmental wall motion abnormality of the right ventricular free wall Decreased descent of the right ventricular base SECONDARY Paradoxical septal motion Tricuspid regurgitation Tricuspid papillary muscle rupture Pulmonary regurgitant jet pressure half-time ≤150 msec Dilated inferior vena cava Right-to-left interatrial septal bowing Right-to-left shunting across patent foramen ovale 258 occurred in the 65 specimens with transmural infarction involving the posterior septum (33 of 65, or 50%). A subsequent pathologic study described that infarction of the right ventricular anterior free wall occasionally can be contiguous with an extensive anteroseptal infarction.[133] The diagnosis of right ventricular infarction should be suspected in a mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 10 patient with evidence of jugular venous distention and clear lung fields in the setting of an inferior myocardial infarction. Although the electrocardiographic sign of ST segment elevation in V4R is both sensitive and specific for the diagnosis,[134] it does not provide information as to the extent of involvement. The 2D echocardiographic signs of right ventricular infarction include right ventricular dilation, decreased right ventricular function, segmental wall motion abnormalities, and paradoxical septal motion (Fig. 12-4) .[135] Quantitative measurement of right ventricular ejection fraction by echocardiography is difficult because of the lack of an adequate geometric model for calculation of volumes; instead, fractional area change and descent of the right ventricular base are commonly used measures of right ventricular function. Right ventricular failure with high right atrial pressures results in bowing of the interatrial septum into the left atrium and dilation of the inferior vena cava with lack of inspiratory collapse.[136] Echocardiographic indicators of right ventricular function correlate with clinical status and prognosis. Goldberger et al[136] compared the echocardiographic characteristics in patients with hemodynamically significant infarction (jugular venous pressure [JVP] > 13 mm Hg; n = 9) with those without (JVP < 13; n = 15). There was no difference in the frequency of detectable wall motion abnormalities between the two groups (77% versus 66%). However, the group with higher estimated JVP had less descent of the base (.7 cm versus 1.3 cm); less inspiratory collapse of the inferior vena cava (22% versus 45%) and a greater right-to-left ventricular size ratio (1.1 versus 0.6). The pressure half-time of the pulmonary regurgitant jet reflects the compliance of the right ventricular Figure 12-4 Four-chamber view of an echocardiogram from a patient after an inferior infarction with right ventricular involvement. There is enlargement of the right ventricle (RV) and right atrium (RA). The left ventricle (LV) appears small and the interatrial septum is deviated from right to left, suggesting elevated right atrial and right ventricular end- diastolic pressures. chamber. In a recent study, a short pressure half-time of the pulmonary regurgitant jet (<150 msec) in patients with right ventricular infarction was the only predictor of in-hospital events.[137] Thrombolytic therapy has been proved efficacious in right ventricular infarction, and echocardiographic features correlate with effective revascularization. In a recent study of 108 consecutive patients with a right ventricular infarction, there was a 78% mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 10 correlation between Thrombolysis in Myocardial Infarction (TIMI) grade III perfusion in and normalization or improvement of right ventricular function by echocardiography.[138] Interatrial septal motion and interventricular septal motion normalized in all reperfused patients. The major complication rate and mortality were higher in patients with echocardiographic findings of right ventricular dysfunction persisting after thrombolytic therapy.[138] Two other complications associated with right ventricular infarction deserve mention. First, papillary muscle dysfunction associated with ischemia and right ventricular dilation may result in functional tricuspid regurgitation. Rarely, papillary muscle rupture may involve the tricuspid valve. Second, severe hypoxemia owing to right-to-left shunting across a patent foramen ovale has been reported with large right ventricular infarctions in association with elevated right atrial pressures. [139] Echocardiography for Prediction of Early Mortality Using echocardiography in the setting of acute myocardial infarction, clinical investigators have identified several important prognostic indices: (1) the extent of the wall motion abnormalities within the infarct zone; (2) the degree of infarct expansion and ventricular dilation; and (3) the presence of wall motion abnormalities outside the infarct zone (i.e., infarct extension). The importance of diastolic function as a prognostic indicator is discussed later. An echocardiographic wall motion score has been the most widely used measure of functional infarct size in clinical practice. The total score is derived by assigning a grade of 1 through 5 (see Table 12-1) to each myocardial segment that is adequately visualized. For a segment to be scored, the majority of the endocardium within that segment must be apparent, and wall thickening and endocardial motion should be examined. The scores for each segment are added and then divided by the number of segments graded for a total wall motion score. Several studies have demonstrated that a higher wall motion score index (12 to 24 hours after admission) is associated with a higher rate of in-hospital complications, including malignant arrhythmias, pump failure, and death.[104] [140] A higher wall motion score index also predicts a higher rate of complications, including free wall rupture, ventricular septal defect or papillary muscle rupture, and death from cardiogenic shock.[140] A higher wall motion score, signifying a more extensive infarction, also is predictive of late mortality. [140] [141] In reviewing the literature on this subject, it is important to mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 10 recognize that many different scoring systems have been described, with consequent variability 259 in the absolute number of the wall motion score index associated with a poor prognosis. Infarct expansion is defined as an increase in the endocardial surface area of the infarcted zone owing to thinning and stretching secondary to necrosis and scar tissue formation. A landmark study in 1979 used serial 2D echocardiography to study 28 patients in the first 2 weeks after myocardial infarction. In eight patients, all with anterior infarctions, there was a progressive increase in the endocardial length of the infarcted segment and progressive ventricular dilation. In the group without infarct expansion (9 inferior myocardial infarction patients, 11 anterior myocardial infarction patients), there was little or no dilation. Although the number of patients in each group was too small from which to draw firm conclusions, the group with infarct expansion had a higher mortality rate (50%) compared with the group without expansion (0%). Other clinical studies have suggested that this mechanism contributes to congestive heart failure and poor functional status after infarction.[142] Later studies in the era of reperfusion confirm that infarct expansion is more common in anterior infarctions, but they suggest that most of the dilation is present by 3 hours.[143] Wall motion abnormalities remote from the infarction site may be present early in the course of the infarction or may develop in the presence of postinfarction angina, suggesting de novo ischemia. The echocardiographic finding of remote asynergy at or soon after clinical presentation is strong evidence of multivessel disease. Abnormal wall motion in a second (or even third) coronary distribution is possibly due to (1) previous infarction, (2) increased myocardial oxygen demands placed on the noninfarcted segment as a result of increased wall stress outstripping its oxygen supply, (3) a cessation in its collateral blood supply that originated from the newly occluded vessel, or (4) simultaneous infarctions in multiple coronary beds, the least likely cause.[144] Infarct extension results from the development of ischemia and infarction in a region remote from the original site after the initial event. Postinfarction angina with electrocardiographic changes distant from the acute infarct (i.e., "ischemia at a distance") is associated with a worse mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 10 prognosis than ischemia within the infarct zone.[145] Although early observations were based on electrocardiographic evidence alone, more recent echocardiographic investigations show similar results.[125] [145] [146] Isaacsohn et al[146] performed echocardiography during 19 episodes of postinfarction ischemia. Echocardiographic extension was detected in seven of nine episodes with clinical evidence of extension (recurrent chest pain, |
new increase in creatinine kinase level, or new electrocardiographic changes). The in-hospital mortality rate was significantly greater in those with echocardiographic evidence of infarct extension (50% versus 12%) and was poorest in those with a high wall motion score. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/105.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 20 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Detecting Complications of Acute Myocardial Infarction The prognosis of myocardial infarction is directly related to the extent of necrosis (Table 12-4) . A large TABLE 12-4 -- Echocardiography in Complications of Myocardial Infarction HEMODYNAMIC STATES Hypovolemia Right ventricular infarction Globally reduced left ventricular contractility MECHANICAL COMPLICATIONS Papillary muscle rupture Ventricular septal rupture Free wall rupture and tamponade OTHER Left ventricular aneurysm Mural thrombus infarction encompassing greater than 40% of the heart is likely to result in severe pump failure. Transmural infarction is more likely to result in complications related to rupture, occurring in up to 3% of patients. Thus, in the hemodynamically unstable patient, it is critical to exclude rupture, a situation that is potentially amenable to surgery, before concluding that cardiogenic shock is on the basis of pump failure. In most cases, TTE (supplemented when necessary by TEE) is sufficient to exclude papillary muscle, free wall, and ventricular septal ruptures. Hemodynamic Classification of Myocardial Infarction Using Doppler Echocardiography mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 20 A carefully performed Doppler echocardiographic study can provide sufficient information to determine a patient's hemodynamic category after infarction. A hemodynamic classification on the basis of these well-studied parameters is given in Table 12-5 . A simple method of estimating stroke volume is to measure the stroke distance, that is, the velocity time integral (VTI) of aortic flow by pulsed wave or continuous wave Doppler. Although continuous wave Doppler measurements are more reproducible, they can be used only in patients with normal semilunar valves; even a mild degree of stenosis increases the VTI. At a heart rate of 70 to 80 beats per minute, the normal stroke distance is 13 to 15 cm for the pulmonary artery and 18 to 20 cm for the aorta.[147] [148] Stroke distance varies inversely with heart rate, but it holds constant over a wide range of body surface areas.[149] This method eliminates the error in cardiac output measurements introduced by estimating the cross-sectional area of the orifice. Moreover, stroke distance measurements are simple to measure online. Recently, automated cardiac output measurements, based on the digital velocities from color flow mapping, have become available on some systems.[150] A more detailed discussion of Doppler measurements of cardiac output is found in Chapter 26 . Mitral inflow, measured at the tips of the leaflets in the four-chamber view, is informative with regard to diastolic function and left ventricular filling pressures.[151] Derived parameters of the time velocity curve include the ratio of peak early filling velocity to atrial filling velocity (E/A 260 TABLE 12-5 -- Hemodynamic Classification of Myocardial Infarction * by Echocardiography Pulmonary PASP Hemodynamic LVOT Mitral Venous (TR Category LVEF RVEF VTI E/A Flow velocity) IV Normal Nl Nl 20 A wave S > D † Nl N cm dom † Hyperdynamic Nl to Nl >20 A wave S > D † Nl to N incr cm dom † slight incr Hypovolemia Variable Nl <20 A wave S > D † Nl to Sm mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 20 cm dom † decr sp co LV Failure Mild Mild Nl to Mild E wave S > D Mild N decr decr decr dom incr pl Severe Mod Nl to Mod E wave S < < D Mod N decr decr decr dom incr pl Cardiogenic Severe Nl to Sev E wave S < < D Mod N shock decr decr decr dom incr pl RV infarction Variable Decr Decr A wave S < D † Decr Se ‡ dom † pl w co MR Nl to Nl to Decr E wave SFR Incr N incr decr dom pl VSD Nl to Nl to Decr Variable S > D Incr N incr decr pl decr, decreased; D, diastolic; dom, dominant; E/A, ratio of early to late (a ventricular diastolic inflow velocity; incr, increased; IVC, inferior vena cava left ventricular ejection fraction; LVOT, left ventricular outflow tract; Mod, MR, mitral regurgitation; Nl, normal; PASP, pulmonary artery systolic pres right ventricular; RVEF, right ventricular ejection fraction; S, systolic; SFR flow reversal; TR, tricuspid regurgitation; VSD, ventricular septal defect; V velocity time integral; w/o, without. *As described by Pasternak, Braunwald, and Sobol.[162] †In the infarction age group. ‡Dependent on extent of LV infarction. ratio), the deceleration time of early filling curve and the isovolemic relaxation time. Two distinct patterns of inflow reflect the two categories of diastolic dysfunction: impaired left ventricular relaxation and decreased left ventricular compliance. Impaired relaxation is characterized by a decreased E/A ratio and prolonged deceleration and isovolumic relaxation times; this pattern is encountered in chronic ischemic heart disease and hypertension and as a result of normal aging. The restrictive flow pattern noted under mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 20 conditions of diminished left ventricular compliance demonstrates an increased E/A ratio and shortened isovolumic relaxation and deceleration times. This inflow pattern occurs in restrictive cardiomyopathies and in association with elevated filling pressures. An intermediate stage of diastolic function is present with "pseudonormalization" of the mitral filling pattern, usually associated with a moderate elevation of filling pressures. In a recent study of postinfarction patients with left ventricular ejection fraction less than 35%, a mitral deceleration time of less than 120 msec was highly predictive of a pulmonary capillary wedge pressure of greater than 20 mm Hg[152] (Fig. 12-5) . In a second study of patients with systolic dysfunction after infarction (ejection fraction >40%), there was an increased rate of adverse events in two years of follow-up in patients with higher mitral E/A ratios and shorter deceleration times.[153] This finding has been confirmed in subsequent studies[11] [154] [155] (Table 12-6) . Several new parameters of diastolic function have been studied in postinfarction patients. The deceleration time of the diastolic component of pulmonary venous flow has a better correlation with wedge pressure in post patients with myocardial infarction than does the mitral deceleration time. The sensitivity and specificity of a pulmonary venous deceleration time less than 160 msec in predicting greater than or equal to 18 mm Hg in pulmonary capillary Figure 12-5 Mitral inflow signal from a patient with a large anterior myocardial infarction. There is an increased E wave velocity and a shortened deceleration time. The deceleration time was measured between the two arrows as 80 msec. This measurement is evidence of elevated filling pressures and is a poor prognostic sign (see text). 261 TABLE 12-6 -- The Role of Diastolic Functional Parameters in Prognosis After Myocardial Infarction Reference n Comment Pozzoli et 107 Patients with cardiac events had significantly higher E/A al[153] ratios and shorter mitral deceleration time Sakata et 206 Decreased A wave was associated with high in-hospital al[154] mortality and congestive heart failure mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 20 Nijland et 95 1-yr survival rate: restrictive filling, 50%; nonrestrictive al[155] filling, 100% Moller et 110 Deceleration time < 140 msec was the most powerful al[11] predictor of cardiac death Total 518 - wedge pressure were 97% and 96%, respectively, compared with 86% and 59%, respectively, for a mitral deceleration time of less than 130 msec.[156] The propagation velocity of mitral inflow measured on M-mode color Doppler echocardiography also has prognostic significance.[11] Technically adequate pulmonary venous flow tracings can be obtained in the majority of patients with surface echocardiography. The predominant pulmonary venous flow pattern is triphasic, with the initial systolic (S) forward flow in pulmonary veins occurring during atrial relaxation (x- descent), a second systolic phase coinciding with basal descent of the left ventricle, and forward flow during diastole (D) occurring in the conduit phase of ventricular filling while the mitral valve is open (y-descent). During atrial systole there is a low-velocity retrograde flow signal (A wave). In subjects older than 40 years of age with normal filling pressures, the peak velocities and VTIs are higher during systole than during diastole, and the duration of the pulmonary venous A wave is less than that of the mitral A wave. With high filling pressures, diastolic filling predominates and the A wave duration exceeds that of the mitral A wave.[110] [157] [158] In patients with acute myocardial infarction, a systolic fraction of pulmonary venous flow less than 45% was highly associated with a pulmonary capillary wedge pressure greater than 18 mm Hg.[150] Additionally, systolic flow reversal in the pulmonary veins is an important sign of hemodynamically significant mitral regurgitation.[159] Measurements of pulmonary artery systolic pressure using tricuspid regurgitant jets with or without contrast enhancement have been well validated in the literature,[160] and the size and respiratory dynamics of the inferior vena cava can be used to estimate right atrial pressure. [161] Combining these parameters with measurements (quantitative or qualitative) of left and right ventricular function and color flow Doppler interrogation for valvular abnormalities results in a comprehensive evaluation of the hemodynamic state after infarction as defined by mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 20 Pasternak, Braunwald, and Sobel[162] using invasive data. A recent study found that a combination of automated Doppler cardiac output and pulmonary venous flow measurements was highly accurate in predicting the hemodynamic subset as measured invasively.[150] When the data are incomplete from a transthoracic examination, one should not hesitate to employ TEE given its established safety even in the critically ill patient. Of course, the hemodynamic information available from an echocardiographic examination is available only at a single point in time, and continued invasive monitoring may be necessary in patients with ongoing instability. Recurrent Ischemia After Infarction Although there have been few studies evaluating the usefulness of echocardiography in patients with recurrent ischemia after myocardial infarction, many clinicians rely on echocardiographic evaluation in this setting, given the sensitivity of this technique for detection of wall motion abnormalities. Worsening of wall motion after initial improvement suggests reocclusion of the infarct-related vessel. Wall motion abnormalities in regions remote from the area of infarction suggest multivessel disease.[146] In addition, alternative causes for chest pain after myocardial infarction (e.g., pericarditis) may be evident on echocardiographic examination. Postinfarction Pericarditis and Pericardial Effusion Postinfarction pericarditis most often occurs after a Q-wave infarction between 3 and 10 days following the myocardial infarction. Onset after 10 days is usually considered Dressler's syndrome. Chest pain caused by pericarditis typically is pleuritic and is accompanied by the auscultatory finding of a pericardial friction rub. Although a pericardial effusion is very common after infarction, it is not pathognomonic of pericarditis. Several investigators have reported on the incidence of pericardial effusion following infarction,[163] [164] [165] [166] [167] as summarized in Table 12-7 . In all the studies reviewed, pericardial effusion was associated with larger infarctions as measured by wall motion scores[163] [166] or degree of creatine kinase elevation.[164] [166] The TABLE 12-7 -- Incidence of Pericardial Effusion After Infarction No. of No. with Study Patients Effusion (%) Comments Pierard et al[166] 66 17 (26) Anterior > inferior Galve et al[165] 138 39 (28) Anterior > inferior mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 20 Peaked on 3rd day Charlap et al 172 30 (17) Echo at 72 hr [164] Sugiura et al 185 44 (24) Inferior MIs only; higher [163] incidence with RV infarct Widimsky and 192 82 (43) Peaked 5th day; CHF or Gregor[167] death more common; no increase with thrombolysis or heparin CHF, congestive heart failure; MI, myocardial infarction; RV, right ventricular. 262 incidence of congestive heart failure and mortality is higher in those patients with effusions apparent on echocardiography.[167] In almost all cases the effusions are small and hemodynamically insignificant. Thus, the effusion did not cause the increase in morbidity and mortality but serves as yet another marker of a large |
infarction. Mitral Regurgitation Ischemic mitral regurgitation can be defined as valvular incompetence associated with myocardial ischemia or infarction in the absence of primary leaflet or chordal pathology (Fig. 12-6) . Acute mitral valve incompetence may occur in the setting of myocardial infarction owing to necrosis and rupture of papillary muscle tissue or incomplete coaptation of the mitral valve leaflets owing to distortion of ventricular architecture. Mitral regurgitation is common in the setting of acute myocardial infarction, with a reported incidence rate between 10% and 50%. Of almost 12,000 postinfarction patients catheterized at Duke University, 19% had evidence of mitral regurgitation by angiography.[168] [169] Hemodynamically significant mitral regurgitation occurs equally in anterior and inferior infarcts. Risk factors for significant postinfarction mitral regurgitation include advanced age, female gender, diabetes, and prior infarction.[170] [171] In patients with myocardial infarction, moderate to severe mitral regurgitation is associated with substantially reduced short- and long-term survival, with up to a 24% early and 54% 1-year mortality rate.[171] [142] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 20 Severe postinfarction mitral regurgitation also is an independent risk factor for coronary artery bypass surgery operative mortality. [168] Moreover, in patients presenting to the emergency room with chest pain, moderate or severe Figure 12-6 (color plate.) Mitral regurgitation in a patient with an inferior myocardial infarction and resultant inferobasal aneurysm. A, Diastolic deformity in this apical two-chamber view (arrow). B, Lack of thickening in this region during systole (arrow). C, Moderately severe mitral regurgitation (double arrow). mitral regurgitation by echocardiography was associated with high risk for overall and cardiovascular mortality (risk ratio = 2.0).[172] Among these patients, only 60% had audible murmurs. The clinical recognition of mitral regurgitation in the setting of myocardial infarction may be confounded by several variables. Up to 50% of patients with hemodynamically significant mitral regurgitation do not have an audible murmur owing to rapid equalization of left ventricular and left atrial pressures (especially in a low output state) or because the murmur is obscured by lung sounds in a patient with pulmonary edema or mechanical ventilation.[171] In view of the adverse prognosis, early diagnosis is desirable to institute medical or surgical interventions that potentially improve outcome. Although some authors have advocated TTE in all patients admitted with myocardial infarction, this approach is probably not cost- effective. However, echocardiography is mandatory in the postinfarction patient with a new systolic murmur, pulmonary edema, or sudden cardiac decompensation. In this situation, TTE is 100% sensitive in detecting mitral regurgitation and in distinguishing mitral regurgitation from ventricular septal defect.[173] Detection and grading of mitral regurgitation is accomplished with 2D, M- mode, color, and spectral Doppler techniques. Two-dimensional imaging detects abnormalities in the mitral valve apparatus, including flail leaflets or ruptured chordae. Although color flow parameters are those most often used, accurate grading of mitral regurgitation severity should encompass other echo-Doppler signs as well.[174] [175] In the patient with pulmonary edema, the unexpected findings of a small infarction, a hyperdynamic left ventricle, increased early mitral inflow velocity, or all three [176] should prompt a careful search for mitral regurgitation even when color flow Doppler mapping is unrevealing. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 20 263 Papillary muscle necrosis with rupture and a flail leaflet is a life-threatening complication of myocardial infarction that requires surgical intervention. The more frequent involvement of the posteromedial papillary muscle is thought to be due to its blood supply from a single coronary artery. Chordae to both leaflets arise from each of the papillary muscles so that in cases of "complete" rupture of the entire trunk of a papillary muscle, both leaflets are affected. In less severe cases, the rupture is "incomplete" and only a single head is torn. The 2D echocardiographic findings include prolapse of one or both leaflets, a flail leaflet, and liberation of a portion of the papillary muscle.[177] In some patients, the ruptured muscle may remain tethered to the chordae and chaotic motion is not present. Spectral and color flow Doppler imaging of the jet is usually easily accomplished with surface imaging, but an eccentric path of flow may complicate its identification. In our experience, TEE is superior in this regard,[36] supported by multiple case reports in the literature[16] [19] [21] (Fig. 12-7) . When only a single head of the papillary muscle is affected (incomplete rupture), medical stabilization often is possible. Initial treatment should include afterload reduction with diuretics, angiotensin converting inhibitors, nitroprusside, and (in cases of severe cardiac decompensation) inotropic support and intra-aortic balloon pump. When rupture is complete, involving the main trunk of the papillary muscle, the complication is uniformly fatal without immediate recognition and prompt repair.[177] [178] In the other forms of ischemic mitral regurgitation, reperfusion therapy with thrombolytics or angioplasty should be considered first-line therapy because reperfusion may improve regurgitant severity and patient prognosis. Coronary bypass in conjunction with mitral valve surgery should be considered in patients who show benefit from medical therapy or nonsurgical revascularization. Coronary bypass with mitral valve surgery is necessary in patients who develop circulatory collapse as a result of mitral regurgitation, despite the relatively high operative mortality in this patient group. In those patients who receive surgery for severe ischemic mitral regurgitation, there is evidence that early surgery, concomitant revascularization, and repair, rather than replacement, improve survival.[179] [180] In the recent SHOCK trial (SHould we use emergently revascularized Occluded Coronaries in cardiogenic shocK?), the survival rate in patients with mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 20 Figure 12-7 (color plate.) Transesophageal echocardiogram of a patient with papillary muscle rupture after an acute inferior myocardial infarction. The papillary muscle rupture was incomplete and the head of the papillary muscle remained tethered to the mitral chordae. A, The triangular density representing the head of the papillary muscle (arrow) can be seen within the body of the left ventricle during systole. B, Associated severe mitral regurgitation with a prominent area of proximal isovelocity surface acceleration (double arrow). acute severe mitral regurgitation who underwent surgery (40%) was higher than in those treated medically (71%, P < .003).[181] Ventricular Septal Rupture Ventricular septal defect owing to myocardial rupture complicates 1% to 3% of all acute myocardial infarctions and up to 5% of all fatal infarctions. In the GUSTO-1 trial (Global Utilization of Streptokinase and TPA for Occluded coronary arteries), the incidence of ventricular septal rupture was only 0.2% (84 of 41,021 enrolled patients), suggesting that thrombolytic therapy has reduced the incidence of rupture.[182] Ruptures occur only in the presence of transmural infarction and result from hemorrhage within the necrotic zone. Independent risk factors for the development of a ventricular septal defect are similar to those for papillary muscle rupture and include first infarction, advanced age (>65), hypertension, and female gender.[183] [184] There appears to be a higher incidence in patients without a history of prior angina and with infarcts in the distribution of a single vessel.[183] [184] [185] Thus, septal rupture appears to be more likely following abrupt occlusion of a single artery that vascularizes a territory for which there is little collateral flow.[184] Unlike papillary muscle rupture, ventricular septal rupture occurs with equal frequency among patients with anterior (LAD) and inferior (RCA) infarctions but less frequently in those with lateral (left circumflex artery) infarctions.[186] Conflicting evidence exists as to the effect of thrombolytic therapy on the development and outcome of postinfarction ventricular septal defect. Thrombolytic administration that is delayed more than 12 hours following the onset of chest pain may increase the incidence of ventricular septal rupture.[97] However, in most cases the slight increase in the risk of rupture is outweighed by the overall benefit of reperfusion therapy. In the GUSTO- 1 study, the onset of rupture was earlier on average (1 day) than that reported previously, suggesting that although thrombolytic therapy reduced the rate of rupture, it tended to occur earlier after thrombolysis. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 20 Ventricular septal defects usually present 3 to 6 days after infarction with recurrent chest pain, dyspnea, and sudden hypotension or shock. A new harsh pansystolic murmur is present in approximately 50% of patients. Bedside 264 echocardiography has been demonstrated to be highly sensitive and specific in the diagnosis of ventricular septal defect. The defect can be visualized by transthoracic 2D imaging in 40% to 70% of patients.[177] [187] The use of contrast and color flow Doppler imaging improves the sensitivity to 86% and 95%, respectively.[21] [97] [173] [177] When TTE is suboptimal, TEE is highly accurate with a reported 100% sensitivity and specificity, [188] [189] with improved delineation of the site of defect, the morphology, and presence of multiple defects[190] (Fig. 12-8) . The most common site for a ventricular septal rupture is the posteroapical septum. Visualization of the area of myocardial dropout is most often accomplished in the parasternal short-axis view just below the level of the papillary muscles or in the apical four-chamber view with slight posterior angulation of the probe. Anterior septal defects most often occur in the distal one third of the septum and are visualized in the apical four-chamber view with anterior angulation or in an apical short-axis view. Post- myocardial infarction ventricular septal defects may be multiple and often have a serpiginous course through the myocardium.[191] Associated echocardiographic findings include evidence of elevated right ventricular pressure including right ventricular dilation, decreased right ventricular systolic function, and paradoxical septal motion. Signs of increased right atrial pressure include right atrial dilation, bowing of the interatrial septum toward the left throughout the cardiac cycle, and plethora of the inferior vena cava. Color flow Doppler imaging is particularly useful in demonstrating the exact position of the defect; the width of the jet correlates with the size of the defect as measured at surgery.[191] Although the peak gradient across the ventricular septal defect measured with continuous wave Doppler allows an estimate of right ventricular systolic pressure, the measurement should be used with caution in patients with complex defects involving indirect tracts through the myocardium. [191] A recent study demonstrated a fair correlation between this Doppler estimate of right ventricular systolic pressure and that measured at catheterization (r = 0.71); the values were similar to those estimated from the tricuspid mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 12 di 20 regurgitant jet. Echocardiography provides prognostic and diagnostic information in patients with ventricular septal rupture. Rupture Figure 12-8 (color plate.) Transesophageal echocardiogram showing a large ventricular septal defect (VSD) involving the posterior septum in a patient with a large inferior myocardial infarction and right ventricular extension. Left, The area of discontinuity can be visualized as a large, irregularly shaped area of myocardial dropout. Right, Color flow demonstrates left-to-right shunting across this ventricular septal defect. LV, left ventricle; RV, right ventricle. of the posterior septum after inferior myocardial infarction is associated with a higher mortality rate, apparently related to the degree of associated right ventricular dysfunction.[186] [192] Moreover, posterior septal ruptures tend to be more complex and associated with remote myocardial involvement. In contrast, anterior septal defects more often have a direct course and involve a discrete myocardial region. Overall mortality is 95% to 100% without surgical intervention.[193] The strongest indicator of poor prognosis is the development of cardiogenic shock associated with as much as a 90% mortality rate.[192] Although early surgery appears to improve survival when cardiogenic shock is present, results in the recent SHOCK trial were disappointing. In the surgically treated group, the survival rate (19%) was only slightly better than that of the medically treated group (5%).[186] Right ventricular systolic pressure tended to be higher and right atrial pressure lower, among the survivors. When the patient can be stabilized medically, operative mortality may be improved when surgical repair is delayed until 6 weeks following the event.[184] In summary, the value of echocardiography in patients with suspected ventricular septal rupture is its ability to provide an accurate, timely diagnosis and important prognostic information that may assist in therapeutic decision making. Rupture of the Ventricular Free Wall and Pseudoaneurysm Free wall rupture occurs in approximately 3% of all acute myocardial infarctions,[194] and it is one of the leading causes of fatality (8% to 20%).[195] [196] [197] [198] [199] Risk factors for free wall rupture are similar to those for papillary muscle and ventricular septal rupture; however, this complication is more likely to occur in patients with a transmural myocardial infarction involving the posterolateral |
wall associated with a left circumflex occlusion mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 13 di 20 [200] or with a LAD occlusion.[201] Early successful reperfusion appears to decrease the risk of rupture. In one study of approximately 1300 patients, the overall incidence of cardiac rupture was lower in those receiving thrombolytic therapy (1.7%) than in those in the conventional therapy group (2.7%). Among 265 patients who receive thrombolytic therapy, patients older than 70 years of age and women had higher rates of rupture.[202] Moreover, patients in whom reperfusion was unsuccessful had a significantly higher rate of rupture than those who were successfully reperfused (5.9% versus 0.5%).[203] Conversely, late reperfusion appears to increase the risk of myocardial rupture though decreasing overall mortality.[97] [204] The use of nitrates in acute myocardial infarction may decrease the risk of rupture by as much as 30%.[205] The intensity of post-thrombolytic anticoagulation with heparin or hirudin does not appear to affect the rate of rupture. [202] Although ventricular free wall rupture usually presents clinically as an acute catastrophic event leading to rapid demise, several recent pathologic and clinical studies have suggested that many cases may involve subacute dissection and tearing of the myocardium before hemodynamic collapse.[194] [196] [200] , [205] Intramural hematoma or hemorrhage at the junction of the necrotic and the normal myocardium results in a small endocardial rent. The tear usually takes a circuitous pathway through the myocardium, ending in a small epicardial opening. Clinically, a prodrome of ongoing or recurrent chest pain (in the absence of an elevation in creatinine kinase), repetitive large volume emesis, unexplained agitation, hypotension or syncope may be associated with the initial small tear.[194] [196] [200] A small amount of hemorrhage into the pericardial space of blood may precede the final catastrophic event. Patients diagnosed during this subacute phase and taken promptly to surgery have a greater chance of survival. A second mechanism of rupture through the wall of an aneurysm has been described. [206] Echocardiography has a high sensitivity for rupture[194] when the diagnosis is sought and all the echocardiographic findings are considered. The most frequent finding is pericardial effusion; the absence of pericardial effusion virtually excludes rupture. Increasing size of effusion and the presence of thrombus in the pericardial space significantly increases the specificity for rupture (>98%). [194] [204] , [207] An intrapericardial thrombus appears as an mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 14 di 20 echo-dense mass; it may be mobile, undulating within the pericardial space or immobile, impinging on the cardiac chambers.[208] Direct visualization of the myocardial tear is possible with TTE in as many as 40% of patients.[201] Other echocardiographic findings include evidence of Figure 12-9 The difference between a true aneurysm (A) and a false aneurysm (B). Note that in the true aneurysm there is continuity of myocardium in the region of dilation, in contrast to the loss of this continuity in the pseudoaneurysm. (Modified from MacKenzie JW, Lemole GM: Tex Heart Inst J 1994;21:296–301.) tamponade with right atrial and right ventricular diastolic collapse (40%), [201] respiratory variation of the tricuspid and mitral inflow pattern, and plethora of the inferior vena cava. Echocardiographic guidance of pericardiocentesis of the hemopericardium may be life saving in the patient with hemodynamic collapse before the patient can be transported to surgery. Patients at risk for rupture may be identified by evidence of infarct expansion with significant wall thinning at the infarct site. The mortality rate of free wall rupture in the absence of surgical intervention approaches 100%,[199] although recent series report as much as a 50% survival rate in patients who underwent pericardiocentesis and conservative medical management.[201] [209] The in-hospital mortality rate for those who undergo surgical repair is in the range of 40%.[193] [201] [204] Those who survive until hospital discharge appear to have a good long-term prognosis. Thus, early echocardiographic diagnosis with prompt surgical or percutaneous drainage is mandatory in patients who develop postinfarction myocardial rupture. A pseudoaneurysm is a myocardial rupture contained by pericardial adhesions resulting in a pouch that communicates with the left ventricular cavity. [177] A distinguishing echocardiographic feature is the narrow neck, compared with the broader "entrance" to the body of a true aneurysm, with a "neck" diameter-to-maximum diameter ratio less than 0.5. An echocardiographic study showed that this sign was only 60% sensitive in patients with post-myocardial infarction pseudoaneurysms.[210] The majority of post-myocardial infarction pseudoaneurysms were located in the inferoposterior or posterolateral regions (associated with right coronary or left circumflex coronary occlusions).[210] The walls of the pseudoaneurysm are composed of pericardium rather than mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 15 di 20 the thin-walled myocardial scar of true aneurysm (Fig. 12-9A) . Occasionally a pseudoaneurysm may occur after rupture of the thin wall of a true aneurysm with the development of a "mixed" aneurysm (see Fig. 12- 9B) . [211] Spectral and color Doppler imaging demonstrate characteristic flow in and out of the pericardial cavity at the site of the tear, as well as abnormal flow within the pseudoaneurysm. Respiratory variation of the peak systolic velocity has also been demonstrated.[212] A meta-analysis suggested that TEE has a higher diagnostic accuracy (>75%) than TTE (26%), although data 266 was available in only a small number of patients[213] (Fig. 12-10) . Surgical repair is the preferred treatment, although new reports have demonstrated that conservative medical treatment in certain high-risk patients is not associated with an increased risk of cardiac rupture.[210] [213] Infarct Expansion and Aneurysm Formation Infarct expansion is an increase in the circumferential extent of the area of infarction that results from stretching and thinning of the infarcted zone. Early clinical studies demonstrated that this phenomenon with a consequent increase in left ventricular volume and wall stress was associated with an adverse prognosis.[85] The importance of infarct expansion has been underscored by clinical trials using angiotensin converting enzyme inhibitors in patients with left ventricular dysfunction after myocardial infarction. In the SAVE trial (Survival and Ventricular Enlargement), which showed a 21% reduction in cardiovascular mortality with the use of captopril,[214] echocardiography demonstrated that ventricular enlargement and reduced fractional area change were independent risk factors for cardiac events. Patients treated with captopril had a lower incidence of ventricular enlargement, which was associated with the lower risk of events,[50] a finding that has been confirmed in subsequent studies.[141] [215] The final expression of infarct expansion is aneurysm formation. In the Coronary Artery Surgery Study (CASS) there was a 7.6% incidence of angiographically documented left ventricular aneurysms.[216] In a study by Visser et al,[218] the incidence of aneurysm was 22% (35 of 158), and most of those occurred in patients with anterior infarction. Formation of an aneurysm occurs only with transmural infarction with a full-thickness scar and, thus, is more frequent following a Q-wave than a non-Q-wave mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 16 di 20 infarction. An aneurysm is more likely to complicate an infarct in the LAD distribution than in the right or circumflex arteries.[218] Spontaneous rupture of an acute aneurysm is rare (see "Rupture of the Ventricular Free Wall"), and late rupture virtually never occurs. Serial 2D echocardiographic studies show that aneurysmal dilation is present as early as 5 days after myocardial infarction (15 of 35, 43%, in the Visser study), and new aneurysms after 3 months are unlikely.[218] Despite the Figure 12-10 Transgastric views in transesophageal echocardiogram showing a large pseudoaneurysm involving the inferolateral wall. Left, short-axis view (horizontal plane); right, long-axis view (longitudinal plane). beneficial clinical course attributed to delayed reperfusion with thrombolytic therapy, there has been no reduction in the frequency of ventricular aneurysms.[219] [220] The echocardiographic appearance of a ventricular aneurysm parallels the pathology. A true aneurysm is defined as a deformity of the thinned infarct segment that is apparent during diastole as well as during systole (see Fig. 12-6) and demonstrates a diastolic contour abnormality. In contrast, a dyskinetic myocardial segment deforms during systole, extending beyond the normal contour of the myocardium. The involved myocardial segment is scarred with thin walls (<7 mm) and increased echogenicity owing to the increased collagen content. [114] The wall of the aneurysm may eventually calcify. The most common location is the left ventricular apex, which is involved in approximately 90% of patients. Aneurysms may vary in size, and very small aneurysms may be difficult to visualize by echocardiography. Technically, the detection of an apical aneurysm is highly dependent on the skill of the operator. Routine employment of high- frequency transducers with a shallow focal point enhances near-field resolution and aids examination of the left ventricular apex. Left-sided contrast agents also may enable detection of small apical aneurysms. Using these methods, the sensitivity of TTE for detection of apical aneurysms should approach 100%. Occasionally, spontaneous echocardiographic contrast may be visible in large aneurysms. It should be noted that TEE may not provide adequate visualization of the left ventricular apex and, therefore, in our experience, is less sensitive than surface imaging. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 17 di 20 Echocardiographic recognition of a left ventricular aneurysm is clinically relevant for the following reasons: 1. The early formation of an aneurysm adversely affects early (in- hospital) and late (1 year) mortality.[218] 2. Thrombi are frequently found within aneurysms. 3. Aneurysms and left ventricular thrombi are associated with systemic embolization. In patients with refractory heart failure and angina or recurrent embolic events, aneurysmectomy may be recommended occasionally. Functional measurements of the residual myocardium using quantitative 2D echocardiography is highly predictive of operative mortality and the clinical success of this procedure.[221] [222] A basal (residual) ejection fraction of greater than 40% was associated with a satisfactory result.[222] Left Ventricular Thrombus 267 Studies in the early 1980s demonstrated a high sensitivity (90% to 95%) and high specificity (80% to 85%) for the echocardiographic identification of left ventricular thrombus.[223] [224] A prerequisite for thrombus formation is the presence of a segmental wall motion abnormality, most commonly in the left ventricular apex. The ultrasonic appearance of a mural thrombus is that of a mass distinct from the endocardium and protruding to a variable extent into the left ventricular cavity. Under ideal conditions, the surface of the thrombus can be distinguished clearly from the underlying endocardium and the mass can be visualized in two different imaging planes. The tissue characteristics of an acute thrombus are usually similar to that of the myocardium (Fig. 12-11) . A chronic thrombus may have increased reflectivity, demonstrate a layered appearance corresponding to the lines of Zahn, and contain areas of calcification (Fig. 12-12) . The base of attachment to the wall may be broad in the case of a sessile thrombus and narrow in a pedunculated thrombus. When multiple characteristics of the thrombus are analyzed, mobility of the thrombus is most closely associated (positive predictive value, 85%) with embolic events.[220] [225] In any given patient, the morphology may spontaneously change from sessile to pedunculated and vice versa; mobility may resolve spontaneously.[226] False-positive echocardiographic diagnoses are usually a result of mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 18 di 20 pseudotendons (i.e., false chordae) spanning the left ventricular apex, coarse trabeculations associated with left ventricular hypertrophy, or near- field artifacts (commonly present with low-frequency transducers). High- frequency transducers with a short focus point can sometimes differentiate true thrombus from these other phenomena. Left-sided contrast agents may outline the contours of the thrombus, creating a filling defect[227] [228] with improved detection of thrombus. Thrombi most commonly develop in the presence of a large infarction during the hospitalization phase of a Figure 12-11 Acute thrombus in the posterior aspect of the apical septum. Note that the large mass is homogeneous in texture, without evidence of calcification. Figure 12-12 Four-chamber view depicting a chronic thrombus within an apical aneurysm. The appearance of the thrombus is layered with areas of calcification. The layers correspond to the lines of Zahn. myocardial infarction.[229] Like aneurysms, they are more likely following a myocardial infarction in the LAD (up to 33%) than in the RCA or left circumflex artery distribution (less than 1%).[230] [231] New data demonstrate that the best predictor of left ventricular thrombus formation after acute anterior myocardial infarction is a high initial end-systolic volume.[232] Anticoagulant therapy appears to decrease the risk of embolic events and enhances the resolution of thrombus, although spontaneous resolution also may occur.[229] [233] Patients with a left ventricular thrombus identified during the initial hospital stay have an increased long-term mortality |
rate (22%) compared with those without thrombi (7%). Left ventricular thrombi usually resolve during the first month after anterior myocardial infarction with routine thrombolytic and aspirin treatment, but appearance and resolution of thrombi can continue in a significant proportion of patients (12%).[234] In general, thrombolytic therapy appears to decrease the rate of mural thrombus development. In the Western Washington Randomized Trial of intracoronary streptokinase, the incidence of thrombus and emboli was similar in both treated and untreated groups,[219] but most other trials of mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 19 di 20 intravenous thrombolytic agents have shown a reduction in the incidence of thrombi and emboli.[235] [236] [237] [238] Moreover, in the GISSI-2 trial there was no significant difference between the four treatment groups (recombinant tissue plasminogen activator ± heparin, streptokinase ± heparin), with an overall incidence of 28%.[239] The overall tendency for reperfusion therapy to decrease the size of the infarction is likely to lower the risk of thrombus formation. In addition, after thrombolysis, most patients receive an in- hospital period of anticoagulation, which is known to decrease the rate of thrombosis and embolization[239] (Table 12-8) . 268 TABLE 12-8 -- Effect of Thrombolytic Therapy on Incidence of Left Ventricular Thrombus in Anterior Wall Myocardial Infarction No. of Mean Time Treated Untreated Study Patients Agent to Rx (hr) (%) (%) P Eigler et al 22 SK <3 1/12 (8) 7/10 (70) <.005 [235] Stratton et al 83 SK * 4.7 7/45 6/38 (16) NS [219] (16) Natarajan et 45 SK <6 0/27 (0) 8/18 (44) <.05 al[237] Lupi et al[236] 63 SK ≤3 4/19 30/44 (54) <.05 (22) Bhatnagar 118 r-TPA <4 3/54 8/44 (18) † <.05 and al-Yusuf (5.5) [238] Mooe et al 99 SK NA 34/74 10/25 (40) NS [234] (46) Domenicucci 222 SK, NA 26/97 71/125 <.005 et al[240] alteplase (27) (57) NA, not available; NS, not significant; r-TPA, recombinant tissue plasminogen activator; SK, streptokinase. *Intracoronary. †Received heparin. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 20 di 20 The decision to prescribe oral anticoagulation following hospital discharge is influenced by two additional considerations. Embolic events occur most likely in the first month after myocardial infarction and rarely occur in the absence of thrombus identified by echocardiography.[240] However, the risk of cerebral or systemic embolization after infarction is increased in patients with large apical aneurysms and poor systolic function independent of echocardiographically documented mural thrombus. Second, chronic mural thrombi, persistent for more than 3 months following a myocardial infarction, are very unlikely to embolize. Changes in the morphology of the thrombus with evidence of protrusion are most likely to predict late embolism (>3 months).[240] Thus, most physicians perform an echocardiogram during the acute phase of an anterior wall infarction to measure left ventricular function and to detect aneurysm, thrombus, or both. In the presence of a large apical aneurysm with or without a visible thrombus, oral anticoagulation is recommended in the absence of contraindications.[241] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/106.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Post-Myocardial Infarction Risk Stratification Echocardiography has an important role in the evaluation of a patient after discharge from the CCU. Echocardiography during low-dose dobutamine infusion is used to detect myocardial viability in segments that have persistent dysfunction following reperfusion.[64] Echocardiography during higher dose dobutamine infusion or with dynamic stress can be used to detect residual ischemia. Caution should be exercised in the first week after a transmural infarction because cases of myocardial rupture during high- dose dobutamine infusion have been reported.[28] [29] Contrast echocardiography will have an important role with the development of reliable perfusion agents. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/107.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Summary Early experimental models employing echocardiography for the detection and quantitation of ischemia and infarction helped investigators elucidate the pathophysiology. This work was directly transferable into the CCU and provided the basis for the clinical diagnostic and prognostic role of echocardiography. Advances in echocardiography, especially color flow Doppler imaging, increased the capabilities of echocardiography in detecting the occurrence of complications, such as ventricular septal defect and papillary muscle rupture. Future directions include the detection of flow deficits using myocardial contrast echocardiography and more accurate quantitation of infarct size using 3D techniques. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/108.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company 275 Chapter 13 - Exercise Echocardiography Stress Testing in the Initial Diagnosis of Coronary Artery Disease and in Patients with Prior Revascularization or Myocardial Infarction Pamela A. Marcovitz MD Stress echocardiography consists of a number of stress techniques used in conjunction with echocardiographic imaging. Exercise echocardiography is the most established of these techniques and has been increasing in popularity since the first paper was published on the use of two- dimensional echocardiography with bicycle exercise in 1979.[1] Although the images were crude, they served to successfully demonstrate ischemia following cardiovascular stress and its resolution following coronary artery bypass grafting (Fig. 13-1) (Figure Not Available) . With technologic advances, including improvements in imaging and digitization, stress echocardiography has seen widespread acceptance as a first-line technique for the diagnosis of coronary disease. Recently, stress echocardiography has been increasingly used for prognostication in various patient subsets, including patients with chronic coronary disease, patients with recent revascularization, patients with recent myocardial infarction, and female patients. Despite recent advances, however, the principles of its use remain mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 the same. In the presence of a significant coronary stenosis, an adequate level of physical exertion results in a transient mismatch between oxygen supply and demand, resulting in a wall motion abnormality within an area of myocardium supplied by a stenotic artery. The wall motion abnormality is detectable by echocardiography and serves as a marker of the degree and severity of ischemia. Future advancements may bring the ability to simultaneously track myocardial perfusion. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/111.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Rationale and Theoretical Basis for Ischemia Detection with Stress Echocardiography The rationale for the use of echocardiography to detect ischemia in conjunction with stress testing is that ultrasonography can visualize wall motion abnormalities that arise as the result of a transient mismatch between oxygen supply and demand, in turn resulting in ischemia.[2] [3] [4] [5] Regardless of the stress modality used to induce ischemia, the echocardiographic response to exercise will reflect the underlying state of the coronary arteries.[6] [7] [8] [9] In the absence of coronary artery disease, there will be inward motion (endocardial excursion of at least 5 mm) and increased wall thickening. These characterize the "normal hyperdynamic response" following exercise and signify normal underlying coronary arteries. Conversely, in myocardium subtended by a critical stenosis, a mismatch between oxygen supply and demand will develop during exercise, resulting in ventricular systolic dysfunction or dyssnergy, in a segment or segments of myocardium during cardiovascular stress. Dyssynergic responses may be classified by the degree of abnormality present: 1. Hypokinesia: less than normal (5 mm) degree of inward myocardial excursion and thickening 2. Akinesia: complete lack of inward motion and thickening 276 3. Dyskinesia: paradoxical outward motion and thinning of affected segment or segments. Figure 13-1 (Figure Not Available) Images from a 30-degree sector scanner demonstrating an exercise-induced apical abnormality prior to coronary artery bypass grafting (A) and normal apical wall motion after revascularization (B). (From Wann LS, Favis JV, Childress RH, et al: Circulation 1979;60:1300–1308. Reproduced with permission. Copyright 1979 American Heart Association.) mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 The observation that abnormal wall motion reflects an underlying mismatch in supply and demand serves as the premise for the use of echocardiographic imaging in stress testing and occurs during a variety of states in which oxygen supply to the myocardium is reduced. Using a stylus attached directly to myocardium in an animal model, Tennant and Wiggers [10] were among the first to demonstrate that disruption of the coronary blood supply produces wall motion abnormality. Immediately after snare occlusion of a coronary artery, a reduction in wall thickening was observed, followed by normalization of wall motion along with release of the snare. This observation has since been validated with echocardiography in clinical settings in which arterial occlusion occurs, including balloon angioplasty and myocardial infarction.[11] [12] A variety of models have been studied to determine, in detail, the temporal and spatial sequence of events that occur during decreased regional blood flow of sufficient severity to create an imbalance in the myocardial oxygen supply-demand relationship. These models have included graded snare coronary occlusion in animals, balloon angioplasty, exercise, atrial pacing, and observation of spontaneous anginal episodes in humans.[13] [14] [15] [16] [17] [18] [19] In the early animal studies, a closely coupled relationship was noted between myocardial wall thickening and coronary flow, such that reductions in blood flow of 10% to 20% were found to impair regional (but not global) wall thickening within an ischemic zone. The observed reduction in wall thickening was found to be proportional to severity of flow reduction, with greater degrees of flow restriction causing greater severity in regional wall motion abnormalities.[16] , [20] Thus, whereas hypokinesis is noted following a threshold reduction in blood flow of around 10% to 20%, akinesis is observed with flow reduction of greater than 80%, and paradoxial motion, or dyskinesis, with transmural reductions in flow. These early studies also noted a tendency for decreased wall thickening to be more closely coupled with subendocardial rather than subepicardial flow and to extend into adjacent regions beyond well- demarcated zones of reduced flow, a phenomenon known as tethering.[3] [21] As the opportunities for echocardiographic monitoring grew, these observations in animals were extended to humans.[22] [23] [24] [25] Taken together, these studies form the basis for what we now regard as standard echocardiographic observations of ischemic myocardium. After acute, complete coronary occlusion, a series of predictable changes takes place in the myocardium, beginning with the development of diastolic and systolic dysfunction, followed by ST segment depression and angina. A mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 wall motion abnormality is one of the initial events seen with the development of ischemia and precedes development of ST segment changes or angina by several minutes. This so-called ischemic cascade, which is known to occur after occlusion of a coronary artery, may occur in ischemic myocardium subtended by a critical stenosis whenever oxygen supply-demand mismatch occurs.[26] [27] [28] A similar temporal relationship between wall motion and electrocardiographic changes has been noted in multiple studies of patients undergoing balloon angioplasty.[12] [29] [30] [31] Hauser et al[31] noted that regional endocardial dysfunction was seen by echocardiography at 19 |
seconds, electrocardiographic changes occurred at 30 seconds, and chest pain occurred at 39 seconds after balloon inflation. In addition to clinical settings involving coronary occlusion, the "ischemic cascade" was found to occur in ischemic myocardium subtended by a severe stenosis subjected to cardiovascular stress. Examining changes following exercise-induced ischemia in the region of a coronary stenosis, Sugishita et al[28] noted that the average time to onset of wall motion abnormality was 30 seconds, versus 90 seconds for electrocardiographic changes. Clinically, the ability to detect exercise-induced regional wall motion abnormalities increases with the severity and number of coronary occlusions.[32] [33] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/112.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 20 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Diagnostic Approach Choosing the Optimal Form of Stress 277 Exercise is one of a number of stress modalities performed in conjunction with echocardiographic imaging. An adequate level of stress is a prerequisite to performing exercise echocardiography. For the purposes of stress testing, clinically adequate exercise is usually defined as the ability to reach at least 85% of predicted heart rate, based on resting heart rate and age. For patients able to exercise maximally, exercise echocardiography provides a wealth of information regarding the overall level of fitness, functional capacity, and the clinical significance of an ischemic response, as well as the prognosis related to coronary disease. Given the additional diagnostic and prognostic information provided by exercise and hemodynamic parameters, exercise should be the stress method of choice whenever feasible. In the event that a patient cannot perform adequate exercise, other stressors are used (Table 13-1) . For patients unable to perform maximal exercise or to reach a target heart rate, pharmacologic methods of inducing stress are commonly used. These are discussed in greater detail in Chapter 14 , but briefly, currently available pharmacologic methods can be divided into one of two general categories: agents that simulate exercise and coronary vasodilators. [34] The first of these are sympathomimetic amines, are infused intravenously, and induce stress in similar fashion to exercise, that is, through increasing heart rate, blood pressure, and contractility. Of the exercise-simulating agents, dobutamine has emerged as the agent of choice in the United States, largely because of its availability and low cost. Dobutamine exerts its physiologic effects through beta agonist activity, increasing myocardial oxygen demand in a similar fashion to exercise. Unlike exercise, however, dobutamine is unable to provide information about level of fitness or electrocardiographic or mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 20 hemodynamic response to exercise. In addition, TABLE 13-1 -- Stress Modalities Used with Echocardiographic Imaging Exercise Treadmill Supine bicycle Upright bicycle Lateral bicycle Pharmacologic stress Dobutamine Dobutamine-atropine Arbutamine (not currently available) Epinephrine Isoproterenol Dipyridamole Dipyridamole-dobutamine Adenosine Pacing Esophageal Atrial Other Hand grip Cold presser Mental stress Hyperventilation Postventricular beats dobutamine frequently does not cause an adequate rise in heart rate, and for this reason, atropine is often needed to increase myocardial oxygen demand.[35] [36] Despite these drawbacks, dobutamine can provide information about the presence or absence of coronary disease, which is valuable in patient management decisions and prognostication. Arbutamine, which is the only pharmacologic stress testing agent approved by the Food and Drug Administration, provides a more balanced heart rate and blood mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 20 pressure response without the need for atropine.[37] [38] Because of cost, however, and because it did not provide a clear advantage over dobutamine, Arbutamine was withdrawn from the market. Isoproterenol, because it produces extreme tachycardia, is no longer used as a stress agent. Atrial pacing, sometimes employed via a transesophageal approach, is reliable but is cumbersome and uncomfortable for the patient and therefore rarely used. Vasodilators, such as dipyridamole and adenosine, create ischemia through the mechanism of coronary steal, or the selective dilation of nonstenotic coronary beds. Following administration of these agents, normal coronary beds dilate preferentially in relation to stenotic beds, in effect shunting flow away from stenotic beds and rendering them ischemic. Some experts believe, and the medical literature suggests, that echocardiography has a lesser sensitivity for the detection of coronary disease when vasodilators are used, as compared with exercise and dobutamine.[39] [40] [41] Nonetheless, dipyridamole continues to be used for the detection of coronary disease, chiefly outside the United States, where the cost of this agent is lower. The type of stress one chooses to apply in conjunction with echocardiography should be based on the patient's ability to exercise and the diagnostic information one wishes to gain from testing. For example, for the initial diagnosis of coronary artery disease in a patient whose chest pain is provoked by physical exertion, exercise would be preferred. For patients unable to exercise maximally because of arthritis, peripheral vascular disease, or general deconditioning, pharmacologic stressors are more appropriate. Rarely, chest pain may be believed to be provoked by vasospasm, and for those patients whose chest pain is suspected to be vasospastic, ergonovine or hyperventilation may be appropriate.[42] [43] The choice of stress should also be governed by the patient's familiarity with types of activities. In the United States, the most popular form of applied physical stress for the purposes of diagnostic testing for coronary disease remains treadmill exercise. Familiarity with walking may lead to achievement of higher cardiovascular workloads. In European countries, upright bicycle exercise is a more familiar activity and has assumed a prominent role. More recently, the supine bike, sometimes with lateral angling, is emerging in the United States as a popular technique for assessment of coronary artery disease. Supine bicycle exercise facilitates imaging whenever a continuous record of echocardiographic images is desired. In the diagnosis of coronary disease, bicycle exercise allows one to determine more precisely the level of exercise at which ischemia develops, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 20 which, as discussed later, may be advantageous in the serial assessment of patients. Bicycle exercise also facilitates assessment of the clinical significance of valvular 278 Figure 13-2 Stress echocardiography laboratory equipment set-up, beginning in the lower left-hand corner and moving clockwise: crash cart, frame grabber, echocardiography machine, bed with shelf above for pulse oximeter and automated blood pressure cuff, electrocardiographic monitoring machine, blood pressure (BP) cuff (manual), treadmill, intravenous (IV) infusion pump for pharmacologic stress echocardiography, and IV equipment. The room measures 15 × 18 feet and requires no more than two steps for the patient between treadmill and bed. heart disease and pulmonary hypertension through assessment of Doppler jets at various workloads. Equipment, Methodology, and Personnel The equipment needed for exercise echocardiography partially depends on the type of stress applied in conjunction with echocardiography. In all cases, high-quality echocardiographic instrumentation with an integrated or free-standing digital frame grabber, an offline analysis system, and either a treadmill or bicycle (supine or upright) connected to a computerized 12- lead electrocardiograph are required. The ergonomics of the stress echocardiography laboratory should facilitate moving from the imaging bed to the treadmill and back to the imaging bed immediately after exercise in as few steps as possible. Following the use of any standard treadmill protocol, the patient steps off the treadmill and onto the imaging bed. Extra steps spent between equipment may result in a critical loss of imaging time during the immediate postexercise period, leading to loss of sensitivity. Thus, the most critical period of time in performing exercise echocardiography is that spent between the termination of exercise and the start of imaging. A typical floor plan for a stress echocardiography laboratory that requires a minimum number of steps for both patient and technician-sonographer is shown in Figure 13-2 . The set-up shown in Figure 13-2 rarely requires multiple steps for the patient between the treadmill and imaging bed. Imaging should take place as quickly as possible, since it has been shown that information about ischemia, particularly single-vessel disease, will be lost as the heart rate returns to mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 20 normal. Some experts believe that special imaging beds with lateral cut-outs for apical imaging facilitate image acquisition. Images are typically captured in four views for side-by-side comparison in a digital format. The parasternal long- and short-axis and apical four- and two-chamber views have traditionally been used, with the substitution of subcostal images, if necessary, for patients with chronic obstructive pulmonary disease or postbypass surgical bandages that interfere with imaging windows.[44] Modification of chest lead placement is sometimes necessary to 279 obtain the best imaging windows and rarely interferes with the integrity of the electrocardiographic response. The question of whether to perform a complete baseline study with Doppler imaging or to simply capture the minimum number of images required for stress imaging often arises. In our laboratory, the practice is to perform a complete baseline study unless one has recently been performed and there has been no interim change in the patient's clinical status. The personnel required to perform exercise echocardiography varies in different laboratories depending on local standards of practice, hospital regulations, and level of billing. In most cases, at least two people are required to carry out exercise echocardiography: a technician-sonographer to perform the imaging and a second technician to monitor the patient's hemodynamic, electrocardiographic, and symptomatic responses to exercise. Regardless of the type of exercise used (i.e., treadmill or bicycle), a sonographer records baseline images at rest, followed by images during or immediately after peak exercise, while a monitoring technician notes and records the hemodynamic and electrocardiographic responses to exercise. At the completion of exercise, the monitoring technician assists the patient in quickly stepping off the treadmill or upright bicycle and reassuming the left lateral decubitus position for postexercise and recovery images, which take place on an imaging table or bed. Alternatively, a nurse or a physician may monitor and assist the patient. One advantage to physician monitoring is that it allows for immediate image interpretation of poststress images. Some laboratories use registered nurses trained as sonographers for both imaging and monitoring functions, eliminating the need for two staff members. Depending on local standards of practice, some hospital laboratories require physician presence in all cases, either in the stress mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 20 echocardiography room itself, or within the immediate area. In our hospital's echocardiography laboratory, all pharmacologic stress tests and high-risk patients referred for exercise tests are supervised directly by a physician. Outpatient clinic echocardiographic laboratories are growing in number. The equipment is the same as for hospital laboratories, but often one technician performs both monitoring and imaging functions, with a physician available within a few steps of the laboratory. The need for frequent hemodynamic monitoring will be facilitated by the use of an automated blood pressure cuff. Obviously, it is best not to perform exercise echocardiography on high-risk patients in this setting. The safety of exercise echocardiography is comparable to the safety of other stress testing modalities. A reported mortality rate of 1 in 10,000 patients with adverse events ranging from 4 to 9 in 10,000 are reported for stress electrocardiography, echocardiography, and nuclear scintigraphy.[45] [46] [47] [48] As with any form of stress testing, a crash cart should be kept within the vicinity of the testing area. Outpatients referred to hospital laboratories may not be well known to the staff performing the test, and for safety reasons, heart rate–lowering medications such as beta blockers and calcium channel blockers are sometimes continued. A question occasionally arises about whether to stop a patient's beta blocker prior to testing, since rapid decay of heart rate response after discontinuing exercise is largely responsible for loss of wall motion information. This may create the problem of achieving a submaximal test because of inadequate heart rate response. One potential solution in clinically stable patients is to decrease their beta blocker dose on the evening prior to testing to one-half dose, and to hold beta blockers on the morning of the test. This simple protocol often allows patients to minimize the antichronotropic effects of beta blockade while still |
retaining some measure of safety with a weaning protocol. Analysis of poststress images has been greatly facilitated by online digitization of images, which allows side-by-side comparison of views.[6] [49] [50] Prior to the development of digital images, the feasibility was lower— around 70%—for successful imaging in an unselected population owing to motion and respiratory artifact. With the advent of digital techniques, feasibility has risen to well over 90% in experienced laboratories. Frame grabbers for digital display allow selection of the optimal images out of multiple cardiac cycles, after all images are obtained. Thus, the technician mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 20 is able to select images without lung interference after all imaging is completed. Asking the patient to perform a breathing maneuver for 2 to 5 seconds during acquisition is another technique that facilitates obtaining high-quality images devoid of respiratory artifact. This maneuver, which works best when practiced during baseline imaging, involves asking the patient to exhale completely or "take in a half breath" and hold his or her breath for a few seconds during the postexercise images. Following optimal image selection, which may be performed by the physician or an experienced sonographer, images are then displayed in side-by-side format with prestress and poststress images adjacent to each other for comparison, generally in right-to-left fashion (Fig. 13-3) . Side-by-side comparison of segments in a gated format facilitates recognition of more subtle abnormalities, raising diagnostic accuracy. Most digitization systems acquire loops of eight frames for each view, with 50 msec allowed for each frame. This time period allows for systolic frames, with a limited portion of diastole, to be captured by triggering image acquisition at the beginning of the R wave of the electrocardiogram. Eight frames are then displayed in a continuous loop format for playback. Imaging acquisition time should be of sufficient duration to digitize all four views but must be performed quickly enough to visualize transient wall motion abnormalities, lest important information be lost as ischemia quickly resolves. Approximately 10 to 20 seconds are needed for digital capture of each view. Ideally, all four views can be digitally captured in approximately 1 minute. In our laboratory, postexercise apical views are captured first to facilitate recording wall motion in distal coronary territories, which are most likely to display ischemic abnormalities. A videotaped recording is made for back-up, and review of these images is recommended to ensure that the captured images are representative of the videotape. Treadmill Exercise Echocardiographic Protocol The most popular form of stress used in exercise echocardiographic testing in the United States is treadmill 280 Figure 13-3 Quad-screen format depicting parasternal long-axis and short- axis views. Diastolic frames (DIAS) and systolic frames (SYS) at baseline (PRE) and immediately after treadmill exercise (POST) are shown. The mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 20 ventricular response is normal after exercise, with increased endocardial excursion and increased wall thickening in all visualized segments. exercise, partly because of the familiarity of walking as a form of exercise and partly because of improved image quality over that of bicycle protocols. Analysis of images depends on the direct comparison of pre- exercise and postexercise images. Parasternal long-axis, short-axis, four- chamber, and two-chamber images are obtained at rest both on videotape and, as noted previously, on an eight-cell cine loop for display in a side-by- side quad-screen format at 50 msec per frame. In our laboratory, a complete baseline study with Doppler examination is usually performed simultaneously. The patient is then asked to step onto the treadmill and to begin exercise on one of various standard protocols available. The Bruce protocol is the most commonly used protocol, but the modified Bruce or the Cornell protocol are options for patients who are not in optimal cardiovascular condition or who require a longer warm-up period. Once baseline images are obtained, treadmill exercise proceeds in usual fashion, limited by symptoms, significant electrocardiographic changes, or a predetermined maximal exercise capacity. After cessation of exercise, the patient steps off the treadmill and reassumes the left lateral decubitus position for 281 Figure 13-4 Wall motion score index incorporating a 16-segment model using the scoring system depicted at the top. Numbers 5 and 7 are arbitrarily assigned a score of 4 (indicating dyskinesis), whereas 6 (akinesis with scar) defaults to 3 (akinesis) for the purposes of calculating the wall motion score index. The report shows scores for pre-exercise and postexercise wall motion and demonstrates apical akinesis after treadmill exercise. The global wall motion score index is normal before exercise (1.0) and worsens (1.3) after exercise. posttreadmill imaging within seconds. This requires a degree of patient agility, as well as considerable operator skill. As noted, because time delays may allow the decay of heart rate, and induced wall motion abnormalities may normalize quickly after exercise, any undue delays during the critical period between cessation of exercise and start of imaging may have the effect of lowering the overall accuracy of the test, particularly in areas of collateral flow, single-vessel disease, and moderately stenotic (50–70%) lesions.[51] Conversely, at higher workloads, greater degrees of ischemia mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 20 occasionally ensue, and prolonged myocardial stunning may take place, with wall motion abnormalities persisting for several minutes after exercise.[1] [52] [53] [54] Because of the technical difficulties involved in the acquisition of images within a limited time frame, a learning curve exists for the experienced technician-sonographer of about 50 stress echocardiographic studies. This learning curve is clearly required prior to smooth performance and acquisition of images within the required 90- second time period. Bicycle Exercise Echocardiographic Protocol Two bicycle protocols are currently in use: upright and supine. Although these are more widely used in Europe in conjunction with echocardiography, both have enjoyed an increase in popularity in the United States. In each of the bicycle protocols, imaging is performed at baseline, at peak exercise, and immediately after exercise. The upright bicycle protocol is shown in Table 13-2 . In the upright bicycle protocol, two-dimensional baseline images are recorded at rest in the parasternal long- and short-axis and apical four-chamber and two-chamber views in the left lateral decubitus position. The patient moves onto the upright bicycle, and the apical views are repeated at rest in the upright position. Using the same view facilitates comparison between rest and peak images. Exercise then begins with the patient pedaling, sometimes following a brief warm-up period, and proceeds in increments of 25 to 50 watts in 2- or 3- minute stages. As the patient exercises, apical views can be recorded on tape throughout the examination. End points for bicycle exercise are the same as for treadmill imaging: predetermined age-related peak heart rate, the development of significant symptoms, or significant electrocardiographic changes. Just prior to stopping at peak exercise, the apical four-chamber and two-chamber views are recorded, and the patient resumes the left lateral decubitus position on an examining bed or table for immediate postexercise parasternal views, as well as repeat apical views. Digital TABLE 13-2 -- Upright Bicycle Protocol 1. Complete baseline study performed in left lateral decubitus position 2. Parasternal long-axis, short-axis, four-chamber, and two-chamber views recorded on tape and digitized 3. Patient assumes upright position on bicycle for apical rest views 4. Pedaling begins at 60 rpm, 25 watts, and increases by 25 watts every 2 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 20 to 3 minutes 5. Peak exercise views obtained at the end of each stage 6. At completion of exercise, patient reassumes left lateral decubitus position for immediate postexercise and recovery images 282 images are captured at the end of each stage, with each subsequent stage overriding the previous peak image. In this way, if a patient suddenly stops exercising early in any stage, the last image captured will be the peak exercise image. The exercise protocol itself may vary. One popular protocol is to have the patient begin pedaling at 60 rpm at 25 watts and to increase the resistance by 25 watts every 2 minutes while the patient continues to pedal at 60 rpm. Maximal exercise is then terminated at 250 watts or at 85% of the predicted maximal heart rate. Because many patients undergoing testing are older, their ability to pedal is highly variable, and tremendous latitude may be necessary in selecting workloads. Smaller increases in resistance are usually necessary in elderly individuals and patients unaccustomed to bicycle exercise. Also, variations in the imaging protocol are sometimes needed because of technical difficulty in obtaining apical views during exercise. One alternative to apical imaging is subcostal views.[44] This approach eliminates superimposition of the air-filled lung and may be more feasible for patients with chest wall deformities or chronic obstructive lung disease. Compared with the upright bicycle, supine bicycle exercise has a simpler protocol in that all imaging takes place with the patient on the bicycle, eliminating the need for an additional imaging table or bed for parasternal views. After acquisition of all four baseline views (parasternal long-axis, parasternal short-axis, four-chamber, and two-chamber) as described earlier, the patient begins pedaling in the supine position while apical views are obtained at each stage and recorded on videotape during exercise in similar fashion to the upright bicycle. At peak exercise, the images are digitized for viewing in quad-screen side-by-side format as previously described. In our laboratory, the four quadrants consist of pre-exercise images on the left and peak exercise images on the right, a display similar to that used in posttreadmill exercise. In addition, recovery images are mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 20 recorded on videotape after the heart rate and blood pressure have returned to pre-exercise levels. Comparison of Stress Modalities As mentioned earlier, all forms of exercise have their relative advantages and disadvantages, and selection of stress modality should be based on individual patient characteristics, the patient's ability to exercise, and the information one wishes to obtain (Table 13-3) . With treadmill exercise, imaging at peak stress is technically difficult and, although a few reports have explored the feasibility of peak treadmill imaging, posttreadmill imaging TABLE 13-3 -- Comparison of Peak Bicycle and Posttreadmill Imaging Peak Bicycle Imaging Posttreadmill Imaging Improved sensitivity Less cumbersome protocol Slightly decreased specificity Improved image quality Lower cardiovascular workloads Higher cardiovascular workloads More leg fatigue More familiar, better tolerated by most patients remains the most widely applied technique. Advantages of treadmill exercise include patient familiarity as well as a lack of need for additional equipment, since most laboratories and hospitals are already equipped with a treadmill for routine exercise testing. In many cases, a digital frame grabber to digitize images at baseline and at peak exercise for side-by-side comparison is the only additional equipment required. One of the main disadvantages of the treadmill is that it relies on capture of images in "all- or-none" fashion after exercise, providing a post-stress "snapshot" of the heart. Unlike with bicycle stress, which provides multiple views of the heart at various intermediate stages of stress, the exact stage of onset of ischemia cannot be detected with treadmill protocols. An advantage of bicycle exercise, therefore, is the ability to image at various levels of stress, allowing the time to onset of ischemia to be recorded and compared between serial studies, possibly providing additional prognostic information. Peak images, rather than posttreadmill images, also have the theoretical advantage of higher sensitivity, since wall motion abnormalities may revert to normal within seconds after exercise.[52] This advantage of bicycle exercise over treadmill exercise may be offset, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 12 di 20 however, by the fact that in the United States patients are usually more accepting of treadmill exercise and less limited by leg fatigue, since walking is a familiar activity. Exercising in the supine position requires that the weight of the legs be supported against gravity and may lead to earlier stopping because of leg discomfort and fatigue. In addition, supine exercise may lead to submaximal heart rate response and lower cardiovascular workloads, with the development of angina at a lower pressure rate product. [55] [56] Thus, maximal workloads attained in the supine position may actually be lower than those obtained in the upright position on the bicycle or the treadmill. Upright bicycle exercise theoretically produces higher workloads at equivalent levels of blood pressure and heart rate but provides a more cumbersome protocol. The major |
potential advantage of imaging performed at peak exercise rather than postexercise is that transient ischemia and its ensuing wall motion abnormalities may resolve quickly and be missed with posttreadmill testing, leading to a lower sensitivity for the detection of coronary artery disease. As noted, however, the higher workload achieved with treadmill exercise may offset the potential benefit of imaging during peak exercise. One study has directly compared the sensitivity and specificity of peak versus postexercise imaging using the same exercise modality in the same patients. Presti et al[52] used upright bicycle echocardiography to evaluate 104 consecutive patients referred for known or suspected coronary disease. Of these, 96 patients had echocardiograms suitable for wall motion analysis at rest, during peak bicycle exercise, and immediately after bicycle exercise (feasibility, 92%). The overall sensitivity of postexercise imaging for the detection of coronary disease was 70%, compared with 100% for peak exercise images. When the parasternal views were added, three additional patients demonstrated postexercise abnormalities. When the coronary anatomy of patients with false-negative studies was examined, it was found that the development of wall motion abnormalities 283 at only peak exercise was more likely to occur in patients with stenotic areas supplied by collateral flow. There have been few direct comparisons of different types of exercise in conjunction with echocardiography in the same patient population. Three studies have compared treadmill testing and bicycle exercise testing in conjunction with echocardiography. The earliest of these, by Applegate et mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 13 di 20 al,[57] evaluated 21 patients after myocardial infarction using low-level, symptom-limited stress testing, with similar workloads achieved in each form of exercise. This study suggested that the delay in posttreadmill imaging did not significantly affect the sensitivity for detection of exercise- induced ischemia in this postmyocardial infarction population. Two studies have compared posttreadmill with peak supine bicycle exercise in a stable population with coronary disease.[58] [59] One of these studies noted an advantage for peak stress bicycle imaging in the identification of coronary disease. Dagianti et al,[58] examining a small series of 10 male patients with coronary disease, noted 100% sensitivity for supine bicycle with only 60% for posttreadmill imaging. In a larger series of 74 patients, Badruddin et al [59] noted a sensitivity of 83% and specificity of 70% for supine bicycle and 75% and 90% for treadmill echocardiography, a difference that did not reach statistical significance. Taken together, these data may indicate a relatively small advantage in the detection of ischemia for selected patients who are able to perform bicycle exercise, particularly patients with single- vessel disease or collateral flow. Interpretation of Stress Echocardiograms Echocardiograms can be interpreted qualitatively, with a descriptive summary of the myocardial response to exercise, or quantitatively, providing a numeric description of wall motion (see Fig. 13-4) . For clinical purposes, a descriptive summary of wall motion response often provides enough information to aid the referring clinician in patient management. Regardless of the chosen scheme, a normal echocardiogram is one in which there is normal resting wall motion and a hyperdynamic response to exercise with symmetric wall thickening and equal excursion in all segments. The development of a wall motion abnormality either at peak exercise or immediately after exercise is sensitive and specific for ischemia and is evidence of underlying coronary disease. Using a qualitative approach, wall motion is often described as "normal," "ischemic," or "fixed," depending on the response to exercise (Table 13-4) . Ischemic segments are labeled as such if they appear normal or mildly hypokinetic at rest and worsen with exercise, whereas fixed areas are akinetic at rest and are unchanged or become dyskinetic with exercise, implying scarred myocardium due to transmural infarction. In most studies, new wall motion abnormalities may be detected when a coronary stenosis of greater than 50% exists, with increased likelihood for detection with stenoses of greater than 70%. Accordingly, using a visual estimate of 50% mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 14 di 20 as a cut-off point would result in a lower sensitivity for detection of coronary disease than using 70%. Hypokinetic TABLE 13-4 -- Categorization of Exercise Echocardiographic Wall Motion Responses Wall Motion During Wall Motion at Rest Exercise Category Normal Normal Normal Normal Abnormal: Worsening Ischemic Abnormal excursion Fixed: No significant Scar: Transmural (thinned) change infarction Abnormal excursion New or worsening Hibernating (preserved thickness) abnormality areas with full-thickness myocardium that worsen after exercise are likely to represent areas that are both viable and ischemic, the resting abnormality representing stunned or hibernating myocardium. Using qualitative terms such as these, one generally reports a description of wall motion and a diagnosis such as "inferior hypokinesis following exercise, consistent with inferior ischemia." Occasionally, lack of hyperdynamic response or frank hypokinesis will be noted in myocardium that is not supplied by a significant stenosis. This situation has been noted in aortic valve disease, in extreme elevations in blood pressure, and, in our experience, occasionally with occult myopathy. The most widely accepted quantitative approach is the wall motion score index recommended by the American Society of Echocardiography, which uses a scoring system from 1 to 4 depending on the degree of abnormality. [60] A grade of 1 is assigned to normal segments and 2 through 4 for hypokinetic, akinetic, or dyskinetic segments, respectively. Some laboratories also grade the lack of development of a hyperdynamic response as abnormal, assigning a grade of 0 to hyperkinetic regions. Grading lack of hyperdynamic response as abnormal results in higher sensitivity for the detection of coronary disease but may result in poorer specificity.[61] Using this wall motion scoring system, one then assigns a number to each of 16 segments and divides by the total number of segments for the calculation of a global wall motion score index (Fig. 13-5) . Alternatively, individual coronary territories can be assigned a "regional" wall motion score index. Either a global score or a regional score can then be used to assess responses to specific medical therapy or to cardiac mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 15 di 20 interventions over time. With use of a regional wall motion score index, it is possible to predict the specific location of a coronary artery stenosis from the area of the wall motion abnormality and thus to provide important prognostic information regarding the nature of the underlying disease. A schematic representation of coronary blood supply in each segment using a 16-segment model is shown in Figure 13-5 . With this scheme, accurate distinction of anterior from posterior circulation is possible. Within the posterior circulation, separating left circumflex from right coronary artery territory is much more difficult because of individual variation in anatomy. In most situations, however, important diagnostic information is provided simply by separating the left anterior descending territory from the posterior circulation. Obviously, segments with normal resting ventricular 284 Figure 13-5 Diagram depicting how coronary artery territory is incorporated into the 16-segment model. Although some overlap is commonly seen, separation of anterior from posterior circulation is 80% to 90% accurate. Individual variation in coronary anatomy usually precludes accurate separation of right coronary from left circumflex territories. (Modified from Segar DS, Brown SE, Sawada SG, et al: J Am Coll Cardiol 1992;19:1199, with permission from the American College of Cardiology.) function that augment during exercise indicate a patent coronary blood supply. Figure 13-3 depicts a normal hyperdynamic ventricular response after exercise, implying normal coronary arteries. As noted, normal resting ventricular function in a segment or segments that worsen during exercise indicates the presence of significant underlying coronary disease and ischemia. Figure 13-6 depicts an ischemic response following treadmill exercise. In this case, a 52-year-old woman with new-onset exertional discomfort demonstrated normal resting systolic function. After 6 minutes of exercise, a wall motion abnormality developed in the anterior septum, signifying left anterior descending artery ischemia (as seen in the postexercise systolic image). This patient was found to have a 75% stenosis of the left anterior descending artery. Abnormal resting ventricular function that worsens during or after exercise is sometimes a confusing picture and may represent one of a number of mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 16 di 20 potential clinical possibilities. Areas of full-thickness myocardium that are hypokinetic at rest may represent areas of chronic repetitive stunning, chronically ischemic (hibernating) myocardium, or previous nontransmural myocardial infarction supplied by a critically stenosed artery. Regardless of the cause of resting hypokinesis, worsening after exercise is likely to represent an ischemic response. Segments that are bright, thin, and akinetic at rest and become dyskinetic after exercise are more likely to represent transmural infarction without significant ischemia. The patient depicted in Figure 13-7 is a 54-year-old man with chest discomfort who was able to exercise for 8 minutes on a Bruce protocol. The wall motion is normal at rest. Following treadmill exercise, an abnormality developed in the basal inferior segments (seen in the lower right-hand frame), and at catheterization the patient was found to have an 80% stenosis of the right coronary artery. One sees a break point in the myocardium (arrow) at the junction of the right coronary and left anterior descending artery territories, signifying left anterior descending artery patency juxtaposed against a stenosed right coronary artery. The patient in Figure 13-8 demonstrates abnormalities in the same myocardial segments of the basal inferior wall; however, in this case the myocardium is thinned and aneurysmal at rest, consistent with prior transmural infarction of the interior wall. Worsening 285 Figure 13-6 Exercise echocardiogram demonstrating anterior ischemia with dyskinesis of the anterior septum in parasternal long-axis view after exercise. The response suggests hemodynamically significant disease in the left anterior descending artery. DIAS, diastolic; POST, postexercise; PRE, pre-exercise (baseline); SYS, systolic. in this case from akinesis to dyskinesis represents a fixed abnormality consistent with scar rather than ischemia. At catheterization, a total occlusion of the right coronary artery was found. As noted, myocardium that is hypokinetic at rest may represent stunning, hibernating, or a mixture of normal and infarcted myocardium. Accurately sorting out and interpreting the responses to exercise in these complex cases often requires integration of angiographic data derived from cardiac catheterization as well as the clinical mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 17 di 20 Figure 13-7 Exercise echocardiogram demonstrating inferior ischemia. Diastolic (DIAS) and systolic (SYS) frames at baseline (PRE) and after exercise (POST) demonstrate normal resting wall motion with outward systolic motion (dyskinesis) of basal inferior segments after exercise. This patient had a critical stenosis of the right coronary artery. (See text for further explanation.) history. Some of these complex responses and the possible relationship to the underlying clinical significance are shown in Table 13-5 . Advantages and Disadvantages of Exercise Echocardiography When compared with routine treadmill exercise, there are a number of advantages to performing exercise echocardiography, 286 Figure 13-8 Exercise echocardiogram demonstrating prior inferior wall myocardial infarction due to right coronary artery occlusion. The basal inferior segments are echogenic and akinetic at rest, suggesting scar. After exercise, the scarred region becomes dyskinetic, indicating "fixed" disease. DIAS, diastolic; POST, postexercise; PRE, pre-exercise (baseline); SYS, systolic. as shown in Table 13-6 . Although routine treadmill testing remains the most prominent form of diagnostic testing for patients with known or suspected coronary disease in the United States, its sensitivity and specificity are limited in many patients in whom the ST segment response is unreliable or uninterpretable.[62] [63] [64] [65] Patients who have a high likelihood of false-positive, false-negative, or nondiagnostic electrocardiographic responses demonstrate improved accuracy for the detection of coronary TABLE 13-5 -- Clinical Interpretation of Complex Responses * Interpretation At Rest After Exercise Normal Excursion Normal Hyperdynamic Wall thickness Normal CAD/No MI Excursion Normal Hypokinetic, akinetic, or dyskinetic mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 18 di 20 Wall thickness Normal CAD/Nontransmural MI Excursion Hypokinetic or Augmented, hypokinetic, akinetic, akinetic or dyskinetic (dependent on infarct artery patency) Wall thickness Partial or full CAD/Transmural MI Excursion Akinetic Akinetic or dyskinetic Wall thickness Thinned CAD/Hibernating/Stunned Excursion Hypokinetic or Incompletely investigated May akinetic augment with mild exercise Wall thickness Partial or full CAD, coronary artery disease; MI, myocardial infarction. * Response depends on extent of residual stenosis. disease with the addition of echocardiography.[6] These include women; patients with left bundle branch block; patients taking digoxin; patients with prior nontransmural myocardial infarction, Wolff-Parkinson-White syndrome, or mitral valve prolapse; patients with hyperventilation ST segment changes; and a large group of patients with nonspecific |
ST-T wave changes at rest. Echocardiographic imaging in conjunction with exercise stress testing has been shown to increase the diagnostic accuracy in patients such as these with resting electrocardiographic abnormalities, which some experts believe make up as much as 30% to 40% of patients presenting for exercise testing. A major advantage of exercise echocardiography is its versatility in the diagnosis of structural heart disease not related to coronary disease. Echocardiography has the ability to diagnose any and all forms of structural heart disease as a cause of angina or other cardiac symptoms. Thus, if exertional symptoms are due to valvular heart disease, pulmonary hypertension, diastolic dysfunction, or pericardial disease, the diagnosis can be made with exercise echocardiography. Figure 13-9 provides an example in which shortness of breath was suspected to be an anginal equivalent in a mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 19 di 20 patient with multiple risk factors TABLE 13-6 -- Relative Advantages and Disadvantages of Stress Echocardiography Advantages Disadvantages Versatile (evaluates all structural Analyzed qualitatively abnormalities) Portable Requires additional trained personnel Minimal space requirements Requires additional equipment Increases sensitivity and specificity Adds time to routine treadmill test Evaluates wall thickening Low risk 287 Figure 13-9 Parasternal long-axis and short-axis views depicting a normal hyperdynamic response to exercise in a patient with severe left ventricular hypertrophy and resting repolarization changes on electrocardiogram. Systolic frames (SYS) are compared before (PRE) and after (POST) treadmill exercise. DIAS, diastolic. for coronary disease. In this case, a patient with chronic renal disease, hypertension, and obvious left ventricular hypertrophy demonstrated baseline secondary ST segment changes and a positive electrocardiographic response to exercise, while the echocardiographic response clearly demonstrates a normal hyperdynamic response, with increased endocardial excursion and symmetric wall thickening in all segments. In some cases, the baseline study may provide clues to diagnosis and reveal a contraindication to stress testing, such as the finding of critical aortic stenosis or significant pericardial effusion. In our laboratory, a previously unsuspected but important cardiac diagnosis occasionally emerges from the resting echocardiographic study and engenders a reason to cancel the stress test. In this respect, exercise echocardiography provides a measure of safety unattainable by routine electrocardiographic monitoring or radionuclide imaging. Another advantage is that echocardiographic equipment can be transported to any area equipped with a treadmill or stationary bicycle, such mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 20 di 20 as the hospital emergency department. Echocardiography is also the only bedside imaging technique that evaluates systolic wall thickening. There are some potential disadvantages to the addition of echocardiography to routine treadmill testing. First, it requires additional personnel and training. In most laboratories this requires two technicians, but one experienced technician may perform both the imaging and monitoring tasks, provided there is a physician in the immediate area (see Equipment, Methodology, and Personnel and also Fig. 13-2) . Another potential disadvantage to exercise echocardiography is the need for additional equipment, which in some cases is only a device for frame-grabbing digital images, since many outpatient clinics and hospitals are already equipped with echocardiographic instrumentation and a treadmill. Echocardiographic imaging also adds approximately 30 minutes to the time of the routine treadmill test. Also, although the results are reproducible, to date no highly quantifiable methods exist to evaluate wall motion or systolic thickening in the clinical setting.[64] Until an easily quantifiable system for wall motion evaluation exists, interpretation of stress echocardiograms remains largely qualitative. Given the overall accuracy reported, this has not proved a major disadvantage. Obviously, these potential disadvantages are a trade-off for increased diagnostic accuracy compared with treadmill testing. It is important to remember, however, that as with any form of imaging in conjunction with exercise testing, the sensitivity of stress echocardiography will be poor in patients who cannot reach an adequate level of cardiovascular stress. For those patients, pharmacologic stress echocardiography is a desirable alternative (see Chapter 14) . Patients who should undergo pharmacologic stress because of high rates of false-negative results due to inadequate exercise levels include patients with peripheral vascular disease, patients with orthopedic problems, elderly persons, and individuals who are deconditioned. For these and other unselected patient populations, the reported accuracy of dobutamine echocardiography for the diagnosis of known or suspected coronary disease has been excellent, around 85% to 95%. This is well within the range of competing nuclear imaging techniques.[7] [8] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/113.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 22 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Clinical Applications of Exercise Echocardiography Accuracy in the Identification of Coronary Artery Disease Several studies have been published reflecting the overall accuracy of exercise echocardiography in the diagnosis 288 of coronary artery disease.[44] [51] [52] [55] , [61] [66] [67] [68] [69] [70] [71] [72] [73] [74] [75] [76] [77] [78] [79] In the first of these studies, published by Wann et al[1] [6] in 1979 at Indiana University, patients were studied with a 30-degree sector scanner during peak supine bicycle exercise. Despite primitive equipment, the overall sensitivity was 87% and the specificity was 100%, not unlike the sensitivities and specificities currently reported with state-of-the-art imaging equipment and digital acquisition techniques. The accuracy of various exercise stress echocardiographic techniques has been verified in numerous laboratories. Many early studies reported sensitivities in the range of 60% to 90%, whereas more recently, particularly with the advent of digital imaging methodologies, sensitivities have more consistently been in the higher end of this range. Table 13-7 compares the sensitivities and specificities of some of the larger reported studies. Many of the early studies focused on the ability of stress echocardiography to detect changes in global function, sometimes using radionuclide ventriculography as the gold standard.[69] [80] [81] [82] These studies demonstrated an increase in indices of global systolic function (such as ejection fraction or pressure/volume ratio) for normal subjects and depressed indices for patients with previous myocardial infarction. One of the first large studies demonstrating increased sensitivity and specificity with the addition of echocardiography to routine treadmill testing using arteriography as the gold standard was that of Armstrong et al, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 22 [6] in which 95 patients underwent both posttreadmill exercise and cardiac catherization. Of the 59 patients in whom there was no evidence of prior infarction, 44 were found to have coronary disease at subsequent coronary arteriography. Exercise echocardiography was abnormal in 35 of these 44 patients, for an overall sensitivity of 80%. In contrast, the exercise electrocardiogram demonstrated ischemia in only 19 of these patients (sensitivity, 43%) and was normal in 13 patients (30%) and nondiagnostic in 12 patients (27%), demonstrating the ability of exercise echocardiography to identify coronary disease in patients with an ambiguous or inaccurate treadmill response. Conversely, exercise echocardiographic results were normal in 13 of 15 patients without coronary disease, for a specificity of 87%. In 36 patients with prior infarction, 35 had rest or exercise-induced wall motion abnormalities, or both, for a sensitivity of 97%. TABLE 13-7 -- Accuracy of Exercise Echocardiography Single Stenosis Vessel Patients, Grade, * Sensitivity, Disease, Sp Study n Modality % % % Limacher 73 Treadmill 50 91 64 et al[69] Armstrong 95 Treadmill 50 88 — et al[6] Armstrong 123 Treadmill 50 88 81 et al[32] Ryan et al 64 Treadmill 50 78 76 [72] Sawada et 57 Treadmill/upright 50 86 88 al[124] bicycle Crouse et 228 Treadmill 50 97 92 al[61] Marwick 150 Treadmill 50 84 77 et al[76] Hecht et al 180 Supine bicycle 50 93 84 [50] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 22 Ryan et al 309 Upright bicycle 50 91 86 [51] Roger et al 150 Treadmill 50 91 — [67] Marangelli 80 Treadmill 50 89 76 et al[143] * Definition of significant coronary artery disease. Because the inclusion of patients with left ventricular wall motion abnormalities at rest falsely elevates the sensitivity of echocardiography for the detection of coronary disease (a fact that is also true for radionuclide imaging), a later study from the same laboratory examined the use of exercise echocardiography in 64 patients with normal wall motion at rest.[72] Twenty-four patients had no angiographic evidence of coronary artery disease, and all 24 had a negative exercise echocardiogram, for a specificity of 100%. Of 40 patients with coronary disease, 31 had a positive exercise echocardiogram (sensitivity, 78%). In a more current era, Marwick et al[76] reported an overall sensitivity of 84% and a specificity of 86% in 150 patients who underwent exercise echocardiography and coronary arteriography, with slightly higher sensitivity and slightly lower specificity when patients with nondiagnostic test results were excluded. Nondiagnostic test results stemming from an inability to reach a target heart rate in the setting of beta blocker use is a common problem in a clinical setting and appears to affect sensitivity more than specificity.[83] Sensitivities and specificities may vary between studies depending on the prevalence of disease in the population under study, the definition of significant disease, and the criteria used for a positive test. Clinical factors such as age, cardiac risk factors, and prior history of angina, all of which affect pretest likelihood of coronary disease, influence sensitivity and specificity, with sensitivities tending to be higher in populations with a higher pretest likelihood of disease. Sensitivity and specificity are also affected by the criteria used to define a positive test. Crouse et al[61] reported a high sensitivity of 97% and a relatively low specificity of 64% in a series of 228 patients undergoing treadmill echocardiography as a screening test. In this study, a normal test was defined as the presence of hypercontractility in addition to the absence of inducible wall motion abnormalities, adding to mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 22 the sensitivity but detracting from the specificity of the results. Probably the biggest influence on specificity is that of posttest referral bias, which alludes to the fact that as a test becomes more accepted by the medical community, more patients with positive tests, and fewer of those with normal studies, are referred for coronary arteriography. Since only a small proportion of those with normal studies are given the opportunity to verify their test results, this 289 tends to lower specificity dramatically. Concomitantly, sensitivity is raised, since more patients with positive tests are referred for angiography. This point was illustrated in a study of 244 men and 96 women by Roger et al[80] that noted that bias in referral patterns for angiography may have a dramatic effect in lowering specificity. Accuracy of all types of stress testing is equally affected by biased referral for cardiac catherization or "verification bias," with lower sensitivities and higher specificities likely compared with those reported. To overcome posttest referral bias, in some studies a "normalcy" rate is calculated for subgroups thought to be at low risk for coronary artery disease within a population. This can then be used as a reasonable substitute for specificity. Thus, through clinical characteristics and demographic factors, subgroups likely to have a less than 5% pretest likelihood of significant coronary disease are identified, and these patients are then assumed to be free of significant coronary artery disease. The number of patients with a normal stress test within this group are identified. Normalcy is then calculated as the number of patients with a normal exercise test divided by the number of those at very low clinical risk for the disease. A few studies have reported normalcy rates when the catheterized population was skewed in the direction of patients with coronary disease. In a published series of 180 patients studied with supine bicycle and coronary arteriography, Hecht[50] reported an overall sensitivity of 93%, a specificity of 86%, and an overall accuracy of 92%. The normalcy rate for 42 patients who had a less than 5% pretest likelihood of significant coronary disease was 100%. Similarly, Marwick et al[36] have reported a normalcy rate of over 90% in 29 of 150 patients with normal results on an exercise echocardiogram and low pretest likelihood. |
Another influence on the accuracy of exercise echocardiography is the definition of significant disease, which is in part determined by the physiologic significance of a stenosis. This was illustrated in a study by mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 22 Sheikh et al[33] who found that stenoses of greater than 75% diameter were more frequently associated with wall motion abnormalities during exercise echocardiography than stenoses of less than 25%. Stenoses in the range of 50% appeared to be evenly divided between positive and negative results when assessed by visual estimates of stenosis. Using quantitative angiographic methods, however, the authors were able to further stratify the ventricular responses into two subgroups. Those patients with wall motion abnormalities were associated with luminal stenoses of greater than 50%, whereas normal wall motion was associated with stenoses of less than 50%, suggesting that visual estimates may be unable to determine which stenoses in the moderate range are significant. This and other studies highlight the limitations inherent in using a diameter stenosis as visually determined to define significant disease.[73] [85] [86] Factors such as proximal location, presence of collateral flows, and plaque morphology have been shown to influence coronary flow, particularly in the setting of submaximal effort. Some recent studies have used intravascular ultrasonography rather than arteriography to define significant stenoses, and these studies further emphasize the limitations of "luminography" as a gold standard. An arteriogram being a two-dimensional representation of a three-dimensional artery may under- or overrepresent the degree of stenosis depending on the views selected. Factors such as bends or kinks in the vessel may cause some areas to falsely appear stenotic, whereas plaque irregularity may lead to underassessment of the functional significance of stenoses.[87] In clinical practice, functional assessment of a stenosis in relation to results of stress testing should always be undertaken along with integration of clinical factors with angiographic results. Currently, the overall accuracy of exercise echocardiography is in the range of 80% to 90%. A recent meta-analysis of 2637 patients reported in 24 articles noted an overall sensitivity of 85% and specificity of 77% for exercise echocardiography, examining only studies in a current era that reported results for all patients such that the calculation of sensitivity and specificity was possible with numbers of patients reported, along with coronary angiography used as the reference test.[88] Taken together, these studies illustrate the ability of exercise echocardiography to identify patients with angiographically significant disease and to provide an assessment of the physiologic significance of stenoses comparable to other stress imaging tests. Exercise Echocardiography After Angioplasty mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 22 Because of its ability to target separate coronary artery distributions, exercise echocardiography may be an ideal tool for surveillance of patients after coronary interventions. Studies suggest that echocardiographic imaging can assess the initial outcome of angioplasty, atherectomy, and stenting, as well as provide valuable information regarding the presence of restenosis.[89] [90] [91] [92] [93] [94] [95] [96] [97] [98] [99] [100] One of the early studies demonstrating the ability of exercise echocardiography to provide a functional assessment in patients before and after angioplasty was that of Broderick et al[91] in which 36 patients were studied before and after coronary angioplasty. Thirty-one patients demonstrated ischemia with either an abnormal exercise test result (exercise-induced ST depression or angina) or an abnormal exercise echocardiogram (exercise-induced wall motion abnormalities). After successful angioplasty, 17 patients continued to demonstrate exercise- induced ischemia by either electrocardiographic or echocardiographic criteria. Although 12 of these 17 patients continued to demonstrate exercise-induced wall motion abnormalities, most were improved compared with the studies prior to angioplasty. Exercise duration, workload, and METS (metabolic equivalents) increased after angioplasty, suggesting that some of the wall motion abnormalities after angioplasty might be explained by a greater ischemic burden. Since follow-up studies were performed 2 weeks or more after angioplasty and no patient had undergone repeat angiography, it is possible that some of these failures to demonstrate improvement represented early restenosis. A few other studies from high-volume laboratories have reported success in the use of exercise echocardiography to evaluate patients before and after angioplasty. Labovitz et al[94] noted new exercise-induced echocardiographic abnormalities in 12 of 17 patients prior to angioplasty and 290 in none of these patients after angioplasty. When 1 mm of ST segment depression was added to the criteria for ischemia, 16 of 17 patients demonstrated ischemia prior to angioplasty. Thus, using a combination of electrocardiographic and echocardiographic criteria increased the sensitivity for the detection of coronary artery disease from 71% to 94%. Both of these studies demonstrate improved accuracy with the addition of two-dimensional echocardiography to exercise testing in postprocedure mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 22 assessment of the functional significance of coronary artery disease. In the study by Labovitz et al,[94] exercise ejection fraction also improved after angioplasty and was similar to that noted in age-matched normal control subjects. In our laboratory, if inducible wall motion abnormalities remain or recur after angioplasty at similar workloads as those noted prior to angioplasty, coronary arteriography is generally undertaken if the patient has symptoms or if a large coronary territory is in jeopardy. Figure 13-10 demonstrates the resting and posttreadmill systolic frames from a patient who had undergone angioplasty of the left anterior descending artery 3 months previously and who had developed atypical chest pain. Postexercise systolic images of the apical four-chamber view demonstrate an apical wall motion abnormality. At catheterization, the patient was found to have restenosis with a 90% luminal narrowing of the middle left anterior descending artery. Limited data have been published on the use of exercise echocardiography in the detection of restenosis, but these have been encouraging in suggesting a role for exercise echocardiography in the long-term follow-up of patients undergoing angioplasty. Hecht et al[93] used supine bicycle echocardiography to examine 80 patients an average of 6 months after angioplasty to determine whether this Figure 13-10 Systolic frames of apical four-chamber (A) and two- chamber (B) views at rest (PRE) and after exercise (POST) demonstrating an apical abnormality in a patient with prior left anterior descending artery angioplasty. This patient was found to have restenosis at the site of previous percutaneous transluminal coronary angioplasty. technique could detect restenosis. The overall sensitivity of supine bicycle exercise echocardiography was 87%, compared with 55% for electrocardiographic sensitivity. The specificity was 95% for exercise echocardiography, compared with 79% for exercise electrocardiography. Sensitivity was highest (91%) for the left anterior descending artery. The sensitivity of supine bicycle echocardiography for the detection of restenosis was surprisingly high, despite a low percentage of patients achieving 85% of predicted maximal heart rate, suggesting that the restenosis lesion was hemodynamically significant at a low cardiovascular workload. The fact that supine bicycle stress echocardiography utilizes peak exercise imaging may account for the higher sensitivities reported with this technique. In another study, Dagianti et al[101] demonstrated the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 22 usefulness of supine bicycle echocardiography shortly after balloon angioplasty to detect clinical restenosis at 6 months. Sixteen of 18 patients who subsequently went on to develop symptomatic restenosis documented angiographically had an early positive bicycle echocardiogram, suggesting that visual estimates may overestimate the early procedural success and that substrate for the restenosis lesion may begin early. Supine bicycle echocardiography was not successful in predicting asymptomatic angiographic restenosis, again pointing out that when performed in an asymptomatic population, percent diameter stenosis as determined by arteriography may not be an accurate reflection of the adequacy of flow. Chest pain is more closely linked to coronary flow reserve than is absolute stenosis diameter.[102] [103] Thus, patients who are asymptomatic despite angiographic evidence of restenosis may be better treated conservatively, particularly if they are able to engage in exercise without limitation. Few studies have compared radionuclide methods with 291 stress echocardiography for assessment of angioplasty results. One study compared single photon emission computed tomography (SPECT) thallium and exercise echocardiography before and after angioplasty. Fioretti et al[92] compared the results of exercise echocardiography with thallium-201 SPECT before and after angioplasty in 23 patients. Prior to angioplasty, the concordance rate between the two techniques was 78%. Nineteen patients were restudied with both techniques within 4 weeks after angioplasty. Echocardiography and SPECT were concordant in 17 of these 19 patients (89%), suggesting that exercise echocardiography is a feasible alternative to thallium-201 SPECT techniques for assessing patients who are undergoing angioplasty. These studies suggest that exercise echocardiography may have a role in serial assessment of patients undergoing coronary revascularization, both in the initial detection of functionally significant stenoses and in the assessment of the results of interventions. In contrast to these, an earlier study by Aboul-Enein et al[104] reported a sensitivity of only 67% using posttreadmill echocardiography to detect restenosis 6 months after successful coronary angioplasty. Looking at maximal predicted heart rate, pressure rate product, and exercise duration, the authors could find no significant differences between the 32 patients in whom exercise echocardiography correctly predicted restenosis and 16 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 22 patients with false-negative results, suggesting a lack of functional significance of the angiographically determined stenosis. Differences in populations between this study and others with better sensitivity for restenosis detection may explain the lower sensitivity noted by these authors. Whereas the patients in the latter study underwent exercise echocardiography and coronary arteriography 6 months after angioplasty as part of a study protocol, regardless of symptoms, the patients in the study by Hecht et al,[93] for example, were evaluated because of recurrent chest pain, suggesting a higher pretest probability. Also, 38 of 48 (80%) of those found to have angiographic restenosis in the study by Aboul-Enein et al[104] had single-vessel disease, which is less likely to produce a positive test result. More recently, Mertes et al[95] examined the role of bicycle stress echocardiography utilizing peak exercise imaging in 86 patients approximately 6 months after nonsurgical revascularization, including angioplasty, stenting, and atherectomy. The overall sensitivity for peak bicycle stress echocardiography in the detection of significant coronary artery disease was 83%, and the specificity was 85%. This is compared with a sensitivity of 42% for stress electrocardiographic detection of significant coronary artery stenoses. In this study, stress echocardiography was also found to be useful for detecting progression of previously existing coronary stenoses that had not undergone revascularization. Interestingly, all patients with false-negative results in this study had failed to achieve the target heart rate at peak exercise. To circumvent the problem of suboptimal exercise, Hoffman et al [105] used transesophageal pacing echocardiography in the detection of restenosis in 60 patients approximately 5 months after successful angioplasty. The sensitivity of transesophageal pacing echocardiography for the detection of restenosis or progression of coronary disease in nondilated vessels was 84% and compared favorably with the 86% sensitivity for technetium-99m sestamibi-SPECT imaging. The sensitivity of electrocardiography in this study was 50%. Many centers have gone to the use of pharmacologic stress echocardiography after revascularization in patients who are unable to perform maximal exercise. Preliminary data suggest that dobutamine stress echocardiography is able to identify patients with significant coronary stenosis prior to angioplasty and to demonstrate improvement in wall motion abnormalities after successful angioplasty (see Chapter 14) . mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 22 Exercise Echocardiography After Coronary Artery Bypass Grafting Although exercise echocardiography has become an accepted modality as a screening test in the initial evaluation of patients with suspected coronary artery disease, limited data exist regarding the use of exercise echocardiography to predict graft patency after coronary artery bypass grafting. Treadmill exercise testing has been the accepted modality for evaluation of patients after bypass surgery, but the high prevalence of resting electrocardiographic abnormalities in this group introduces a high rate of nondiagnostic electrocardiographic responses. For this reason, thallium SPECT imaging was recognized early on as a valuable adjunct in sorting out the nondiagnostic electrocardiographic responses in such patients.[106] It seems logical that if exercise echocardiography is able to accurately detect ischemic segments in territories deprived of blood supply via native vessels, segments supplied by stenotic grafts would be similarly detected. Although few in number, published studies using exercise echocardiography to detect graft patency have been extremely encouraging; these are summarized in Table 13-8 .[107] [108] [109] Sawada et al[107] used upright bicycle exercise echocardiography to assess bypass graft patency in 41 patients at a mean of 6 years |
after coronary artery bypass surgery. The presence of inducible ischemia was correlated with vessel stenoses, including obstructed bypass grafts, obstructed native vessels without prior revascularization, and diseased native vessels distal to anastomotic sites. In the 35 patients with graft stenosis, exercise echocardiography demonstrated ischemia in 33 patients, a sensitivity of 94%. Exercise echocardiography also correctly identified five of six patients without significant disease, with a specificity of 83%. Through the use of segmental wall motion analysis, accurate identification of the location of significant stenoses (i.e., anterior vs. posterior circulation) was possible. The sensitivity for detection of TABLE 13-8 -- Accuracy of Exercise Echocardiography After Coronary Artery Bypass Grafting (CABG) Years After Sensitivity, Specificity, Study Patients, n CABG % % Sawada et al[107] 41 6 94 83 Crouse et al[108] 125 7 98 92 Kafka et al[109] 182 3.6 79 82 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 22 292 compromised arterial supply in the left anterior descending distribution was 89%, and in the posterior circulation it was 88%. Crouse et al[108] studied 125 patients a mean of 7 years after coronary artery bypass grafting and reported a sensitivity of 98% and a specificity of 92% for the detection of graft or native vessel stenoses of 50% or greater reduction in luminal diameter. More recently, Kafka et al[109] reported that exercise echocardiography was able to successfully detect both single- vessel disease and multivessel disease, with a sensitivity of 77% and 96%, respectively, in a population of 182 patients undergoing symptom-limited treadmill exercise, electrocardiography, and exercise echocardiography for routine follow-up. Patients in this study had undergone revascularization with coronary artery bypass grafting 3½ years previously. Despite a lower prevalence of disease in this series when compared to the series of Sawada et al[107] and Crouse et al, [108] the overall sensitivity and positive predictive value were high (85%) when compared with exercise electrocardiography, which had a positive predictive value of only 62%. The negative predictive value for the corresponding techniques was 81% and 52% for exercise electrocardiography and echocardiography, respectively. In summary, the results of exercise echocardiography compare favorably to results of studies using thallium SPECT in the detection of ischemia in the region of coronary artery bypass grafts. Echocardiography performed in conjunction with exercise electrocardiography has a high feasibility rate— greater than 90% in these reported series—and provides superior sensitivity and specificity than exercise electrocardiography alone. These studies illustrate the ability of exercise echocardiography to identify graft as well as native disease stenosis in a population in whom interpretation of electrocardiographic response is less than optimal. Exercise Echocardiography After Acute Myocardial Infarction Following successful reperfusion for acute myocardial infarction, accurate prognostic assessment is critical in directing expensive and limited invasive resources to those patients who will receive the greatest benefit. Two important determinants of prognosis are left ventricular systolic function and the severity of underlying coronary artery disease. Medical centers performing primary angioplasty may use the results of cardiac catheterization to provide risk assessment, but most clinicians have traditionally performed noninvasive testing to predict prognosis and guide mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 12 di 22 future therapy. The practitioner has a choice of tests with which to accomplish this assessment. In the past, two tests have frequently been called upon to provide assessment of systolic function and ischemia: radionuclide ventriculography or echocardiography to determine systolic function and submaximal exercise testing for the assessment of ischemic burden. More recently, stress echocardiography has been used to provide data about both left ventricular function and the presence of residual ischemia to assess future risk of cardiac events. Future ischemic events appear to involve increasingly complex interactions between an ischemic milieu and inflammation, but stress echocardiography is a relatively inexpensive test that has been shown to correctly stratify patients into high- and low-risk subgroups. Submaximal exercise testing can be safely performed after myocardial infarction and has been shown to provide useful prognostic information with regard to subsequent cardiac events.[110] [111] Treadmill testing, however, while able to identify some patients who are at high risk for subsequent cardiac events, has a sensitivity of only 50% to 70% for the prediction of subsequent coronary events.[112] [113] Thallium scintigraphy has been shown to improve the sensitivity for prediction of cardiac events after myocardial infarction.[114] More recently, two-dimensional echocardiography after low-level treadmill exercise has been shown to provide useful information for the purposes of risk stratification and prediction of subsequent cardiac events.[57] [115] [116] Most of the studies examining exercise echocardiography for postmyocardial infarction assessment were performed before the widespread use of reperfusion therapy and included as events the "soft" events of revascularization. Nonetheless, these studies demonstrate the ability of exercise echocardiography to identify a high-risk group, particularly when combined with clinical risk assessment. Jaarsma et al[115] studied a group of 43 patients with exercise echocardiography within 3 weeks of acute myocardial infarction. All patients were noted to have resting wall motion abnormalities. Images obtained immediately after exercise demonstrated new wall motion abnormalities, remote from the site of myocardial infarction, in 18 patients, 17 of whom were shown to have multivessel coronary artery disease. This is compared with only 5 of 25 patients without remote wall motion abnormality who were found at catheterization to have multivessel disease. The development of a new wall motion abnormality, remote from the site of myocardial infarction, predicted multivessel coronary disease with a mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 13 di 22 sensitivity of 77% and a specificity of 95%. It also predicted a high-risk group for reinfarction or recurrent angina within 12 weeks, demonstrating the ability of exercise echocardiography to predict a higher risk group for cardiac events based on the identification of patients with multivessel disease. Transient remote ischemia during the first several hours of acute myocardial infarction has been attributed to a supply-demand imbalance in areas perfused by a critically stenosed vessel in noninfarcted segments of myocardium. Because remote ischemia signifies multivessel disease, these patients would presumably be at high risk for the development of subsequent events. Ryan et al[116] examined the predictive value of either remote or adjacent asynergy in 40 patients shortly after myocardial infarction using posttreadmill exercise echocardiography and found it to have an excellent predictive value for subsequent cardiac events. In a 6- to 10-month follow-up period, cardiac events occurred in 20 patients, 16 of whom had a positive exercise echocardiogram (80% sensitivity). A negative exercise echocardiogram was predictive of a good clinical outcome without subsequent cardiac events in 19 of 20 patients (specificity, 95%). In this group of postmyocardial infarction patients, treadmill characteristics were unable to identify high- and low-risk groups. Likewise, Applegate 293 et al[57] found that neither electrocardiographic nor clinical characteristics could identify a high-risk group in another study of 21 patients who underwent symptom-limited treadmill exercise shortly after acute myocardial infarction. In this study, multivariate logistic regression analysis was performed on several clinical, treadmill, and electrocardiographic characteristics. Wall motion abnormalities immediately after exercise and echocardiographically determined ejection fraction had the highest predictive value (P < .001) for the prediction of future cardiac events. In patients treated with thrombolysis, the ability to exclude significant multivessel disease may help to avoid cardiac catheterization and to direct expensive resources and higher risk technologies to those patients who are at higher risk for poor outcome. Quintana et al[117] examined exercise echocardiography within a week after myocardial infarction in 70 patients, about half of whom had received thrombolytic therapy. Exercise mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 14 di 22 echocardiography correctly identified a high-risk group for cardiac events within 2 weeks after myocardial infarction. Twenty-two percent (6 of 27) of those with a positive exercise echocardiogram, versus only 5% (2 of 43) of those with negative studies, suffered an early cardiac event. At 4-year follow-up, the cumulative event-free survival rate was significantly better in patients with a negative exercise echocardiography. While the electrocardiographic response also identified patients in whom events were more likely to occur, exercise electrocardiography was unable to identify a low-risk group. These studies demonstrate the usefulness of two- dimensional exercise echocardiography in helping to stratify patients into high- and low-risk groups after myocardial infarction and to predict a high- risk group for subsequent cardiac events on the basis of ischemia. An area of current active clinical investigation is the application of pharmacologic stress echocardiography to identify stunned and hibernating myocardium after myocardial infarction. The goal of these techniques is to determine potentially viable segments of myocardium that would be expected to recover function without revascularization after myocardial infarction, as opposed to those that are more likely to benefit from revascularization. Dobutamine echocardiography, discussed in Chapter 14 , has shown promise in the area of identification of stunned segments in the immediate post-infarction period and has been widely utilized for this purpose. Recruitment of myocardial segments with low-dose dobutamine shortly after acute myocardial infarction identifies segments that are likely to recover function without further intervention.[118] [119] Subsequent deterioration of some segments with higher doses of dobutamine (the so- called "biphasic" response) signify segments that may improve only after revascularization is performed. In theory, a low level of exercise could potentially be used to identify viable myocardium in analogous fashion to low levels of dobutamine infusion. A study by Hoffer et al[120] has investigated the utility of low-level bicycle exercise shortly after myocardial infarction to identify reversible dysfunction through augmentation of stunned segments. These authors noted improvement with low-level bicycle exercise in some akinetic segments within the infarction zone of patients with recent myocardial infarction, similar to the augmented response seen in viable segments with low-dose dobutamine infusion. Segments that improved with exercise were more likely to recover function at follow-up, signifying reversible dysfunction. Since multiple graded levels of exercise were not tested, it is unknown whether some segments that improve with low levels of exercise would demonstrate a biphasic response as well, with higher cardiac workloads. Whether mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 15 di 22 echocardiographic monitoring during multiple graded levels of exercise could detect ischemic segments suitable for revascularization has not been investigated. Exercise Echocardiography in Women Despite the fact that cardiovascular disease is the number one killer of women in the United States, accounting for approximately 500,000 deaths annually, most studies involving noninvasive techniques to identify patients with coronary artery disease focused exclusively on men, until relatively recently. Because of a variety of social, economic, and medical beliefs, women were excluded from populations with coronary disease under study. Even in the current era, there are surprisingly few studies examining diagnostic and prognostic implications of noninvasive testing of women (Table 13-9) . One reason for the paucity of published data in the noninvasive assessment of coronary disease in women is the fact that stress testing is believed to be less accurate in women. Indeed, early studies of electrocardiographic stress testing in women usually displayed poorer sensitivity and specificity for the identification of significant coronary disease.[63] [121] [122] In retrospect, however, the majority of these studies were performed in women who, according to Bayesian theory, were of low pretest likelihood with lower disease prevalence than their male cohorts, a factor that adversely affects specificity. The low disease prevalence in populations under study contributed to the belief that women are less likely to suffer from coronary disease and less likely to need referral for invasive testing. As discussed previously, verification bias, or the tendency to avoid sending those with negative test results for cardiac catheterization, is also a major contributor to lower test specificity in women. Contributing to the lower sensitivity of stress testing in women is the fact that, in many early studies, women appear to have lower exercise capacity, achieving submaximal levels of cardiovascular stress more often, thereby rendering it less likely that ischemia would be provoked. In addition, hormonal and autonomic factors, inappropriate catecholamine release, syndrome X, and the presence of more comorbid diseases at the time TABLE 13-9 -- Studies Examining the Accuracy of Exercise Echocardiography in Women Study Year Patients, n Sensitivity, % Specificity, % Sawada et al[124] 1989 57 86 86 Williams et al[125] 1994 70 88 84 Marwick et al[126] 1995 161 80 81 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 16 di 22 Roger et al[84] 1997 96 79 37 294 of diagnosis, may further contribute to test inaccuracies in women. In an effort to increase the overall accuracy of stress |
testing in women, some practitioners have advocated the use of imaging techniques as an initial test. Recent studies have focused on the addition of echocardiographic imaging as a means to increase the accuracy of stress testing as an initial diagnostic test in women.[123] Recent studies have examined the echocardiographic responses to treadmill or bicycle exercise in women also undergoing diagnostic catheterization. [84] [124] [125] [126] Sawada et al[124] examined the diagnostic value of exercise echocardiography in 57 women with chest pain syndromes using coronary arteriography as the gold standard. Sensitivity and specificity for echocardiographic detection of coronary stenosis of 50% or greater were both 86%. Exercise echocardiography was particularly useful in sorting out patients with atypical chest pain with coronary disease (sensitivity, 84%) from those with a nondiagnostic exercise electrocardiogram who were free of coronary disease (specificity, 82%). Similarly, Williams et al[125] compared the accuracy of the exercise echocardiogram to the accuracy of 12-lead electrocardiography performed during maximal treadmill exercise in 70 women with a 53% pretest probability for coronary disease. Defining significant coronary disease as greater than 50% stenosis, exercise echocardiography had a sensitivity of 88% for the detection of coronary artery disease, compared with 57% for electrocardiographic analysis using ST depression of greater than 0.1 mV. The specificity of exercise echocardiography was 84%, compared with 51% for echocardiographic analysis. In both of these studies, the accuracy of exercise echocardiography significantly exceeded that of exercise electrocardiography and paralleled larger studies of predominantly male patients. [6] [51] , [61] [76] Marwick et al[126] investigated the use of exercise echocardiography in the detection of coronary disease in women and found it to have an overall accuracy of 81%, compared with overall accuracy of 64% for exercise electrocardiography. In addition, these authors examined the cost of exercise echocardiography and noted that it compared favorably with mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 17 di 22 several potential diagnostic strategies in the work-up of cardiac symptoms in women. These authors sought to identify a diagnostic strategy that would balance the cost of diagnostic testing (defined as local Medicare reimbursement) with the lowest number of false-negative results and the fewest inappropriate referrals for cardiac catheterization. Compared with electrocardiography or echocardiography as an initial test (with and without Bayesian analysis) or angiography alone as the only diagnostic work-up, exercise echocardiography provided the best overall accuracy at the least cost. Data continue to accumulate that exercise echocardiography, because of preserved accuracy in patients with low to intermediate pretest likelihood of disease and because Medicare reimbursement rates are roughly half of those for radionuclide methods, may be the initial stress test of choice for women. The ultimate test of any noninvasive strategy may not be its ability to detect disease but its ability to predict future events. Recent studies have examined the ability of exercise echocardiography to predict prognosis in patients with known or suspected coronary artery disease.[127] [128] [129] Some of these studies focus on outcomes of women or include women as a major proportion of patients. One of the first of these studies was that of Sawada et al,[127] which encompassed 71 women among 148 patients who were followed for 28 ± 8 months after having a normal exercise echocardiogram. Cardiac events occurred in 2.8% (2 women) at 28 months without evidence of abnormality on exercise echocardiogram, demonstrating the ability of exercise echocardiography to identify a low-risk group for future events. Likewise, McCully et al[128] reported, in a large group of patients of whom about half were women, an excellent event-free survival rate for patients with normal treadmill echocardiograms who achieved an adequate level of cardiovascular stress (>5 METs for women). Another study examining prognosis in women reported that exercise-induced ischemia predicted cardiac events. In a multivariate analysis, Heupler et al[129] demonstrated incremental predictive value for exercise echocardiography in addition to clinical factors and exercise electrocardiography. Many of these studies have been performed in academic centers where referral of higher risk patients may falsely elevate the sensitivity of diagnostic testing and its ability to prognosticate. Exercise echocardiography has also been shown to correctly stratify women as to risk in a community setting. In a study of 1188 women with known or suspected coronary disease who underwent treadmill exercise echocardiography, the degree of ischemic wall motion abnormality was an mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 18 di 22 important factor in identifying a very high risk group.[130] Patients with resting wall motion abnormalities in addition to exercise-induced ischemic abnormalities had the highest rate of cardiac death and myocardial infarction. These studies highlight the ability of echocardiography to risk-stratify patients into high-, intermediate-, and low-risk subsets based on echocardiographic response to exercise and to select patients who will most benefit from further invasive procedures. Further studies will need to be performed. Exercise Echocardiography in the Determination of Prognosis The acceptance of stress echocardiography as a diagnostic tool able to guide decision making for medical and interventional procedures has allowed for follow-up of patients with coronary disease. Published event rates for patients with myocardial infarction undergoing exercise echocardiography were discussed earlier and demonstrate a higher rate of cardiac events in patients with significant degrees of inducible ischemia after infarction. As with acute myocardial infarction, the major determinants of prognosis in chronic coronary artery disease are overall left ventricular function and the presence and severity of ischemia. Echocardiography, in its ability to evaluate both of these factors, makes an ideal tool for the determination of prognosis. Event rates for patients with chronic coronary disease with normal or abnormal test results have been examined with regard to "hard" cardiac events such as myocardial infarction and cardiac death as well as "soft" cardiac events such as revascularization. These findings demonstrate a more benign prognosis for patients with normal exercise echocardiograms, with higher event rates noted for those with inducible ischemia (Table 13-10) 295 TABLE 13-10 -- Exercise Echocardiography for Prognostic Assessment of Patients with Known or Suspected Coronary Artery Disease Event Rates * Patients, Abnormal Normal Study n Follow-up, mos SE SE Sawada et al[127] 148 28 — 1.7/.85 * mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 19 di 22 Marwick et al[132] 463 44 9/6.5 7/2 Krivokapich et al 360 12 34/9 9/2 [131] McCully et al[128] 1325 23 — 2.5/<1 * Percentage of events at 12 months, total/spontaneous. SE, stress echocardiography. Two studies have noted low event rates of less than 1% per year in patients with normal resting function and no exercise-induced wall motion abnormality.[127] [128] Importantly, in both of these studies, a normal study finding is defined as one that is normal both at rest and with exercise. In some cases, higher event rates have been noted for patients with negative test results, and often these higher event rates were reported in studies that allowed patients with resting wall motion abnormalities to be included within the "negative" group. Krivokapich et al,[131] defining a negative test result as lack of ischemia with exercise, noted a higher event rate of 9% in patients with a negative exercise echocardiogram. In this study, soft events such as revascularization were also included as events, obviously having had an adverse affect on total event rate. When only myocardial infarction is examined, the event rate dropped to only 2%. Likewise, Marwick et al[132] noted in a group of 463 patients an event rate of 7% for patients with a negative exercise echocardiogram but when 15 of 20 patients with revascularization as the only event were excluded, the event rate was reduced to less than 2% per year for spontaneous events. These studies demonstrate that exercise echocardiography in patients undergoing stress testing for known or suspected coronary disease is able to effectively stratify patients as to future risk and to guide therapy for patients at higher risk. The presence of electrocardiographic ST depression appears to add prognostic information to the value of the echocardiographic response. For example, in the study of Marwick et al[132] , the rate of events including revascularization was highest in patients with both echocardiographic and electrocardiographic evidence of ischemia (event rate, 45%), with a lower event rate of 38% in patients without exercise-induced electrocardiographic changes. Likewise, Krivokapich et al[131] noted highest event rates for patients with both electrocardiographic and echocardiographic evidence of ischemia. In patients without echocardiographic evidence of ischemia, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 20 di 22 however, event rates were still higher in patients with a positive exercise electrocardiogram compared with a negative electrocardiogram. In both of these studies, although echocardiographic wall motion response appears to provide the greatest prognostic information, the electrocardiographic response appears to add prognostic value. Dobutamine echocardiography, discussed elsewhere, has provided the largest group of data for prognostication in patients referred for known or suspected coronary disease.[133] [134] In particular, dobutamine echocardiography appears to be able to accurately stratify risk in patients scheduled for vascular surgery, with published data encompassing more than 1500 patients.[135] Together, exercise and pharmacologic stress echocardiography is quickly gaining momentum as a test that can accurately and effectively stratify patient risk and guide therapeutic decisions. Cost-Effectiveness Issues The rising tide of health care costs, along with recent government budget cuts for reimbursement for many inpatient procedures, mandates that physicians be aware of the relative costs of procedures they order or perform on their patients. The cost of any procedure can be examined from a variety of viewpoints, including the cost to the patient—that is, insurance or Medicare reimbursement—the actual cost to the hospital or physician performing the test, and the cost of further diagnostic testing that the test result initiates. Cost-effectiveness examines cost versus healthcare outcome, usually expressed as a unit of effect on health care, such as survival or quality-assisted life-years. This is not meant to be a comprehensive discussion of cost analysis but a simple comparison of stress echocardiography with other testing strategies that provide similar information at similar risk to the patient. Several authors have addressed the issue of cost-effectiveness of stress testing as an initial strategy as compared with proceeding directly to invasive tests, and many of these assessments highlight the importance of determining pretest likelihood of disease prior to testing.[136] [137] [138] [139] If a high degree of likelihood exists that a patient has coronary disease, (greater than 75%), then the best initial strategy is likely to be proceeding directly to angiography, as suggested by Bayes' theorem. On the other hand, in case of very low pretest likelihood (i.e., less than 20%), perhaps no further testing is recommended. For patients with intermediate pretest likelihood of disease, the best initial strategy has been shown to be noninvasive testing mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 21 di 22 followed by catheterization in patients with high likelihood of significant coronary disease based on results of noninvasive testing. In contrast, Shaw et al[136] examined the use of radionuclide imaging as an initial strategy in women and found that noninvasive testing was approximately $1000 less over a 2.5-year period as compared with proceeding directly to catheterization for patients with intermediate pretest likelihood of disease. Similarly, Marwick et al[126] examined multiple different strategies involving stress electrocardiography or echocardiography versus catheterization as an initial strategy, noting that exercise echocardiography led to the least number of false results, providing the greatest sensitivity and specificity for detection of coronary disease. False-positive test results were presumed 296 to lead to inappropriate angiography. Thus, although exercise electrocardiography was a less costly test from the standpoint of reimbursement, it was assumed to lead to a higher number of inappropriate catheterizations. Medicare fees and volumes for various stress testing techniques, which were published in 1996, compared professional and technical fees as well as relative value units (RVUs), which provide an estimate of relative cost.[140] Within the published guidelines of the American College of Cardiology and the American Heart Association for exercise testing, while treadmill testing alone was noted to be least costly (3.30 RVUs), performing this test in all cases would not necessarily result in lower cost of patient care, since test inaccuracies can be expected to lead to further unnecessary testing. Imaging adds considerably to the cost of reimbursement (5.3 times that of treadmill), as does echocardiography (2.3 times higher). However, as discussed previously, given the improved accuracy of exercise echocardiography, its relatively lower expense as an imaging modality when compared with radionuclide technology makes it an attractive alternative. In comparison with |
radionuclide techniques, echocardiography is likely to be reimbursed at roughly half the relative cost, based on Medicare reimbursement. In this light, few studies have examined nuclear techniques with echocardiography as a screening test. Garber et al[137] compared an initial strategy of arteriography with one of five noninvasive strategies, initially including echocardiography, nuclear techniques with SPECT, positron emission tomography, or treadmill electrocardiography. There were no significant differences in life expectancy based on the initial diagnostic test. The total cost of a strategy mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 22 di 22 that used echocardiography was less than one that began with radionuclide based on a cost-effectiveness ratio. Because of improved sensitivity compared with treadmill testing, exercise echocardiography resulted in better outcome. Thus, echocardiography was a highly cost-effective alternative to treadmill or radionuclide imaging. Kuntz et al[138] examined the cost-effectiveness of noninvasive strategies with exercise treadmill electrocardiography, exercise echocardiography, or SPECT nuclear imaging versus arteriography in the initial diagnosis of coronary disease. These authors found that either exercise electrocardiography or exercise echocardiography resulted in "reasonable" cost-effectiveness ratios for patients with mild to moderate risk for coronary artery disease. Proceeding directly to arteriography was cost- effective for patients with high pretest probability of coronary artery disease. Further studies of both cost and outcome will need to be performed in randomized fashion with longer term follow-up to determine whether exercise echocardiography will continue to assume a greater role in settings where HMO-driven decisions mandate the most information at the least cost. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/114.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Exercise Echocardiography Compared with Other Imaging Modalities A number of studies have compared exercise echocardiography with the more well established radionuclide techniques for the diagnosis of coronary disease. An early study compared two-dimensional echocardiography with radionuclide angiography during left lateral decubitus bicycle ergometry.[44] This study noted a higher sensitivity, 91%, for radionuclide angiography versus 76% for exercise echocardiography using a bicycle protocol. The problem with this and many subsequent studies is that such comparisons take place in centers where one or the other of the techniques being compared is more widely utilized, and different levels of expertise exist for the competing technologies. An exception to this is the large study of 292 patients reported by Quinones et al[141] that analyzed all patients with both exercise echocardiography and SPECT thallium for the diagnosis of coronary disease. Sensitivity for single-vessel disease was quite low with both techniques (58% for echocardiography and 61% for thallium SPECT), and both techniques correctly identified three-vessel disease with a 94% sensitivity. Specificity was similar in both groups (88% for echocardiography and 81% for thallium SPECT). In a comparison of exercise echocardiography with technetium-99m MIBI-SPECT, Pozzoli et al[142] found a good correlation between perfusion and wall motion in 103 consecutive patients, with concordance in 84% of segments overall. Concordance was especially high (91%) in patients with previous myocardial infarction. These studies, while limited, demonstrate the ability of both techniques to detect patients with significant disease, providing similar clinical information about the functional significance of underlying coronary disease. The advantage of echocardiography lies in its ability to provide additional information about left ventricular function and underlying valvular disease without adding significantly to the time of the echocardiographic study. The accuracy of exercise echocardiography has also been compared to that mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 of echocardiography with different forms of cardiovascular stress. Beleslin et al[40] compared exercise, dobutamine, and dipyridamole echocardiography in 136 consecutive patients with a high prevalence of coronary artery disease. The sensitivity of exercise echocardiography was 88%, compared with 82% for dobutamine echocardiography and 74% for dipyridamole echocardiography. Specificity for exercise, dobutamine, and dipyridamole echocardiography was 82%, 77%, and 94%, respectively. All three tests were noted to have acceptable diagnostic value, with a higher diagnostic accuracy for stress echocardiography in patients with single- vessel disease. Similarly, Marangelli et al[143] compared exercise, dipyridamole, and transesophageal atrial pacing in conjunction with echocardiography in 104 consecutive patients with normal resting wall motion who underwent coronary arteriography. The sensitivities for exercise, transesophageal atrial pacing, and dipyridamole were 89%, 83%, and 43%, respectively, suggesting that exercise and atrial pacing have similar sensitivities and may exceed the sensitivity of pharmacologic stress with vasodilators. In comparison with nonexercise forms of cardiovascular stress, the additional information gleaned from analysis of the hemodynamic response to exercise proves to be an invaluable adjunct in the clinical assessment of patients. If the patient is able to exercise, the additional clinical value gained in analyzing the physiologic exercise data adds 297 incrementally to the information learned from wall motion analysis alone. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/115.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Summary Exercise echocardiography is an accurate technique for initial diagnosis of coronary disease and can provide prognostic information in many subgroups with known disease. Over the past decade, its acceptance by the medical community has grown and current applications have expanded to include diagnosis and prognosis in a wide range of patients, including women, for whom accuracy and cost appear better than other comparable techniques. Current clinical applications of exercise echocardiography include diagnosis of suspected coronary disease, guiding percutaneous intervention, surveillance of patients following coronary bypass surgery, and prediction of prognosis in chronic coronary disease as well as acute myocardial infarction. Accuracy of exercise echocardiography is now considered to be at parity with other noninvasive imaging techniques with a cost roughly half that of competing nuclear techniques. Its lower cost makes exercise echocardiography an attractive alternative as an initial diagnostic test and in follow-up of patients with coronary disease. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/116.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 5 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company 301 Chapter 14 - Stress Echocardiography with Nonexercise Techniques Principles, Protocols, Interpretation, and Clinical Applications Thomas H. Marwick MD, PhD 302 TABLE 14-1 -- Indications for Nonexercise Stressors Unable to Exercise Able to Exercise Inability to exercise maximally Specific indications Diagnosis of coronary artery disease, Coronary spasm decision making Myocardial viability Risk stratification Developing indications Situations preventing exercise Onset of ischemia Angiography laboratory, operating room New technologies (TDI, CK, contrast) CK, color kinesis; TDI, tissue Doppler imaging. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 5 Background Indications for Nonexercise Stress Testing The performance of a maximal level of exercise is a critical determinant of the sensitivity of all stress modalities for the detection of coronary artery disease. Unfortunately, many patients—fully 30% to 40% at some tertiary centers (Fig. 14-1) (Figure Not Available) —either cannot exercise at all or cannot exercise maximally,[1] but these patients may still need to undergo stress testing for diagnostic, decision making, or prognostic purposes. The most common causes of limited exercise capacity are vascular disease (either peripheral or cerebrovascular) and orthopedic problems. Other situations warranting nonexercise stress testing include severe cardiopulmonary disease and general debility, especially among the elderly, in whom pharmacologic testing with both dobutamine and vasodilators has been shown to be well tolerated and reliable.[2] [3] [4] [5] Although the inability of a patient to exercise maximally constitutes the main indication for the use of nonexercise stressors, such stressors are less commonly indicated in other situations (Table 14-1) . The most important of these situations include circumstances in which the use of a pharmacologic agent may offer diagnostic dimensions that are not available from exercise stress, for example, the diagnosis of coronary spasm using ergonovine stress testing.[6] [7] A similar scenario involves patients early or late after myocardial infarction, after which left ventricular dysfunction may not be permanent. The diagnostic challenge in this situation is that whereas stunned myocardium improves spontaneously, the revascularization of hibernating Figure 14-1 (Figure Not Available) Proportion of patients undergoing exercise testing who are unable to exercise maximally. (From Marwick T: Acta Clin Belg 1992;47:1– 51.) myocardium has implications for functional capacity and prognosis. As discussed later in the chapter, echocardiography can be used with dobutamine[8] or dipyridamole[9] [10] stress, or both,[11] for the identification of viable myocardium. Pharmacologic agents are more appropriate than exercise for stress testing in some environments, such as the cardiac catheterization laboratory or operating rooms. Finally, nonexercise methods have been used in mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 5 preference to exercise echocardiography even in patients who are able to exercise because of their relative technical ease. The incremental nature of these stressors means that the time-course of ischemia can be identified; these data are not available using posttreadmill stress and are more difficult to obtain with bicycle exercise testing. Although the decision to use a nonexercise stress may not be justifiable with routine echocardiographic imaging at present, the facilitation of adjunctive techniques discussed subsequently—such as tissue Doppler, color kinesis, and contrast echocardiography (which may be less feasible during exercise than nonexercise stress)—could in the future justify the use of nonexercise techniques in patients who are able to exercise. Choice and Mechanism of Action of Nonexercise Stressors There are two general groups of nonexercise stress agents: those that induce ischemia by increasing myocardial work and oxygen consumption (exercise-simulating agents), and those that induce ischemia by influencing coronary perfusion and therefore myocardial oxygen supply (vasoactive agents). The latter include the coronary vasodilators dipyridamole and adenosine, which cause ischemia by provoking coronary steal, and ergonovine, which can be used to provoke coronary spasm. In addition to these stressors, nonpharmacologic approaches including hand-grip and the cold pressor test[12] [13] have been used. Hand-grip testing is often combined with dobutamine-atropine testing,[14] but the cold pressor test has not been widely adopted clinically because of limited efficacy and patient discomfort. Exercise-Simulating Agents The exercise simulators include dobutamine and other sympathomimetic agents, pacing stress, and atropine 303 (usually used as an adjunct to the other approaches), all of which increase cardiac work and myocardial oxygen requirement. Thus, the induction of ischemia and regional dysfunction reflects the inability of the diseased coronary circulation to respond to this increased oxygen demand, a process that parallels the response to exercise. However, processes additional to classic "demand" ischemia may be active, and sympathomimetic agents may place an additional stress on the heart through effects on cardiac metabolism—an "oxygen-wasting" effect. In a group of patients with mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 5 ischemic responses to both dobutamine and exercise, ischemia appeared at a significantly lower rate-pressure product during dobutamine than during exercise stress, consistent with the presence of a factor additive to that of cardiac work suggested experimentally.[15] [16] [17] Another contributor to this process might include concurrent "supply" ischemia due to reduction of coronary flow; certainly, sympathomimetic agents cause a dose-dependent reduction of subendocardial perfusion and maldistribution of coronary flow, in the face of mild coronary stenoses.[18] The latter component, together with regional flow heterogeneity based on tachycardia-induced coronary vasodilation, [19] is responsible for perfusion defects detected at myocardial perfusion imaging. Because increased cardiac workload and oxygen demand is the usual mechanism underlying ischemia in most ambulatory situations, the exercise-simulating agents are often considered to be a more physiologic means of stressing the heart, although "demand" ischemia may |
be combined with reduction in coronary supply due to vasospasm or coronary steal. Vasoactive Agents The use of dipyridamole in combination with myocardial perfusion imaging is based on the induction of maximal coronary vasodilation in all territories. Flow heterogeneities (and therefore apparent perfusion defects) develop if a coronary stenosis limits the regional hyperemic response.[20] Of note, this process does not involve the provocation of ischemia in a functional or metabolic sense. In contrast, the development of regional wall motion abnormalities at stress echocardiography necessitates the induction of ischemia. The chief mechanism of vasodilator-induced ischemia is coronary steal,[20] which may be either "vertical" or "horizontal" through the left ventricular wall. The best known mechanism is horizontal steal, in which blood flows to nonstenosed from stenosed territory, owing to reduced collateral flow into the stenosed territory because of depressurization of vessels supplying the collaterals due to increased runoff. Vertical steal also occurs because of vasodilator-induced depressurization of the microcirculation, causing subendocardial vessels to collapse under the greater extravascular pressure in this region and "stealing" flow to the subepicardium from the subendocardium. Other mechanisms of vasodilator-induced ischemia, unrelated to coronary steal, include reduced coronary supply because of coronary spasm (which is the major effect of ergotamine), systemic hypotension, or collapse of the stenosis. Under conditions of maximal coronary hyperemia, driving pressure is the main determinant of mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 5 myocardial perfusion because vasodilator reserve is exhausted. Hence, systemic hypotension may accentuate hypoperfusion due to coronary steal. Stenosis "collapse" may be provoked if profound microcirculatory vasodilation causes a reduction of lateral pressure induced by increased flow. Finally, myocardial oxygen demand may be increased in response to increased cardiac workload because of increased sympathetic activity secondary to angina. Agents Used to Identify Myocardial Viability In the presence of dysfunctional but viable myocardium, regional function is enhanced by the inotropic effect of low-dose dobutamine, although this appears to require both recruitable perfusion and an increment in metabolism.[21] The mechanism of this is ill-defined but most likely pertains to enhanced calcium cycling. Viable myocardium supplied by a patent infarct-related vessel (generally corresponding to stunned myocardium) demonstrates a sustained improvement during the infusion, which then reverses after the test. Viable tissue supplied by a stenosed infarct-related artery (which may involve stunned or chronically ischemic— "hibernating"—tissue) is characterized by an initial improvement, occurring at low doses (<20 µg/kg/minute), or low heart rates, or both, followed by deterioration of regional function as the chronotropic effect becomes more prominent and myocardial work increases.[8] If the region is supplied by a critically stenosed artery, however, it may be possible for the territory to become ischemic before there is a noticeable enhancement of contractility. Moreover, the ability of the myocardium to thicken is determined by the amount of infarcted tissue within the segment.[22] Myocardial viability may also be inferred from the contractile response to dipyridamole. The mechanism of this is also putative but probably relates to myocardial congestion with interstitial fluid due to vasodilation. A so- called mini-Starling effect may be caused by this congestive process, producing additional tension on the myofibrils.[23] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/118.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 11 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Principles of Nonexercise Stress Techniques Pharmacology and Physiopathology of Nonexercise Stress Techniques Exercise-Simulating Agents The exercise-simulating agents include dobutamine, dopamine, epinephrine, and isoproterenol. Of these, dobutamine has become the most commonly administered exercise-simulating agent, and the majority of published data on pharmacologic stress echocardiography have involved this agent. Arbutamine, a dobutamine isomer, was developed in the last decade but showed no substantial clinical merits compared with its parent compound, and distribution of the agent has been discontinued.[24] [25] Dopamine 304 stimulates alpha receptors and, if it extravasates, may cause localized limb ischemia due to vasoconstriction. Dopamine may also be a less effective precipitant of myocardial ischemia than is dobutamine.[26] Although other sympathomimetic agents have been used for stress testing,[27] epinephrine and isoproterenol are probably the more arrhythmogenic. This side effect is dose dependent, but its avoidance by conservative dosing may compromise the sensitivity of the test by limiting the amount of stress on the heart. Dobutamine is predominantly a beta-1 agonist, and normal areas become hyperkinetic in response to its inotropic effect. Myocardial segments supplied by a stenosed coronary artery may become akinetic or dyskinetic but more commonly are unable to augment their thickening and excursion, and the contrast between this response and the hyperkinetic function of normal segments facilitates the detection of zones with abnormal function. Vasodilation and chronotropy appear at higher doses, [26] usually at the 20 µg/kg/minute level of the routine dobutamine stress protocols, reflecting mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 11 the stimulation of other receptors to a lesser degree. This chronotropic response appears to be the most important factor in terms of precipitating ischemia; most dobutamine stress protocols cause a mean heart rate increment of 40 to 50 beats per minute and mean peak heart rates of 110 to 120 beats per minute.[28] [29] [30] [31] [32] [33] [34] However, reflex bradycardia may occur in response to hypertension. The vasodilator effects of dobutamine may cause blood pressure to fall at peak doses, although blood pressure normally rises in response to the inotropic effect of the drug. Increases in myocardial oxygen demand due to increased cardiac work, as well as a weak vasodilator effect, lead to the development of coronary hyperemia in territories supplied by normal coronary arteries. Although this response is probably less than that induced by coronary vasodilators, the coronary hyperemic response to dobutamine stress permits its combination with perfusion scintigraphy.[34] [35] [36] [37] The detection of myocardial perfusion defects in the presence of coronary disease may be augmented by partial volume effects due to thinning of the ischemic wall. Vasoactive Agents Most of the experience with pharmacologic stress echocardiography using vasoactive agents has been obtained with the coronary vasodilators dipyridamole and adenosine. The coronary vasodilators differ with respect to the onset and duration of their effects. Dipyridamole increases endogenous adenosine levels by reducing cellular reuptake and metabolism, and thereby acts indirectly.[20] This indirect mechanism causes some delay between the administration of this agent and the timing of peak vasodilation, the half-life of this effect being 6 hours. The indirect action of dipyridamole may account for interindividual variations in the magnitude of its effects. Adenosine acts directly on the vasculature, its vasodilator efficacy being equivalent to that of papaverine.[38] The potency and speed of onset of adenosine cause its side effects to be more intense but also more short-lived than those of dipyridamole. An increasing amount of literature describes the combination of ergonovine with echocardiography. This agent has a direct effect on the vessel; responsiveness to acetylcholine may be related to loss of nitric oxide production at the site of disease. Exercise Simulation Using Pacing Stress Several nonpharmacologic approaches have been used for stress echocardiography, including "physiologic" stresses such as the cold pressor mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 11 test, which are poorly tolerated. Pacing is an alternative means of increasing cardiac work without resorting to pharmacologic techniques. Pacing-induced tachycardia increases myocardial oxygen consumption and thereby causes myocardial ischemia in the setting of significant coronary stenoses.[39] [40] The reduction of subendocardial perfusion with pacing[40] may also contribute to the development of ischemia. Ventricular pacing is not favored, as it causes both abnormal regional contractility and abnormal perfusion, so that pacing stress techniques generally involve atrial stimulation, either transvenously or via the esophagus (only the latter having gained acceptance as a routine stress modality). Of these, direct atrial pacing has been used for other stress imaging tests, but it is invasive and therefore has not achieved acceptance. Of the transesophageal pacing approaches, the "pill" electrode has formerly been studied, but although this technique is effective, it has the disadvantage of causing significant discomfort. Attachment of pacing electrodes to transesophageal echocardiography probes has been reported in trials[41] [42] but has not moved into commercial production; perhaps miniaturized transnasal probes could make this feasible. The development of a small esophageal pacing catheter offers enhanced contact between the electrodes and the esophagus, which facilitates the test. In particular, the technique causes less discomfort than other pacing techniques because of the presence of smaller pacing thresholds.[43] Atrial pacing stress is more invasive than pharmacologic stress echocardiography but may be useful in patients in whom the pharmacologic approaches are contraindicated or associated with side effects. Moreover, this technique has additional attractions that might justify its use in preference to pharmacologic testing. These include the capacity to achieve a target heart rate in virtually all patients, the potential to immediately terminate the tachycardia if the patient develops complications (in contrast to pharmacologic methods, which require a period of time for the effects to dissipate), and the ability to perform measurements in the ischemic ventricle at a low heart rate (after cessation of pacing). The latter may be of particular value if Doppler indices of diastolic function are being assessed, as these are difficult to measure in the presence of tachycardia (which with dobutamine takes some time to resolve, by which time the ischemia may also have dissipated). Using atrial pacing stress, ischemic myocardium has been shown to have reduced ventricular compliance.[44] Sudden termination of stress during ischemia may also be of value in the combination of stress testing with color flow Doppler echocardiography, as the use of low frame- mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 11 rates may pose a problem at high heart 305 rates. However, despite the benefits of transesophageal atrial pacing, its availability for many years,[45] and recent data showing correlation with dobutamine echocardiography despite a shorter test duration and better patient tolerance,[43] this technique has not become widely used because it remains somewhat invasive. Combined Approaches Atropine reduces the depressant effect of vagal stimulation on heart rate and may be particularly useful when reflex reduction of the heart rate occurs in response to blood pressure elevation. The combination of atropine with dobutamine has been found to be useful in patients who fail to develop an adequate degree of tachycardia in response to dobutamine, the most common situation involving patients taking beta receptor antagonists.[46] [47] [48] An additional component of tachycardia (and therefore ischemia due to increased oxygen demand) can also be obtained by combining atropine with dipyridamole.[49] [50] [51] In both circumstances, the addition of atropine to other stressors has been associated with an increment in sensitivity. Indeed, there is a trend toward earlier use of atropine during the dobutamine protocol,[52] [53] especially in beta-blocked patients. However, although nondiagnostic results of a submaximal heart-rate response can be avoided by the use of atropine, this adjunct does not help the results of submaximal tests that reflect premature termination of pharmacologic stress due to side effects. The rationale for combining dobutamine and dipyridamole Figure 14-2 End-diastolic apical four-chamber image in fundamental (A) and harmonic (B) modes. The use of harmonic imaging substantially improves visibility of the lateral wall and distal structures. reflects their action through different mechanisms. The sequence of drug administration can be used to produce a stepwise stress on the heart. The initial administration of dipyridamole permits detection of the most severe coronary stenoses due to the development of coronary steal. The subsequent incremental administration of dobutamine progressively increases oxygen demand, permitting the identification of progressively mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 11 more moderate stenoses.[54] The combination has also been used to enhance the accuracy of detection of myocardial viability.[11] Although the combination of these techniques has afforded higher levels of sensitivity than the individual tests can provide, using the current methodology, this is obtained at the cost of an unacceptably long stress protocol.[54] Echocardiographic Approach to Nonexercise Stress Techniques Image Acquisition The technical challenges of pharmacologic and pacing stress, although less extreme than those posed by exercise echocardiography (as the patient is neither moving nor hyperventilating), mandate |
the use of the best available echocardiography equipment. The development of harmonic imaging has made a substantial impact on endocardial visualization[55] [56] [57] (Fig. 14-2) and therefore the feasibility of stress echocardiography.[58] Although very few patients (<2%) have completely uninterpretable images, 306 failure to detect the endocardium in every myocardial segment is very common, and contrast is indicated if two to four segments are completely or partially obscured (Fig. 14-3) . Typically, transthoracic images are obtained in the four standard views (parasternal long- and short-axis and apical four- and two-chamber). Transesophageal echocardiography has been employed in combination with both pharmacologic[59] [60] [61] and pacing stress,[41] [42] [62] usually for patients with inadequate transthoracic images. During transesophageal imaging with pharmacologic stress, we approximate the standard imaging planes as closely as possible by recording transverse and longitudinal esophageal and transgastric short- and long-axis views. During pacing with electrodes attached to the transesophageal echocardiography probe, the need to stimulate the esophagus inhibits the ability to move the transducer, so that imaging is performed in the transgastric planes only. Although the constraints of a busy stress echocardiography schedule may preclude the performance of a detailed examination in every patient, a "screening" M-mode, pulsed wave (especially for left ventricular inflow), and color Doppler echocardiographic examination should be performed at the beginning of every study. Time should also be taken to optimize two- dimensional echocardiographic images, gain settings (for endocardial mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 11 detection), and image size (to obtain the best spatial resolution and frame- rate). During the stress, the patient is imaged continuously, and the images are stored on videotape. When the study is performed for the diagnosis of coronary disease, the digital quad-screen display is filled with a resting image, a low-dose image (10 µg/kg/minute dobutamine, 0.56 mg/kg dipyridamole, or a small heart rate increment with pacing), and two high- dose images (40 µg/kg/minute dobutamine or 0.84 mg/kg dipyridamole with or without atropine), or a peak and early poststress image. When a resting wall motion abnormality is present, and the clinical question pertains to the possibility Figure 14-3 Use of myocardial contrast for left ventricular opacification during stress echocardiography. Compared with harmonic imaging (A), the post-contrast end-diastolic apical four-chamber image (B) shows significant improvement of lateral wall resolution. of viable myocardium, we obtain two low-dose images (5 and 10 µg/kg/minute dobutamine) and one high-dose image. Image Processing Both videotape and digital techniques are used for interpretation and archiving of stress echocardiograms. Because modern echocardiography systems are fully digital, digital image capture is an easy process that permits rapid acquisition. Moreover, digital image processing facilitates image display and interpretation by allowing a side-by-side display of resting, low-dose, and high-dose images, as well as the ability to review individual frames (the latter permitting an effective evaluation of the temporal sequence of contraction). Although the use of digital echocardiography enhances the accuracy of nonexercise echocardiography, however, all studies should be recorded on videotape as well as in digital format. This provides a back-up in case technical problems with the digital capture (especially triggering) or corruption of the archived data threaten loss of the study. Indeed, routine review of videotape has a significant impact on diagnosis, probably by permitting review of off-axis images and regions that are not adequately represented by saving a single cardiac cycle. [63] Qualitative Interpretation The interpretation of stress echocardiograms for clinical purposes is based on a qualitative evaluation of regional function at rest and stress.[64] Some mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 11 standardization is obtained by scoring regional wall motion and thickening in a number of segments, the most widely used being a model based on that of the American Society of Echocardiography,[65] wherein the left ventricle is divided into 16 307 Figure 14-4 (Figure Not Available) Effect of a training period on the accuracy of interpretation of dipyridamole stress echocardiograms by learning and experienced groups of observers (shown at initial [Before] and follow-up [After] periods). (From Marwick T: Stress Echocardiography. Amsterdam, Kluwer Academic Publishers, 1994.) segments (anterior, septal, lateral, and inferior at the apex, with these segments as well as anteroseptal and posterior segments at the base and midpapillary muscle level). Despite this standardization, however, the expertise of the physician interpreting the test is critical, and even accomplished echocardiographers require a significant learning period. In a study of echocardiographers learning dipyridamole stress echocardiography, Picano et al[66] reported that 100 supervised studies were required to bring the accuracy of "novices" to the level of "experts" (Fig. 14-4) (Figure Not Available) . The standard qualitative algorithm for interpretation of pharmacologic stress echocardiography is summarized in Table 14-2 . With the exception of the low-dose responses to dobutamine and dipyridamole, which denote myocardial viability (see later discussion), it may also be applied to pacing or other stressors. Regional wall motion at rest may be classified as normal, hypokinetic, akinetic, or dyskinetic. Severe hypokinesia may be difficult to distinguish from akinesia; a useful guide is based on endocardial excursion, with less than 2 mm identifying akinesia and less than 5 mm indicating hypokinesia. Regions that fail to thicken or that move only in late systole (after movement of the adjacent myocardium) may be moving passively and should be considered akinetic, irrespective of endocardial excursion. Segments with resting akinesis or dyskinesis are most likely composed of infarcted myocardium if the wall is TABLE 14-2 -- Interpretation of Myocardial Viability and Ischemia Using Dobutamine Echocardiography Resting Peak/Poststress mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 11 Diagnosis Function Low-Dose Function Normal Normal Normal Hyperkinetic Ischemic Normal Normal (unless Reduction vs. rest severe CAD) Reduction vs. other segments Delayed contraction Viable, patent Hypo/akinetic Improvement Sustained IRA improvement Viable, Hypo/akinetic Improvement Reduction (c/w low- stenosed IRA dose) Infarction A/dyskinetic No change No change CAD, coronary artery disease; c/w, compared with; IRA, infarct-related artery. thinned and dense,[67] but in the absence of thinning are quite likely to consist of viable tissue. Indeed, hypokinetic segments are not identified as being infarcted, on the basis that residual contraction implies the presence of residual viability. Because the process of thinning and fibrosis takes some time after infarction, myocardium of normal thickness is commonly seen after recent or non-transmural infarction. Improvement of abnormal function in response to low doses of dobutamine (5 or 10 µg/kg/minute) or dipyridamole (0.28 or 0.56 mg/kg) suggests the presence of viable myocardium (Fig. 14-5) , although this finding is more reliable if the segment subsequently deteriorates, which indicates ischemia. The global left ventricular responses to dobutamine stress include an increase in cardiac output and reduction of left ventricular cavity size, although neither is as prominent with vasodilator stress. Left ventricular dilation implies multivessel or left main coronary artery disease, but this is less commonly seen with pharmacologic than exercise stress,[68] probably because of reduction of left ventricular loading. Together with an extreme inotropic response, this afterload reduction may produce cavity obliteration, and although this response is favorable prognostically (presumably reflecting a low probability of multivessel disease), it may impair sensitivity because endocardial excursion is reduced and small areas of wall motion are unrecognized.[69] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 11 The normal regional response of segments to maximal 308 Figure 14-5 End-diastolic and end-systolic freeze-frame images illustrating left ventricular enlargement at dobutamine echocardiography in a patient with left ventricular dysfunction and multivessel coronary artery disease. There is a resting wall motion abnormality in the apex, which is unchanged with stress. At peak stress, there is left ventricular enlargement with reduction of systolic motion and thickening of the lateral (and to a lesser degree the septal) wall. inotropic stress is to increase endocardial excursion, speed of contraction, and degree of myocardial thickening. A deterioration of function from rest, or after an initial enhancement of function, indicates the development of ischemia with either dipyridamole or dobutamine (Fig. 14-6) . Variants of an overt deterioration include delayed contraction ("tardokinesis") and a reduction of myocardial thickening. Caution should be applied in the assessment of areas adjacent to zones of myocardial infarction, which may be tethered by the infarcted zone and hence fail to improve function with stress, or even appear dyskinetic if the infarct bulges during stress. Careful examination of wall thickening may assist in distinguishing peri-infarct ischemia and tethering. The diagnosis of ischemia in segments with abnormal resting function depends on the stress agent and is more difficult. At dobutamine echocardiography, if a segment shows akinesia or dyskinesia at rest, a further deterioration of function probably reflects increased loading rather than ischemia.[70] The most challenging interpretation is the diagnosis of ischemia in segments with resting hypokinesis. Segments demonstrating a stress-induced improvement are classified as normal, and those showing a deterioration (compared with either rest or low-dose) are identified as ischemic. However, differentiation between degrees of hypokinesia may be difficult, even with side-by-side cine-loop analysis. Some caution needs to be applied in the interpretation of regional variations in the degree of hyperkinesis, as these may occur in normal patients.[71] The diagnosis in hypokinetic regions that fail to improve function in response to stress is debated; if adjacent segments mount a hyperkinetic response, we characterize these as ischemic. The greatest limitations of the current application of stress mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 11 echocardiography are concerns related to subjectivity and reproducibility. Although single-center studies 309 Figure 14-6 Apical two-chamber views illustrating the development of myocardial ischemia (reduced wall thickening) of the apex during dobutamine stress echocardiography. End-diastolic images are given on the left and systolic images on the right, with resting images above and peak dose below. have suggested that the interobserver variation in interpretation is small,[72] interinstitution variability (although similar to that of other imaging techniques) is significant.[73] Interinstitution variability is particularly a problem in studies of poor image quality and in patients with mild ischemia. This discordance has been progressively reduced by definition of standard reading criteria[74] and more recently by the adoption of harmonic imaging.[75] The following reading guidelines are useful for controlling variation: minor degrees of hypokinesia are not identified as ischemia (especially if only apparent at peak and not at poststress readings); focal abnormalities that do not follow angiographic territories are ignored; abnormalities are corroborated whenever possible with another view; basal inferior and septal segments are not identified as abnormal in the absence of a neighboring abnormal segment; studies are read by multiple observers whenever possible; and reading is blinded to all other data. Finally, we find a standard sequence to be of value in the interpretation of stress echocardiograms (both exercise and nonexercise). We first review the video images of the resting examination, including M-mode and Doppler components. On beginning the review of the digital images, we first check that images are triggered correctly and the prestress, peak stress, and poststress views are comparable. We then briefly review the side-by- side display to see if there are new wall motion abnormalities or obvious changes in cavity size (suggesting multivessel disease) or cavity shape. Segmental analysis is carried out by careful comparison of regional function in each of the 16 segments, comparing the same site at rest and at stress. Both wall motion and thickening are compared, using both cine-loop and frame-by-frame review of the digital images. If image quality is not good enough to permit the use of thickening criteria, the reader should focus on the first part of systole to minimize the contribution of rotational or translational movement. Finally, videotaped stress images are examined, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 11 to review nonstandard views 310 and to check on conclusions based on the digitized images. From review of digital and video data, the site, extent (number of abnormal segments), severity (segmental wall motion score), time of onset and offset of ischemia, and the effect of ischemia on global left ventricular function can be derived. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/119.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 10 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright |
© 2002 W. B. Saunders Company Technical Aspects of Nonexercise Stress Techniques General Considerations The preparation for nonexercise stress testing does not deviate substantially from preparation for exercise stress testing. These tests should be performed in the fasting state, partly because nausea is a side effect with some agents (especially transesophageal pacing, dipyridamole, and adenosine), and also in case complications ensue, with attending risks of aspiration. For dipyridamole stress testing, coffee, tea, and cola drinks should be avoided for 12 hours before the examination, as xanthines antagonize the effects of dipyridamole on adenosine metabolism, as well as by direct competitive inhibition of adenosine activity. For diagnostic testing, patients should be instructed to stop anti-ischemic drugs on the day of the procedure, but medications may be continued if testing is being performed to assess the adequacy of therapy. During the preparatory stage of the test, intravenous access is secured, and electrocardiographic monitoring may be modified to remove electrodes from the echocardiographic windows. A minimum of two personnel (sonographer and physician) is mandatory for performance of these protocols, and many centers involve a nurse as well. Clinical and electrocardiographic monitoring during the tests parallels the monitoring undertaken during exercise stress testing. In addition to the usual resuscitation equipment, intravenous beta-adrenoreceptor blocking agents and nitrates should be available to treat severe ischemia, and for dipyridamole testing, aminophylline should be available for the treatment of severe ischemia, which occurs occasionally. Exercise-Simulating Agents Protocols for Administration of Sympathomimetic Agents Dobutamine has been administered using various empirical dose regimens, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 10 but the relative plasma levels with these have not been studied, and none is clearly superior to the others. The most widely used is an incremental administration (Fig. 14-7) from 5 µg/kg/minute to 40 µg/kg/minute in 2- or 3-minute stages.[28] [29] [30] [31] [32] [33] [34] Variants include maximal doses of up to 50 µg/kg/minute and down to 20 µg/kg/minute; lower dose-rates administered over longer periods are able to attain hemodynamic effects similar to those obtained by the high-dose protocols.[33] New accelerated dobutamine protocols are currently being used to reduce the duration of the test, but whichever regimen is applied, a reasonable (i.e., 2- to 3-minute) period at peak heart rate is desirable, as ischemic wall motion abnormalities may take a short time to become apparent. If atropine is added to induce an increase in heart rate, the usual dose is 1 to 2 mg total in 0.25-mg increments. Arbutamine is no longer marketed, but other agents might be applied using a similar closed-loop computerized delivery system. The age and weight of the patient, target heart rate, and rate of heart rate augmentation (heart rate slope) were entered into the device. Based on the response to an initial dose, the microprocessor automatically increased the infusion rate to achieve the required rate of augmentation and eventually the desired peak. As the target rate was approached, the infusion was reduced and stopped. The device had a number of alarms to alert the supervising physician to responses that require attention, as well as safety features that permitted automatic shut-off of the system. Such a system could reduce the need for a nurse to increase the drug and monitor the hemodynamics. Hemodynamic Responses to Sympathomimetics Dobutamine enhances left ventricular contractility at low doses, usually without the development of tachycardia. At doses greater than 20 µg/kg/minute, systolic blood pressure increases, and the heart rate augments to more than 100 beats per minute. Using a standard protocol without atropine, heart rate can be expected to increase to about 120 beats per minute in most patients, reflecting a heart rate increment of 40 to 50 beats per minute. In normotensive patients, the systolic blood pressure usually increases to about 170 mm Hg (an increment of 30 to 40 mm Hg), without a significant change of diastolic blood pressure. The systolic pressure response may be marked in hypertensive patients and blunted in patients with left ventricular dysfunction or multivessel coronary disease. The peak rate-pressure product increases to the range of 16,500 to 20,000. Although the development of ischemia at lower dobutamine doses and cardiac workloads indicates the presence of more extensive coronary mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 10 disease, there is too much overlap for the hemodynamic response to be a reliable predictor of one-, two-, or three-vessel disease. The hemodynamic response to dobutamine shows significant variability between patients. Beta-adrenergic blockade may attenuate the physiologic responses to dobutamine through a process of competitive antagonism at the receptor level. Patients taking beta blockers have a significantly lower heart rate response (to a peak of 90 to 100 beats per minute), and a lower double-product (to levels of around 14,000), although this may be attenuated by use of atropine. The peak systolic blood pressure is less during dobutamine than exercise, although this difference is less than with heart rate.[29] Indeed, the cardiac stress imposed by dobutamine (even at maximal dobutamine dosage) is less than that obtainable with maximal exercise testing. In several head-to-head comparisons between 311 Figure 14-7 Standard incremental dobutamine protocol, starting at 5 µg/kg/min and going to 40 µg/kg/min with incremental atropine. Images and hemodynamics are obtained at the end of each stage. dobutamine and exercise stress in the same patients, systolic blood pressure levels were comparable, but peak heart rate and double product were significantly greater during exercise than dobutamine stress.[33] [76] [77] [78] [79] [80] [81] These disparities have important implications for the relative sensitivity of dobutamine and exercise echocardiography (see later discussion). Side Effects of Stress Testing with Sympathomimetic Agents Other than the development of myocardial ischemia, dose-limiting side effects experienced during dobutamine protocols generally reflect intense adrenergic stimulation. Consequently, dobutamine stress is contraindicated in patients with severe hypertension and serious arrhythmias. Serious side effects are rare during dobutamine stress testing. In more than 1000 dobutamine studies reported by Mertes et al,[82] no patients died or suffered myocardial infarction or sustained tachyarrhythmias. Similarly, in 650 studies with dobutamine and atropine reported by Poldermans et al,[83] no patients died or suffered myocardial infarction, and cardiac arrhythmias were most likely in patients with left ventricular dysfunction or pre-existing mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 10 ventricular arrhythmias. In a multicenter study reported by Picano et al,[50] nine major cardiac events occurred in nearly 3000 studies (three due to ventricular tachycardia, two from ventricular fibrillation, two from myocardial infarction, one with severe ischemia, and one with hypotension). In this study, atropine psychosis was observed in five patients, but this finding has not been reported from other studies and this author has yet to see this complication in a personal experience of over 5000 studies, many of which have involved atropine usage. In our experience, serious side effects of dobutamine stress occurred in 3 per 1000 patients,[84] a similar result to that of a large German study.[85] Nonetheless, in case reports, fatalities have been reported from ventricular fibrillation and cardiac rupture.[86] Moreover, the safety of the test in patients at highest risk—those with severe left ventricular dysfunction—has been described only in small populations.[87] Nonetheless, considering that the sickest patients (those unable to exercise and those with questions of myocardial viability) undergo the test, this safety profile can be considered to be quite favorable and may in part reflect the detection of the extent and severity of ischemia by online echocardiographic imaging, permitting termination of the stress before serious problems arise. The most frequent serious but nonfatal complications are myocardial infarction and arrhythmias, although atrial fibrillation and sustained ventricular tachycardia are rare, and more common rhythm problems include atrial and ventricular extra systoles and nonsustained atrial and (less often) ventricular tachycardias. Other problems include palpitations (due to increased contractility), hypertension, anxiety (sometimes manifested as dyspnea or vagal reactions), tremor, and urinary urgency. Hypotension may arise from the vasodilator effect of high-dose dobutamine, the development of outflow tract obstruction, or the development of severe ischemia. [88] [89] [90] [91] Unlike hypotension during exercise testing, it does not denote the presence of serious coronary disease or left ventricular dysfunction. [92] All of the studies documenting the sensitivity and specificity of dobutamine stress echocardiography have documented these complications, but the recorded frequency of these side effects has varied from 5% if only serious, dose-limiting side effects are considered[28] to 82% if all side effects are included.[33] One source of variability relates to the definitions used to identify side effects. For example, in the initial experience with dobutamine stress testing, hypotension (which is usually asymptomatic) provoked termination of the test if the systolic blood pressure decreased by more than mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 10 20 to 30 mm Hg or a greater than 15 mm Hg fall from baseline, whereas most centers now continue the infusion unless the systolic blood pressure falls to less than 100 mm Hg or the patient becomes symptomatic. Another source of variability relates to the type of stress protocol, the incidence being lower if the test is terminated for attainment of a target heart rate or when echocardiographic evidence of ischemia is seen[28] or if submaximal test responses are excluded.[29] Vasodilator Stress Protocols Stress Protocols For dipyridamole stress, an intravenous line is inserted into a large proximal arm vein to minimize local discomfort from this strongly alkaline compound. Various dipyridamole administration regimens have been used, both intravenous and oral, although the absorption of the latter is variable and the approval of the intravenous form of 312 this agent by the Food and Drug Administration has removed the main reason for using this route. For myocardial perfusion imaging, the most commonly administered dose is 0.56 mg/kg IV,[93] but this infusion protocol has unsatisfactory levels of sensitivity when combined with stress echocardiography. The sensitivity of dipyridamole echocardiography can be significantly enhanced[94] [95] by an additional 2 minutes of infusion if the initial response is negative and no major side effects have appeared. Because the time of onset of ischemia correlates with the severity of coronary disease and prognosis (see later discussion), we record images every 2 minutes from the conclusion of the first dose until 18 minutes from the start of the study. Digitized images are saved at rest, before the start of the second dose (8 minutes), after the second dose (12 minutes, which is the most common time for the onset of ischemia), and at 16 minutes. Aminophylline (in aliquots of 50 to 75 mg IV) can be used to counteract the effects of dipyridamole if severe ischemia or side effects arise; the threshold for using this agent is influenced by the overall left ventricular function and the clinical state of the patient. Because dipyridamole acts via endogenous adenosine release, there is some delay between the time of its administration and the development of its effects. In contrast, because exogenous adenosine is able to act directly, it rapidly achieves steady state, and its biologic effects are of rapid onset.[38] It mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 10 is therefore suitable for injection using an incremental dose schedule, with echocardiographic imaging at the end of each stage. Various dosing regimens have been used for echocardiographic studies, including a fixed dose of 0.14 or 0.17 mg/kg/minute and incremental protocols (3-minute stages starting at 0.10 mg/kg/minute, increasing to 0.14 and 0.18 mg/kg/minute).[96] [97] [98] [99] The use of aminophylline is rarely required for side effects, as these resolve within a minute of stopping the infusion. Hemodynamic Responses to Vasodilators The mechanism of action of vasodilator agents is chiefly through the phenomenon of coronary steal. There is a small contribution of increasing oxygen demand from tachycardia,[23] which may be a response to angina and side effects rather than arising from the agents themselves. Similarly, blood pressure is usually little changed by these stressors, which may cause hypotension. The addition of atropine leads to an augmentation of heart rate and cardiac work, [49] [51] effectively combining reduced coronary supply with increased oxygen demand. Side Effects of Dipyridamole and Adenosine The development of side effects during dipyridamole stress usually follows completion of the infusion and rarely precludes completion of the study. Side effects usually resolve spontaneously, but, if necessary, aminophylline can be used to reverse the effects of dipyridamole. Minor side effects, including flushing and headache (which reflect the systemic vasodilator effects of the compound), |
occur in about two thirds of patients studied with high-dose dipyridamole.[100] Severe or prolonged myocardial ischemia is infrequent but can be treated with nitrates or aminophylline. Serious side effects are very rare[50] [101] severe myocardial ischemia and infarction, bronchospasm, and complete heart block and even death have been reported. The frequency of these serious complications is probably less than with dobutamine, although ensuring that the comparison groups are matched for baseline risk is always difficult. Dipyridamole stress is contraindicated in patients with untreated atrioventricular block and bronchospastic disorders, although patients with chronic obstructive airway disease with no or minimal airway reactivity may undergo the test. Adenosine differs from dipyridamole stress only to the extent that the adenosine causing the physiologic effects is exogenous rather than endogenous. The side effect profile is therefore similar, and although the intensity and frequency of side effects with adenosine exceed those of mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 10 dipyridamole, they are of shorter duration. Some form of side effect occurs in most patients undergoing adenosine stress.[102] In response to a high-dose protocol, [99] side effects prevented about one third of patients from achieving peak dose, a comparable frequency to that found with dobutamine. As the effect of adenosine is very transient, cessation of the infusion is usually the only treatment required for side effects. Vasoconstrictor Protocols An increasing amount of literature has developed regarding the use of ergonovine for the diagnosis of coronary spasm, especially in regions where this diagnosis is made in the absence of fixed coronary stenoses. In the West, however, this finding is considered unusual, with spasm being recorded in 4% of patients in whom it is suspected clinically, although the return may be increased significantly by focusing on smokers and patients with some coronary disease.[103] Although most practitioners feel more comfortable with the use of this agent in the angiography laboratory,[103] because spasm can be visualized directly and intracoronary nitrates infused to treat severe spasm, a significant evidence base attests to its safety when applied noninvasively in patients without significant stenoses.[104] [105] [106] Although most of the evidence base relates to patients in whom significant stenoses have been excluded, the test has been applied to some patient groups without previous angiography.[6] [7] The standard protocol involves repeated bolus doses of ergonovine maleate at 5-minute intervals up to a total cumulative dose of 0.35 mg, unless echocardiographic evidence of abnormal left ventricular wall motion is detected. Pacing Stress Stress Protocols The use of transesophageal pacing requires topical pharyngeal anesthesia and mild sedation. The end points of the test are the same as those for other nonexercise stressors; 313 in the absence of these end points, pacing at peak heart rate is continued for 3 minutes. No protocol has been uniformly accepted. Although formerly we used an incremental protocol commencing at 100 beats per minute, with increases in 2-minute stages, we now take the heart rate to 85% of predicted maximum immediately, followed by 100% of predicted mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 10 maximum. The benefit of a short protocol is that electrode movement and loss of capture are less likely. Atropine is often required to overcome Wenckebach's atrioventricular block. In our practice, we digitize resting, 100 beats per minute, peak, and post-pacing images and apply the usual guidelines for interpretation. Hemodynamic Responses The hemodynamic response to pacing stress is more controllable than the response to pharmacologic agents. The heart rate is usually increased to 150 or 160 beats per minute, and systolic blood pressure is increased by only a small amount, giving a rate-pressure product of 15,000 to 20,000. In the case of atrial pacing using transesophageal imaging, the insertion of the transesophageal probe in an awake patient may itself provoke hemodynamic TABLE 14-3 -- Sensitivity and Specificity of Echocardiography with Dob 50 Patients) Significant Multivessel Myocard Dobutamine Stenosis Disease, n Infarctio Patients, Protocol, Diameter, (% All n (% Al Study N µ/kg/min % CAD) CAD) Sawada et al 103 30 >50 14 (40) 35 (43) [28] Cohen et al[29] 70 40 >70 35 (69) 19 (37) Salustri et al 52 40 >50 17 (46) 14 (38) [31] Marcovitz & 141 30 >50 47 (43) — Armstrong[32] Mazeika et al 50 20 >70 24 (67) 13 (36) [33] McNeill et al 80 40 + >50 15 (32) 28 (60) [46] atropine Marwick et al 217 40 >50 74 (52) 0 (0) [34] Hoffmann et 66 40 >70 21 (42) 0 (0) al[81] Previtali et al 80 40 >50 33 (58) 15 (26) [78] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 10 Takeuchi et al 120 30 >50 37 (50) 62 (84) [214] Prince et al[215] 81 40 + TEE >70 16 (76) 7 (33) Panza et al[59] 76 40 + TEE >70 37 (60) 23 (37) Beleslin et al 136 40 >50 11 (9) 41 (34) [79] Senior et al[216] 61 40 >50 21 (49) 9 (21) Ostojic et al[54] 150 40 >50 16 (12) 38 (29) Ostojic et al[54] 55 40 + >50 16 (12) 38 (29) dipyridamole Daoud et al[217] 76 30 >50 36 (55) 24 (37) Ho et al[218] 54 40 >50 27 (67) 18 (41) Dagianti et al 60 40 >70 15 (60) 41 (39) [219] Pingitore et al 110 40 + >50 42 (46) 25 (27) [51] atropine Ling et al[220] 183 40 + >70 109 (74) 105 (71) atropine San Roman et 102 40 + >50 34 (54) 0 (0) al[221] atropine Anthopoulos 120 40 + >50 48 (40) 38 (30) et al[222] atropine Dionisopoulos 288 40 + >50 122 (58) — et al[223] atropine Elhendy et al 96 f 40 + >50 142 (61) 214 (70) [224] atropine 210 m Hennessy et al 219 40 + >50 113 (66) 55 (24) [225] atropine Huang et al[226] 93 40 >50 — — Lewis et al[227] 93 Modified >50 15 (60) — protocol Nagel et al[228] 208 40 + >50 70 (64) 0 (0) atropine mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 10 Beleslin et al 168 40 >50 0 (0) 40 (24) [117] SVD = single vessel disease, TEE = transesophageal echocardiography. changes and hence ischemia, so that "resting" transesophageal echocardiographic images may not be truly acquired at rest. Side Effects Fewer side effects occur during transesophageal pacing than with pharmacologic stressors. The frequency of esophageal discomfort, gagging, or nausea is much lower with modern pacing electrodes. Angina may be provoked by stress but is usually self-limiting after cessation of pacing. Atrial flutter or fibrillation may also be precipitated. Esophageal injury is theoretically possible in response to high levels of stimulation over a prolonged period, but this has not been reported clinically. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/120.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 10 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Accuracy of Nonexercise Stress Echocardiography for Diagnosis of Coronary Artery Disease Dobutamine Stress Echocardiography The sensitivity and specificity of dobutamine echocardiography for the detection of coronary artery disease and results of recent studies are summarized in Table 14-3 . The 314 sensitivity for significant disease (defined as visually assessed stenoses of greater than 50% or greater than 70%) is variable between studies, with an interquartile range of 75% to 92%. The addition of atropine appears to enhance the sensitivity of the test, as does transesophageal imaging. The interquartile range for specificity ranged from 77% to 93%, which is comparable to that of exercise echocardiography. No single feature accounts for these false-positive results, although the most frequent site of false-positive results[107] is the basal inferior wall. Patients with apparent abnormalities in this segment should be identified as having coronary disease only if an adjacent segment (basal septal, mid-inferior, posterior) is also involved. One problem with assessments of sensitivity and specificity is that a 50% or 70% stenosis cutoff is arbitrary and does not take into account stenosis location or vessel size, both of which clearly influence the likelihood of an abnormal response. This concern has been addressed in several studies that have compared the results of dobutamine echocardiography with stenosis diameter at quantitative coronary angiography.[108] [109] [110] The angiographic cut-off value with the best predictive value for a positive dobutamine test was a luminal diameter of 1.07 mm, percent diameter stenosis of 52%, and percent area stenosis of 75%, of which minimal lumen diameter was found to have the best predictive value for a positive dobutamine stress test (odds mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 10 ratio, 51; sensitivity, 94%; specificity, 75%).[108] Stenoses smaller than 1 mm in diameter can be identified with a sensitivity of 86%. [109] [110] The previous analyses were limited by comparison with the anatomic severity of stenosis, whereas a more physiologic comparison would be more meaningful. Myocardial fractional flow reserve is a functional index of coronary stenosis severity that takes into account collateral flow and is calculated as the ratio of mean hyperemic distal coronary to aortic pressure. The degree of dobutamine-induced dyssynergy correlates significantly better with myocardial fractional flow reserve than percent stenosis or minimal lumen diameter, and the sensitivity of dobutamine echocardiography is significantly lower for lesions in vessels smaller than 2.6 mm than for larger vessels.[109] Because the existence of a regional wall motion abnormality identifies the presence of coronary disease, dobutamine echocardiography demonstrates higher sensitivities in patients with myocardial infarction. In patients with single-vessel coronary disease, the sensitivity of dobutamine echocardiography (ranging from 40% to 70%) is lower than in patients with multivessel disease. As dobutamine produces a less potent stress on the heart than exercise (see earlier discussion), the results of dobutamine stress are probably more susceptible to external influences than are those of exercise echocardiography or myocardial perfusion scintigraphy. This may be pertinent to the extrapolation of results from clinical trials (in which patients were carefully supervised and tested under optimal conditions, off therapy), to routine clinical practice, in which patients are often tested on therapy and are more likely to have a "suboptimal" test result because of inability to complete the protocol or interference by beta-blocker therapy.[34] Stress Echocardiography Using Other Sympathomimetic Agents Combination of echocardiography with other agents, such as epinephrine and isoproterenol, offers moderate sensitivity in the diagnosis of coronary artery disease.[111] Failure to attain higher levels of sensitivity with these compounds has in part reflected limitations in the administered dose brought about by concerns about side effects. The sensitivity of arbutamine echocardiography for the identification of ischemia was 76%, and the sensitivity for identification of coronary disease was 84%. No specificity data were obtained, but in a group at low probability of coronary disease, the normalcy was 96%.[112] As in the case of dobutamine and exercise echocardiography, the sensitivity was lower in mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 10 patients with less extensive disease and also in patients who were stressed submaximally. However, arbutamine stress echocardiography seems unlikely to be developed further for commercial reasons. Dipyridamole Stress Echocardiography Studies of more than 50 patients that address the accuracy of vasodilator stress echocardiography for the identification of coronary artery disease are summarized in Table 14-4 . The use of the low-dose (0.56 mg/kg) protocol is associated with lower sensitivities than those generally reported with the high-dose regimen, which range from 58% to 94%. The addition of atropine to dipyridamole appears to enhance the sensitivity of the test.[49] [113] In patients with single-vessel coronary disease, the sensitivity of dipyridamole echocardiography is in the range of 50%, and this has an important influence on the sensitivity of this test in comparison with dobutamine. Most studies show the specificity of the technique to be excellent. As in the case of dobutamine, the use of transesophageal imaging has enhanced the accuracy of dipyridamole stress echocardiography.[114] There appears to be more variation in the sensitivity of vasodilator stress echocardiography than for dobutamine and exercise echocardiography. The main variables that account for this heterogeneity are patient selection and the definition of "significant" |
disease. The use of greater than 70% diameter stenosis as a criterion of significant coronary disease has tended to enhance the sensitivity, as patients with milder stenoses (who would be more difficult to detect) are not included. Of more importance, however, are clinical factors, such as the prevalence of myocardial infarction and multivessel disease and the cessation of antianginal therapy[115] many of the more favorable results pertain to populations with a high percentage of patients with more severe coronary disease. As in the case of dobutamine stress, investigators have sought to address the accuracy of dipyridamole stress with physiologic rather than anatomic criteria of significant stenosis.[116] In 30 patients with isolated stenoses of the left anterior descending coronary artery, predictors of an abnormal dipyridamole echocardiogram were a stenotic flow reserve of less than 2.8, stenosis diameter greater than 59%, lumen diameter less than 1.35 mm, and coronary flow reserve less than 2.0, of which stenotic flow reserve was the only independent predictor of ischemia. This 315 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 10 TABLE 14-4 -- Accuracy of Vasodilator (Dipyridamole and Exercise) Ech of More Than 50 Patients) Multivessel Myocardia Definition Disease, n Infarction Patients, of CAD, (% ALL n (% All Study N Agent Dose % CAD) CAD) Picano et al 66 Dipyridamole, >70 20 (40) 9 (18) [94] 0.56 mg/kg Picano et al 93 Dipyridamole, >70 48 (67) 17 (24) [100] 0.84 mg/kg * Masini et al 83 Dipyridamole, >70 24 (62) 15 (38) [229] 0.84 mg/kg * Massa et al 52 Dipyridamole, >70 12 (23) 9 (17) [156] 0.84 mg/kg * Cohen et al 50 Dipyridamole, >70 28 (78) 16 (44) [230] 400 mg PO Picano et al 445 Dipyridamole, >50 119 (46) 0 (0) [231] 0.84 mg/kg * Simonetti et 51 Dipyridamole, >70 al[232] 0.84 mg/kg * Zoghbi et al 73 Adenosine, >75 24 (44) 38 (70) [97] 0.14 µg/kg/min * Severi et al 429 Dipyridamole, >75 114 (46) 0 [126] 0.84 mg/kg * Mazeika et 55 Dipyridamole, >70 30 (75) 18 (45) al[233] 1.00 mg/kg * Picano et al 130 Dipyridamole, >50 — — [49] 0.84 mg/kg + atropine Previtali et 80 Dipyridamole, >50 33 (58) 15 (26) al[78] 0.84 mg/kg * Marwick et 97 Adenosine, >50 28 (47) 0 (0) al[99] 0.18 µg/kg/min * mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 10 Ostojic et al 150 Dipyridamole, >50 16 (12) 38 (29) [54] 0.84 mg/kg * Marangelli 60 Dipyridamole, >75 19 (54) — et al[123] 0.84 mg/kg * Beleslin et 136 Dipyridamole, >50 11 (9) 41 (34) al[79] 0.84 mg/kg * Dagianti et 60 Dipyridamole, >50 15 (60) 41 (39) al[219] 0.84 mg/kg * Tawa et al[98] 67 Adenosine, 0.17 µg/kg/min + HG Djordevic et 58 Adenosine, >50 7 (18) 22 (55) al[234] 200 µg/kg/min * San Roman 102 Dipyridamole, >50 34 (54) 0 (0) et al[221] 0.84 mg/kg * Pingitore et 110 Dipyridamole, >50 al[51] 0.84 mg/kg + atropine Anthopoulos 120 Adenosine, >50 48 (40) 38 (30) et al[222] 0.14 µg/kg/min * Beleslin et 168 Dipyridamole, >50 0 (0) 40 (24) al[117] 0.84 mg/kg * HG, hand grip. * Low-dose positivity permits conclusion of study before stated "peak" dose. study was interesting on two grounds: First, it implies that dipyridamole identifies fewer mild stenoses than dobutamine echocardiography, and second, it identified angiographic variables of stenosis severity to relate to dipyridamole echocardiographic results better than intracoronary Doppler variables. Other studies have confirmed that the optimal angiographic cut- off point for dipyridamole stress echocardiography is 60%, as compared with 58% for dobutamine and 54% for exercise echocardiography.[117] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 10 Vasodilator Stress with Adenosine Echocardiography The accuracy of adenosine stress echocardiography is also detailed in Table 14-4 . There is less of an evidence base for this test than for other pharmacologic approaches, and the published data show significant variations in accuracy. The most favorable results may be influenced by a high prevalence of multivessel coronary disease or prior infarction, the sensitivity being only 60% in patients with a normal electrocardiogram.[97] In patients without prior infarction, the sensitivity of this test was less than 60%.[99] The dose and duration of adenosine have an important influence on sensitivity, as does the coadministration of atropine. The accuracy of adenosine echocardiography has recently become the source of considerable interest because of the possibility of combining standard stress echocardiography and assessment of myocardial perfusion, either using contrast echocardiography or coronary flow reserve. Several studies have now shown that the intense coronary vasodilation induced by adenosine permits the comparison 316 of rest and hyperemic images using contrast echocardiography.[118] , [119] Although this comparison is certainly also feasible with dipyridamole,[120] adenosine may be superior. Similarly, coronary flow reserve may be measured at transthoracic or transesophageal echocardiography, using adenosine[121] as a vasodilator. The longer time course and less predictable peak flow with dipyridamole make this a less attractive agent, and if this is selected, high dose is certainly required. [122] Pacing Stress Echocardiography Table 14-5 details the accuracy of studies that have combined atrial pacing with echocardiography. Generally, very favorable results have been obtained with this stress, although the number of studies and patients within studies is still limited. The accuracy of both transesophageal imaging and pacing probably reflects the benefits of high-quality images as much as the role of pacing stress, as similar favorable findings have been obtained using transesophageal echocardiography with dobutamine and dipyridamole, as discussed earlier. The discrepancy between the reported accuracy in contrast with the limited application of the test is striking. Indeed, this became more prominent after mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 10 a recent landmark study[43] found that transesophageal atrial pacing had a high level of feasibility, and safety, duration, and patient acceptance were more favorable than with dobutamine stress echocardiography. Moreover, the tests showed a high level of concordance in inducing regional wall motion abnormalities. Although the lack of clinical uptake for this modality may not appear to be readily understood, the following are important issues that influence our continued use of pharmacologic stress. First, the evidence base for diagnostic, management, and prognostic information using pharmacologic agents is substantially greater than with pacing stress. Second, the pacing test is unlikely to be useful for the detection of viable myocardium, and even when this is not needed from a clinical standpoint (e.g., the patient is not being evaluated for possible revascularization), the biphasic response has been shown to facilitate the distinction of ischemia in the setting of resting wall motion abnormalities. Third, although advances in pacing catheter technology have improved patient tolerance, as documented earlier, most patients and some TABLE 14-5 -- Sensitivity and Specificity of Atrial Pacing Stress Ech Definition Sensitivity: Patients, Feasibility, of CAD, Overall, % Sensi Study N Method % % (n) SVD, Iliceto et al 85 TTE 95 >75 91 (56) 80 (2 [45] Lambertz 50 TEE 100 >50 93 (41) 85 (2 et al[42] Zabalgoitia 36 TEE 90 >70 90 (21) 100 (1 et al[235] Kamp et al 71 TEE 99 >50 83 (52) 69 (1 [41] Norris et al 32 TEE 94 >70 86 (20) — [236] Anselmi et 31 TTE — 75 92 (26) — al[237] Marangelli 80 TTE 77 >75 83 (35) 75 (1 et al[123] Michael et 65 TTE >50 87 — al[238] Schroder 69 TTE 52 >50 82 (69) 82 (6 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 10 et al[239] SVD, single vessel disease; TEE, transesophageal echocardiography; TTE echocardiography. clinicians look upon the test as being excessively invasive. We believe the test will have several "niche" applications for situations in which dobutamine is unattractive: patients with hypertension or rhythm contraindications to dobutamine, potentially unstable patients (because the stress can be stopped suddenly), or patients with chronotropic incompetence of various causes. Comparison Between Nonexercise Stressors for the Diagnosis of Coronary Artery Disease Selection of the Optimal Pharmacologic Stress It is clear from Table 14-3 and Table 14-4 that both dobutamine and vasodilator stress echocardiography are effective for the diagnosis of coronary artery disease. However, the relative efficacy of the stressors cannot be assessed by merely comparing the results of individual studies in the literature, because of variations in the study groups. The optimal study design should be based on a head-to-head comparison of the tests in the same patients, under the same conditions, as summarized in Table 14-6 . Such studies have generally demonstrated similar levels of feasibility with dobutamine and vasodilator stress. The sensitivity of dobutamine stress echocardiography has been shown to exceed that of vasodilator stress almost exclusively, although the two are close enough to be considered comparable in several studies. The main source of discrepancy appears to be patients with single-vessel coronary disease, among whom dobutamine appears to be superior to dipyridamole echocardiography. This difference parallels a significantly greater cardiac workload with dobutamine compared with vasodilator stress. As the contraindications to inotropes and vasodilators vary, the selection between them may be individualized; patients with hypertension or arrhythmias should undergo a vasodilator stress, and patients with bronchospasm or conduction disorders should be submitted to inotropic stress. However, in the majority of patients who do not have these contraindications, dobutamine appears to be the most sensitive agent for pharmacologic stress echocardiography, at least for diagnostic purposes. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 10 317 TABLE 14-6 -- Studies Comparing Sensitivity and Specificity of D Echocardiography Multivessel Myocardial CAD, Disease, n Infarction, Sensitivity: S Patients, n (% All n (% All Dobutamine, Dip Study N (%) CAD) CAD) % Martin et al 40 25 18 (72) — 76 56 [240] (63) Salustri et al 46 18 18 (64) 15 (83) 79 82 [152] (39) Marwick et 97 59 28 (47) 0 (0) 85 58 al[99] * (61) Previtali et 80 57 33 (58) 15 (26) 79 60 al[78] (71) Beleslin et 136 119 11 (9) 41 (34) 82 74 al[79] (88) Ostojic et al 150 131 16 (12) 38 (29) 75 71 [54] (87) Dagianti et 60 25 15 (60) 41 (39) 72 52 al[219] (42) Anthopoulos 120 89 48 (40) 38 (30) 87 66 et al[222] * (74) San Roman 102 63 34 (54) 0 (0) 77 77 et al[221] (62) Loimaala et 60 44 18 (41) 0 (0) 93 95 al[205] (73) Fragasso et 101 56 37 (65) 0 (0) 88 61 al[241] (56) CAD, coronary artery disease. * Adenosine used instead of dipyridamole. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 10 Selection of Pacing Rather than Other Nonexercise Stress Few data are available to evaluate the relative status of pacing in relation to pharmacologic approaches to nonexercise stress testing. A recent comparison of pacing to dipyridamole stress echocardiography in 80 patients with suspected coronary disease and without prior infarction[123] showed the feasibility of the test was less with pacing stress than dipyridamole (77% versus 96%, P < .0001). In patients in whom pacing and dipyridamole testing were feasible, the respective sensitivities were 83% and 43% (P = .0005), and specificities were 76% and 92% (P = NS). Although these favorable results for pacing stress may reflect the inadequacies of dipyridamole echocardiography for diagnostic stress testing, a recent comparison with dobutamine stress echocardiography recently documented[43] that transesophageal atrial pacing showed safety, duration, and patient acceptance results more favorable than those achieved with dobutamine stress echocardiography, with a high level of concordance in inducing regional wall motion abnormalities. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/121.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Assessment of Disease Significance Using Nonexercise Echocardiography In patients with known coronary artery disease, stress imaging procedures are often performed to facilitate clinical decision making, for example, regarding the referral of patients for coronary intervention. The location, extent, and severity of coronary disease can be important in this respect, and all can be determined using nonexercise echocardiography. The use of stress echocardiography for identification of the "culprit" coronary lesion |
is often constrained by the assumptions inherent in allocating territories of the heart to individual coronary vessels. The most ambiguous areas in this respect are the apex (usually assumed to be within the territory of the left anterior descending coronary artery) and the posterior wall (usually assumed to be supplied by the left circumflex artery). Because of the equivocal involvement of the right coronary or left circumflex vessels in the posterior territory, investigators have examined the ability to discern the presence of coronary disease in the anterior and posterior circulations. Although in the pre-harmonic imaging era the lateral wall was a source of false-negative results, the accuracy of dobutamine echocardiography in each territory appears to be equivalent (Fig. 14-8) . More severe disease in the vessel supplying an ischemic region generally correlates with a more severe wall motion disturbance. Likewise, multivessel disease usually corresponds to extensive areas of ischemia or the development of global ventricular dysfunction, or both, evidenced by poststress reduction of ejection fraction or increase of end-systolic volume, although these are much less common than with exercise, probably because of left ventricular unloading at peak stress. The presence of stenoses in multiple vessels is well known to be predictive of an adverse prognosis in patients with coronary artery disease. Consequently, the recognition of multivessel disease as such may be important in planning revascularization rather than medical therapy. The ability of dobutamine stress mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 echocardiography to predict multivessel disease is greatest in patients with a history of previous myocardial infarction, under which circumstances its sensitivity for the correct identification of disease is 80% to 85% and its specificity is 88%.[28] [124] In contrast, the sensitivity for multivessel disease in patients without previous infarction is approximately 70%[28] and exceeds the levels reported in this situation using exercise echocardiography. A close correlation has been demonstrated between the extent of ischemia defined by dobutamine echocardiography and perfusion scintigraphy, although both underestimate the angiographic extent of disease as measured by the Gensini score,[34] a reflection of the difficulties of assessing the functional implications of disease extent on anatomic grounds. In addition to the "space coordinate" (i.e., extent of abnormal segments),[20] another physiologic indication of the extent of coronary disease is the "time coordinate" (i.e., ischemic threshold). Using dobutamine stress, multivessel disease may also be predicted if ischemia has an early onset (similar to the "ischemia-free" time at 318 Figure 14-8 Lateral wall ischemia. Freeze-frame images in the apical four-chamber view demonstrate normal thickening at rest (above), with reduced thickening at peak stress (arrows). exercise testing), corresponding to its occurrence at a low dose or provocation at a low heart rate and rate-pressure product.[29] [125] Similarly, at dipyridamole stress, ischemia at "standard dose" (0.56 mg/kg) correlates with the presence of multivessel disease, [100] a lower ischemic threshold at exercise testing [126] as well as a worse prognosis (see later discussion). Nonetheless, patients with severe single-vessel disease may also demonstrate an early onset of ischemia, so that this relationship is only an approximate guide to lesion severity. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/122.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 8 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Prognostic Evaluation Using Nonexercise Echocardiography Comparison of the results of nonexercise echocardiography with those of angiography validates the accuracy of these tests for diagnostic purposes and permits comparison with other noninvasive methodologies. The disadvantage of this approach, however, is that the angiographic criteria of stenotic significance are somewhat arbitrary and may not correlate with "physiologic" significance. A less artificial analysis is to use patient outcome to judge the efficacy of testing. Functional testing is commonly used for cardiac risk stratification in various groups of patients, such as those with chronic, stable angina or those who have had a myocardial infarction; for predicting complications at major noncardiac surgery; and in planning which patients should undergo coronary intervention. Prediction of Cardiac Events in Patients Undergoing Major Noncardiac Surgery Coronary artery disease is highly prevalent in patients with vascular disease elsewhere,[127] and cardiac events are the leading cause of perioperative complications at vascular surgery.[128] However, whereas coronary disease and 319 "soft" end points (postoperative unstable angina and heart failure) are frequent in patients with vascular disease, "hard" end points (death, myocardial infarction) occur in less than 10% of patients in the perioperative period, even in the absence of preoperative coronary intervention.[129] As the pretest probability of an event is low, Bayes' theorem would suggest that even if a noninvasive test were positive, the chance of an event would remain small. This explains the low predictive value of a positive test in many previous studies of stress testing in this setting. However, it is also important to remember that severe coronary mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 8 disease is also the major contributor to late deaths after vascular surgery, and the screening of vascular patients for significant coronary disease is important for both perioperative and late risk stratification. The first step in preoperative risk stratification is clinical evaluation.[130] Patients with unstable coronary syndromes within the last 6 months constitute a high-risk group and, if surgery is mandatory, warrant careful functional testing to delineate the extent of jeopardized myocardium and possible intervention preoperatively. Those with previous bypass surgery (within 5 years) or coronary investigations (within 2 years) do not require reinvestigation in the absence of recurrent symptoms. The nature of the planned surgery is important; procedures carrying low cardiac risk such as ophthalmic or laparoscopic surgery should not provoke extensive risk evaluation, whereas vascular, major orthopedic, and major abdominal operations engender significant cardiac risk. Finally, the patient history has an important influence on risk, but the standard anesthetic risk scores[131] have limited applicability among vascular patients, who have greater cardiac risk than the general surgical populations from whom these risk scores were initially obtained. A simple score derived from the patient's age, presence of diabetes, angina, prior infarction, and congestive heart failure has been shown to identify low-risk patients, who do not need further investigation.[132] In a recent series of more than 4300 patients[133] undergoing high-risk surgery, history of ischemic heart disease, congestive heart failure or cerebrovascular disease, insulin treatment, and preoperative serum TABLE 14-7 -- Use of Stress Echocardiography to Predict Events in Patients Undergoing Vascular Surgery Predictive Value, % Patients, Events, POSITIVE NEGATIVE Study Stress N n TEST TEST Even Tischler et Dipyridamole 109 8 78 99 MI, al[242] UAP, CHF Sicari et al Dipyridamole 121 9 25 98 Death [243] MI, UAP Rossi et al Dipyridamole 110 10 100 Death [244] MI, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 8 UAP Pasquet et al Dipyridamole 129 9 30 97 Death [136] MI, UAP Lane et al Dobutamine 57 4 21 100 Death [245] MI, CABG Lalka et al Dobutamine 60 13 29 93 Death [246] MI, UAP Eichelberger Dobutamine 70 5 19 100 MI, et al[247] UAP Langan et al Dobutamine 74 3 48 100 MI, [248] AP, CABG Davila- Dobutamine 93 4 74 100 MI, Roman et al + atropine UAP, [249] CABG Poldermans Dobutamine 131 15 43 100 Death et al[250] + atropine MI, UAP, CHF Poldermans Dobutamine 181 18 32 100 Death et al[251] + atropine MI, UAP, CHF Poldermans Dobutamine 300 27 38 100 MI, et al[125] + atropine AP, LVF Pellikka et Dobutamine 80 8 29 98 Death al[252] + atropine MI, UAP, CHF Ballal et al Dobutamine 233 8 all rvs 96 Death [253] + atropine MI, UAP mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 8 AP, angina pectoris; CABG, coronary artery bypass graft surgery; CHF, congestive heart failure; LVF, left ventricular failure; MI, myocardial infarction; UAP, unstable angina pectoris. creatinine level greater than 2.0 mg/dL were markers of risk; patients with none, one, two, or three or more of these factors had major cardiac complication rates of 0.4% to 0.5%, 0.9% to 1.3%, 4% to 7%, and 9% to 11%, respectively. It is important to keep in mind that patients with vascular disease are often inactive and are usually asymptomatic even in the presence of significant coronary disease. For patients at intermediate risk, stress imaging techniques with nonexercise stressors are required if screening is to be undertaken, as limitations of their exercise capacity render exercise testing approaches inadequate for the diagnosis of coronary artery disease, and the low sensitivity of pharmacologic stress electrocardiograms mandates the use of an imaging test. The relative availability and low cost of stress echocardiography, along with the potential for combining this approach with nonexercise stress, makes this an attractive technique for preoperative risk stratification. Table 14-7 shows that both dipyridamole and dobutamine stress echocardiography are effective for this purpose. The predictive value of a negative test is very high (usually greater than 90%), but as is the case with perfusion scintigraphy, the predictive value of a positive test is intermediate, varying from 20% to 70%. This value may be further stratified by paying attention to the ischemic threshold and the clinical risk factor status (Fig. 14-9) (Figure Not Available) . Clearly, the occurrence of cardiac events at the time of surgery does not only relate to the presence of coronary stenoses but is also modulated by medical treatment and anesthetic intervention. Only a handful of studies have compared stress echocardiography with single photon emission computed tomography (SPECT) for the prediction of perioperative cardiac events. From a meta-analysis of published work with dobutamine echocardiography and SPECT (mainly with dipyridamole stress), Shaw et al[134] concluded that the tests had comparable levels of accuracy but that cost features weighed in favor of echocardiography. A direct comparison by the group in Liege, Belgium showed the techniques to have similar prognostic value,[135] but another 320 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 8 Figure 14-9 (Figure Not Available) Evaluation of risk in patients undergoing vascular surgery. Patients without clinical predictors of risk rarely have a positive dobutamine study (DSE), are unlikely to suffer events, and usually do not require testing. The presence of ischemia is predictive of events, especially if the patient has multiple clinical risk factors or a low ischemic threshold. MI, myocardial infarction; neg, negative; pos, positive; preop, preoperative. (From Poldermans D, et al: J Am Coll Cardiol 1995;26:648–653.) comparison by a different Belgian group showed echocardiography to be significantly more specific than SPECT.[136] Prognostic Evaluation of Patients with Stable Coronary Disease Although the frequency of major cardiac events is low in stable chronic coronary disease (less than 1% per year), risk stratification is an important aspect of these patients because some have been shown to have a more favorable prognosis with intervention. The detection of left main or multivessel disease at coronary angiography is often used to identify subgroups likely to benefit from revascularization, but this procedure is too costly and invasive to be used for prognostic evaluation of all patients. As in the case of preoperative risk stratification, clinical data (including the severity of angina, prior infarction, heart failure, and diabetes) may identify high- and low-risk subgroups,[137] [138] and additional investigations are of most value in those at intermediate or greater risk. Exercise capacity and ST segment depression at exercise testing offer important prognostic information in patients who are able to exercise,[139] [140] and exercise SPECT [141] or exercise echocardiography have been shown to provide incremental data in some patients.[142] In those patients who are unable to exercise, pharmacologic stress echocardiography is a useful prognostic tool (Table 14-8) . The detection of ischemia at pharmacologic stress echocardiography has been shown to be an independent predictor of adverse outcomes, incremental to clinical and resting echocardiographic data. During dipyridamole stress, cardiac events occurred in 41% of patients with wall motion abnormalities occurring at low dose and 26% of those with high-dose responses (a reflection of the prognostic importance of ischemic threshold). Even in patients with known exercise electrocardiographic and coronary angiographic data,[143] ischemia at dipyridamole echocardiography was a better predictor of cardiac events |
(relative risk, 1.9) than either coronary stenoses or age (relative risks, 1.3 and 1.0, respectively). Similar data have been gathered during dobutamine stress testing (see Table 14-8) . The prognostic value of pharmacologic stress appears to be preserved within various subgroups, including mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 8 hypertensive patients.[144] Few data have been gathered regarding comparisons between the stressors. Dobutamine and dipyridamole have been shown to offer effective and comparable efficacy of risk stratification in patients at low to moderate risk of cardiac events.[145] The prognostic content of stress echocardiography seems to be similar to that of SPECT.[146] The prognostic components of both tests include the presence, severity, and extent of induced ischemia. Perhaps the most important aspect of the prognostic literature is that a negative test portends extremely low risk, evidenced by an event rate of 1% or less per year. Prognostic Evaluation of Patients after Myocardial Infarction The frequency of cardiac events in the first year after myocardial infarction exceeds that in patients with chronic stable angina. Although clinical features such as age and the presence of heart failure should be used in the initial stratification of patients, the amount of infarcted and 321 TABLE 14-8 -- Use of Stress Echocardiography to Predict Events in Patie with Chronic Stable Coronary Disease Predictive Value, % Mean Patients, Follow- POSITIVE NEGATIVE Study Stress N up, mo TEST TEST Comm Mazeika et Dobutamine 51 24 68 77 High ri al[254] Afridi et al Dobutamine 77 10 50 87 [255] Poldermans Dobutamine 430 17 26 87 et al[256] Kamaran et Dobutamine 210 16 43 92 al[257] Marcovitz Dobutamine 291 15 10–17 99 et al[258] Schroder et Dobutamine 134 19 31 94 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 8 al[259] Steinberg Dobutamine 120 60 67 67 All eve et al[260] 13 95 Hard events Senior et al Dobutamine 121 15 45 88 [261] Chuah et al Dobutamine 860 52 14 96 [262] Davar et al Dobutamine 72 F 13 — 100 Norma [263] studies Poldermans Dobutamine 1659 36 8–20 96 Hard et al[264] events Picano et al Dipyridamole 539 36 26 94 [144] (high dose) Dipyridamole 539 36 41 94 (low dose) Schroder et Dipyridamole 134 19 27 92 al[259] residual ischemic myocardium are major determinants of outcome that cannot be quantified clinically. Previously, the techniques used for this purpose included the exercise electrocardiogram, resting echocardiography, nuclear ventriculography, and thallium imaging. In a comparison of these alternatives,[147] the optimal approach for prediction of postinfarction complications was shown to be thallium imaging and nuclear ventriculography. Stress echocardiography, however, offers a means of replacing these two tests with one. Ischemia may be assessed as homozonal dyssynergy (peri-infarct ischemia) or heterozonal dyssynergy (multivessel disease), and infarction may be estimated from the resting wall motion score index. Exercise testing offers prognostically important adjunctive data on functional capacity. However, the majority of the postinfarction stress echocardiography literature (Table 14-9) concerns pharmacologic stress studies for three reasons: first, nonexercise studies are useful in patients who cannot exercise; second, they are useful for assessment of myocardial viability (see later discussion); finally, they provide an opportunity for mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 8 obtaining a near-maximal stress reading early in the patient's admission, before many patients and physicians feel comfortable about performing maximal exercise stress testing. The last aspect is perhaps the most important, as early risk evaluation may identify at-risk patients before the occurrence of an event, permitting a reduction in hospital length of stay for low-risk patients and justifying angiography and possible intervention in those at higher risk. Both pharmacologic and atrial pacing stress tests have been used for risk assessment after myocardial infarction. All have proven to be effective for the detection of multivessel disease[124] [148] [149] and predictive for the subsequent development of cardiac events. Although atrial pacing is very safe (as the stress may be terminated instantly), it remains invasive and uncomfortable, and the pharmacologic techniques are best validated for this purpose. Moreover, the use of pharmacologic stress permits evaluation of myocardial viability, the detection of which has important implications for revascularization decisions. Table 14-9 summarizes the prognostic implications of positive and negative nonexercise stress echocardiography in patients after infarction. With dipyridamole stress echocardiography, the presence of ischemia and its time of onset are important predictors of cardiac events[150] in elderly patients, ischemia was an independent predictor of mortality.[151] An equivalent evidence base has been reported with dobutamine in the postinfarct period. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/123.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 4 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Evaluation of Therapy Using Nonexercise Echocardiography Medical Therapy In contrast to myocardial perfusion scintigraphy, the identification of ischemia with stress echocardiography is dependent on the development of ischemia. This is a disadvantage to the extent that antianginal therapy reduces the sensitivity of stress echocardiography, particularly when dipyridamole stress is used.[115] Patients on beta blockers account for most patients who fail to attain a heart rate greater than 85% of age-predicted maximum. With dobutamine echocardiography, the interaction between dobutamine and beta blockers involves competitive inhibition, and if enough dobutamine is administered, this effect may be overcome, leading several studies to suggest that concurrent drug therapy has no effect.[152] Atropine can be used to enhance the sensitivity of dobutamine stress testing, without reducing specificity or inducing serious side effects. The interaction between medical therapy and the development of ischemia may be of use in evaluating the adequacy of therapy.[153] [154] Although some data are being gathered with exercise echocardiography, the role of nonexercise stress remains largely unexplored. [155] In large part, this lack of data reflects the subjectivity of wall motion scoring, and use of stress echocardiography should become more feasible with a truly quantifiable approach. Follow-up after Coronary Interventions After angioplasty and bypass surgery, recurrent symptoms of chest discomfort may result because of restenosis 322 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 4 TABLE 14-9 -- Application of Nonexercise Stressors to Post Patients, Follow- Study Year N Timing Stress up, mo Outcomes Iliceto[44] 90 83 <3 wks Atrial Pacing 14 Reinfarction, angina Res * 95 69 3–5 Atrial Pacing 12.6 Cardiac death, days reinfarction, revascularizatio Bolognese 92 217 Dipyridamole 24 Cardiac death [202] Cardiac death, reinfarction Cardiac death, reinfarction, angina Sclavo † 92 103 5–8 Dipyridamole 14.5 Cardiac death days Cardiac death, reinfarction Cardiac death, reinfarction, angina Picano[49] 93 925 10 days Dipyridamole 14 Cardiac death Chiarella ‡ 94 251 70 hrs Dipyridamole 13 days Cardiac death Cardiac death, reinfarction Cardiac death, reinfarction, angina Picano § 95 1080 10 days Dipyridamole 14 Reinfarction Neskovic 95 93 2–3 Dipyridamole 16 Cardiac death wks Cardiac death, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 4 reinfarction Cardiac death, reinfarction, angina Sclavo ¶ 97 60 3–4 Dipyridamole 15 Cardiac death, days reinfarction, angina, revascularizatio Lanzarini 96 41 8 days Dobutamine 7.5 Reinfarction, [129] angina, revascularizatio Carlos £ 97 214 2–7 Dobutamine >12 Cardiac death, days reinfarction, angina, ventricular tachycardia, congestive hea failure Sicari[166] 97 778 12 days Dobutamine 9 Cardiac death Cardiac death, reinfarction Cardiac death, reinfarction, angina Greco 97 178 12 days Dobutamine 17 Cardiac death Cardiac death, reinfarction Cardiac death, reinfarction, angina Previtali 98 152 9 days Dobutamine 15 Cardiac death [30] Cardiac death, reinfarction Cardiac death, reinfarction, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 4 angina Picano[237] 98 314 12 days Dobutamine 9 Cardiac death Cardiac death, reinfarction Cardiac death, reinfarction, angina * Res et al: Am J Cardiol 1995;76:1112–1114 † Sclavo et al: Eur Heart J 1992;13:1348–1355 ‡ Chiarella et al: Eur Heart J 1994;15:842–850 § Picano et al: J Am Coll Cardiol 1995;26:908–913 Neskovic et al: Am Heart J 1995;129:31–39 ¶ Sclavo et al: G Ital Cardiol 1997;27:1000–1007 £ Carlos et al: Circulation 1997;95:1402–1410 Greco et al: J Am Coll Cardiol 1997;29:261–267 and graft closure, respectively. Because angioplasty is most often performed for single-vessel disease, routine exercise testing is usually considered to be insensitive for the diagnosis of restenosis, and exercise echocardiography or exercise myocardial perfusion imaging are often performed. Pharmacologic stress echocardiography performed before and after angioplasty has been shown to predict resolution of ischemia using dipyridamole[156] [157] and dobutamine stress.[158] [159] If the patient cannot exercise, pharmacologic stress echocardiography can be used effectively for the diagnosis of restenosis,[160] [161] the sensitivity being significantly greater than that of the stress electrocardiogram.[162] Similarly, after bypass surgery, stress imaging tests are usually obtained for diagnostic purposes (because the resting eletrocardiogram is often nondiagnostic). Exercise echocardiography has been shown to be accurate in this context, and if the patient cannot exercise, pacing or pharmacologic stresses can reasonably be used.[163] [164] The major application of echocardiography and perhaps stress echocardiography after revascularization, however, is to assess the improvement of dysfunctional but viable myocardium.[165] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/124.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 4 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Assessment of Myocardial Viability Using Nonexercise Echocardiography Clinical Significance Left ventricular dysfunction after myocardial infarction is due not only to loss of myocardium but also to stunned and hibernating myocardium. Stunned myocardium shows spontaneous resolution of dysfunction,[166] but hibernating tissue requires myocardial revascularization to 323 resume normal function.[167] [168] Myocardial revascularization in patients with viable myocardium may be indicated to improve cardiac function or overall functional capacity, as well as to avoid subsequent cardiac events from this inherently unstable tissue. Thus, clinical decisions about whether to revascularize, which vessel to revascularize, and how to do it may be influenced by the detection of viable myocardium. In the following section, evaluation of the accuracy of various tests for the identification of viable myocardium is based on recovery of function after myocardial revascularization. This criterion is an imperfect gold standard, being influenced by the adequacy of revascularization, bypass graft closure, and restenosis, but it has the attraction of having direct clinical relevance. By this criterion, conventional techniques used for the detection of myocardial scar and viability (Q waves on the electrocardiogram, regional left ventricular dysfunction at ventriculography, and "fixed" perfusion defects at conventional scintigraphic procedures) have been found to be inaccurate. More accurate alternatives include position emission tomography and thallium scintigraphy using rest-redistribution or stress- redistribution-reinjection protocols, both of which have a high negative predictive value.[169] A positive test result is less predictive of functional recovery, however, probably manifesting the sensitivity of these tests for mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 4 small regions of viable myocardium that may not be able to contribute to regional function when revascularized. The use of dobutamine and dipyridamole stress echocardiography to detect viable myocardium has a large evidence base and is now part of standard practice. Use of Dobutamine Echocardiography for the Diagnosis of Viable Myocardium Administration of sympathomimetic agents (such as isoproterenol, dopamine, and dobutamine) has been shown to reverse postischemic left ventricular dysfunction.[170] [171] [172] [173] The typical response of viable myocardium is to increase thickening in response to low doses of dobutamine; in the presence of a stenosed infarct-related artery, function subsequently deteriorates as the tissue becomes ischemic. Indeed, there is a balance between the recovery of function and the development of ischemia, and, at least in theory, the development of ischemia may compromise the functional recovery of areas that are marginally perfused at rest. The high- dose response (>20 µg/kg/minute) has been shown to be a less reliable predictor of recovery.[8] Although some investigators start at lower doses, or use only a low-dose protocol for the assessment of viability, and others use 5-minute rather than 3-minute increments, [174] there does not appear |
to be a clear benefit in favor of any of these alternatives. Dipyridamole has been shown to enhance both segmental shortening and load-independent indices of ventricular function in stunned myocardium.[175] The mechanism of this phenomenon is unclear, but a "local Frank-Starling response" (whereby augmentation of myocardial blood volume leads to increased sarcomere separation) appears to be the most likely explanation. Additionally, an indirect sympathomimetic response to dipyridamole- induced ischemia may contribute to improvement of regional function, as may resolution of ischemia secondary to improvement of coronary perfusion. Dipyridamole appears to be an effective alternative in low-dose and "infra-low-dose" protocols[176] the choice of agent is dependent on local expertise and preference. The interpretive criteria are similar, irrespective of the stressor. Viable segments are characterized by reduced resting function, which augments in response to low-dose dobutamine (usually 7.5 to 10 µg/kg/minute). There is continued augmentation if there is a patent infarct-related artery or the tissue is well collateralized. In the presence of a stenosed infarct-related artery, an increasing proportion of segments become ischemic at dobutamine doses greater than 10 µg/kg/minute.[177] This initial mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 4 improvement followed by deterioration in function constitutes the "biphasic response," which is strongly predictive of eventual functional recovery of the tissue.[177] A uniphasic response is less predictive of recovery, and a classic ischemic response is not very predictive of the recovery of resting function. Because the biphasic response is the most reliable finding (Fig. 14-10) , our preference is to induce ischemia whenever possible by proceeding to maximal stress (i.e., 40 µg/kg/minute dobutamine with or without atropine), rather than using a discreet "viability" or low-dose protocol. In patients with severe left ventricular dysfunction, this approach warrants caution, and early termination may be needed if ischemia is progressive or if other responses might induce instability. Finally, viability studies are the most difficult to interpret, and we commonly use both digital display, including doses of both 5 and 10 µg/kg/minute, and videotape for review of the study. The response of regional function to dobutamine is influenced by the extent of viable tissue, the degree of residual stenosis, the extent and magnitude of collateral vessels, the size of the risk area (which influences tethering), and the presence of drug therapy,[178] of which the extent of viable tissue and perfusion warrant further attention. The uniphasic response is an ambiguous signal that may be caused by part of the wall mounting a dobutamine response (i.e., admixture of scar and normal tissue) or all of the wall mounting a partial response (i.e., viable myocardium). The ability to discriminate the extent of subendocardial damage, with its implications for the likelihood of subsequent functional recovery, is poor. With respect to perfusion, augmentation of function is dependent on delivery of more substrate; thus, tissue supplied by more severe stenosis may become ischemic before it augments function. This may compromise the recognition of viability. The accuracy of dobutamine for prediction of regional functional recovery is summarized in Table 14-10 , although there is a large evidence base, most studies are relatively small and derive from expert centers. The overall sensitivity of dobutamine (approximately 80%) appears greater than that of dipyridamole stress (approximately 60%), although the specificity of the former is less (78% vs. 87%). Moreover, the nuclear approaches are more sensitive but less specific than these echocardiographic techniques. 324 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 4 Figure 14-10 Apical four-chamber diastolic (right) and systolic (left) views at rest (top), with low-dose dobutamine (middle), and with peak- dose dobutamine (below), illustrating a "biphasic" response to dobutamine stress (reduced systolic thickening at rest, increment with low dose, and deterioration at peak dose) in the lateral wall. Prediction of Recovery of Global Function and Outcome Improvement of left ventricular function within individual segments is not usually the goal of revascularization, whereas improvements in ejection fraction, exercise capacity, and outcome are therapeutic goals. Recent work has sought to address the ability to predict these parameters. Stress echocardiography can be used to predict improvement of global left ventricular function after revascularization. Cornel et al[179] has reported an 89% sensitivity and 81% specificity for prediction of a significant (5%) improvement in ejection fraction, using a cut-off point of 4 of 16 viable (biphasic) segments at dobutamine echocardiography. Similarly, the global ventricular response to low-dose dobutamine is a strong predictor of global functional recovery.[180] Other factors clearly influence the likelihood of recovery, including an inverse relationship with the number of thinned and akinetic segments or ventricular volumes. [181] The revascularization of patients with adequate amounts of viable myocardium (usually >25% of left ventricular mass) is associated with improved functional class. The presence of viable myocardium may influence outcome in two ways. First, revascularized viable tissue may lead to improved function and thereby improved outcome.[182] Second, non-revascularized viable tissue may be unstable and act as a substrate for recurrent events,[183] including mortality.[184] These outcomes have not been reported in all series,[185] probably because of heterogeneity in populations studied and responses; for example, a uniphasic response early after infarction may be a benign finding. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/125.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 6 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company New Technologies that May Solve Limitations of Stress Echocardiography Image Quality Although perfect image quality is certainly not essential for a stress echocardiographic study to be interpretable, 325 TABLE 14-10 -- Sensitivity and Specificity of Dobutamine Echocardiogra for Identification of Myocardial Viability (Segmental Analysis) * Patients, Sensitivity, Specificity, Study Stress N % (n) % (n) Comm Pierard † Dobutamine 17 83 (6) 73 (8/11) Early p MI Smart * [8] Dobutamine 51 86 (22) 90 (26/29) Early p MI Previtali[30] Dobutamine 42 79 (63) 70 Early p (109/158) MI Cigarroa ‡ Dobutamine 25 82 (11) 86 (12/14) Marzullo[275] Dobutamine 14 82 (49) 92 (24/26) Alfieri § Dobutamine 14 91 (93) 78 (25/32) Watada Dobutamine 21 83 (66) 86 (43/50) Early p MI La Canna ¶ Dobutamine 33 87 (205) 82 (89/109) Charney[276] Dobutamine 17 71 (31) 93 (27) Perrone-Filardi Dobutamine 18 88 (48) 87 (27/31) mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 6 £ Afridi Dobutamine 20 74 (38) 73 (55/76) Arnese[70] Dobutamine 38 74 (33) 95 (130/137) Senior[110] Dobutamine 45 87 (45) 82 (123) Bolognese[202] Dobutamine 30 89 (27) 91 (45) Early p MI Poli # Dobutamine 51 72 (78) 68 (176) Early p MI Dipyridamole 51 51 (78) 82 (176) Early p MI Varga[10] Dipyridamole 40 78 (40) 94 (133) Dobutamine 40 76 (40) 94 (133) Bax[283] Dobutamine 36 85 (27) 63 (65) Vanoverschelde Dobutamine 73 76 (167) 86 [285] (238/277) Perrone-Filardi Dobutamine 40 79 (73) 83 (36) [282] Furukawa[67] Dobutamine 53 69 (32) 100 (26) Akinet Dobutamine 86 (50) 57 (46) Hypok Cornel[87] Dobutamine 30 89 (62) 82 (106) Nagueh[279] Dobutamine 18 68 (46) 83 (63) Biphas respon Total Dobutamine 726 81 78 (1065/1312) (1401/1796) Dipyridamole 91 60 (71/118) 87 (269/309) MI, myocardial infarction. * Average ejection fraction approximately 35%. † Pierard et al: J Am Coll Cardiol 1990;15:1021–1031 ‡ Cigarroa et al: Circulation 1993;88:430–436 § Alfieri et al: Eur J Cardiothoracic Surgery 1993;7:325–330 Watada et al: J Am Coll Cardiol 1994;24:624–630 ¶ La Canna et al: J Am Coll Cardiol 1994;23:617–626 £ Perrone-Filardi et al: Circulation 1995;91:2556–2565 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 6 Afridi et al: Circulation 1995;91:663–670 # Poli et al: Heart 1996;75:240–246 it certainly favors concordance between observers[73] and facilitates an accurate diagnosis of disease extent and distinction of ischemia and scar. Major improvements in image quality obtained from harmonic imaging have translated into improvements in the accuracy of stress echocardiography.[58] Likewise, the use of contrast echocardiography may facilitate delineation of the endocardial border; the implications of this finding are addressed in another chapter. Quantitative Approaches to Interpretation As mentioned earlier, the current qualitative algorithm for interpretation of stress echocardiograms requires a significant level of expertise on the part of the observer. A less subjective means of interpretation would be attractive on the grounds of feasibility and reproducibility. Either semiquantitative or fully quantitative strategies of examining wall motion can be used to evaluate global and regional left ventricular function. Global indices (ejection fraction or end-systolic volume) are insensitive to milder degrees of ischemia and are not an answer to the shortcomings of qualitative interpretation. Wall motion scoring offers a semiquantitative regional approach, which may improve the reproducibility of observers, but this does not constitute a major deviation from the regional approach used by most experienced readers and does not measure function independent of the observer. True quantitation of regional function may be based on following either radial or longitudinal myocardial motion (see Chapter 5) . The simplest approach involves tracing of endocardial (and for some methods, epicardial) interfaces and their superimposition using a fixed or floating reference system and measurement of endocardial excursion or myocardial thickening. Historically, this approach has been limited by three major technical limitations, but recent developments have addressed some of these limitations. First, excellent border definition of both endocardium and epicardium (especially in the apical views) was obtainable in less than 50% of images, but harmonic imaging has improved image quality substantially, and contrast echocardiography may also be of value. Second, failure to mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 6 compensate for rotational or translational cardiac movement may be associated with false-positive results, but correction for movement of the heart may also compromise sensitivity. A postprocessing approach (using color-enhanced digitized cine-loops) may be used to correct translational movement.[186] Third, the 326 process of tracing multiple systolic and diastolic frames is tedious, time- consuming, and unattractive for clinical practice. However, recent developments in edge-tracking have led to automated programs for measuring endocardial excursion. Along similar lines, Perez has developed an online quantification of ventricular function during dobutamine echocardiography using acoustic quantification.[187] The feasibility and accuracy of this approach has now been documented in several studies[188] [189] (Fig. 14-11) (Figure Not Available) . Myocardial tissue Doppler may provide another means of quantifying regional function. A unique aspect of this approach is that it can be used to quantify motion in the longitudinal (base-apex) direction, which corresponds to the contribution of longitudinal subendocardial muscle fibers.[190] Tissue Doppler measurements can be obtained using color or pulsed wave modalities to gather peak velocity and timing parameters. Pulsed wave Doppler, although useful for resting imaging,[191] is less feasible during stress because of the need to acquire all values online within a limited time at peak stress. Tissue velocity profiles within each segment of a color myocardial Doppler image may be obtained by postprocessing, but this requires a high frame-rate (at least 80 to 100 frames per second) to ensure that true peak systolic velocity is captured (Fig. 14-12) . The development of ischemia causes a reduction of peak velocity and transmyocardial velocity gradient and a delay in the development of peak velocity, of which the first is the most reproducible. Peak velocity has been shown to correlate with wall motion interpretation[192] [193] and ischemia with dual isotope SPECT.[194] More recently, normal ranges at peak stress have been described, and these ranges have been applied to the identification of angiographically defined coronary disease, [195] providing comparable accuracy to an expert reader. This technique presents some unresolved problems; it appears to be more amenable to dobutamine than exercise stress, and further efforts are needed to remove the contribution of translational movement. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 6 Another quantitative approach that is independent of edge detection is the analysis of myocardial backscatter. Cyclic variation of backscatter has been shown to change during ischemia,[196] [197] but, until recently, backscatter analysis was strictly a research technique that was dependent Figure 14-11 (Figure Not Available) (color plate.) Color kinesis images with color coding showing sequential frames in systole and diastole in short-axis and apical four- chamber views. The graphics express regional fractional area change in each segment. (From Mor-Avi V et al: Circulation |
1997;95:2087–2097.) on the ability to export and process voluminous raw data from the echocardiography machine. Recent developments in computer technology, especially storage, have made this approach more feasible,[198] although whether it can be incorporated into clinical imaging remains to be seen. Stress Doppler Echocardiography Stress Doppler echocardiography has been used to examine systolic or diastolic blood flow alterations caused by ischemia. Unfortunately, because compensatory hyperkinesis of the nonischemic wall tends to preserve overall ventricular function, changes in stroke volume occur mainly in the presence of extensive ischemia,[199] and stress-induced alterations in global cardiac function are not specific for coronary disease. The development or worsening of mitral regurgitation on color flow mapping (which may explain the occurrence of dyspnea disproportionate to the severity of coronary disease) is another systolic parameter that may be predictive of ischemia during dobutamine stress testing,[33] but the frequency of this finding is low,[200] as vasodilation at peak dobutamine dose tends to reduce left ventricular cavity size and therefore regurgitation. Left ventricular relaxation is an active process that may be altered by the development of myocardial ischemia. These changes can be examined by transmitral flow measurements of the peak E and A wave velocities, E/A ratio, E wave deceleration time, diastolic time intervals, and flow-velocity integrals of passive and active flow.[201] Unfortunately, tachycardia causes the E and A waves to merge at higher heart rates. Nonetheless, reductions in passive left ventricular filling (probably reflecting impaired relaxation secondary to ischemia) have been correlated with ischemia during dobutamine stress echocardiography.[202] The same pattern has been recorded with other stressors that provoke ischemia without tachycardia, such as dipyridamole and pacing with cessation after the development of ischemia.[203] Unfortunately, however, the effects of ischemia (delayed mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 6 relaxation) may be pseudonormalized by ischemia-induced increases in left atrial pressure (Fig. 14-13) . Tissue Doppler assessment may be of value in 327 Figure 14-12 (color plate.) Importance of high frame-rate to tissue Doppler velocity. Doppler velocity profiles are shown in the same segment at different frame-rates. A high frame-rate (>100 frames per second [f/s]) is necessary to obtain the true peak velocity as well as timing variables. examining regional diastolic function with less influence from left atrial pressure. [204] Changes of diastolic function in response to stress are not specific for ischemia, however, and may be induced by left ventricular hypertrophy, for example. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/126.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 10 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Alternatives to Nonexercise Stress Echocardiography Exercise Stress Echocardiography Nonexercise stress approaches are invaluable in patients who are unable to exercise maximally. Attempts to use exercise stress in such patients are attended by suboptimal sensitivity, and this is true also of isometric exercise. [205] Pharmacologic stressors have also been used in patients who are able to exercise, among whom the results of Figure 14-13 Development of a pseudonormal pattern, probably due to ischemia-induced increment in left atrial pressure. This patient with resting left ventricular dysfunction developed extensive ischemia by wall motion assessment. However, there is an increment of E wave velocity and shortening of the deceleration time, rather than development of a delayed relaxation pattern. exercise and pharmacologic techniques can be compared. Table 14-11 summarizes several studies that compared exercise and nonexercise stress echocardiography on a "head-to-head" basis. Most studies have shown no significant differences in sensitivity or specificity between exercise and nonexercise stress echocardiography. Some of these comparisons have suggested that the nonexercise technique has greater feasibility, although this may be colored by greater expertise in pharmacologic than in exercise echocardiography at some centers. However, several of these comparisons have involved designs that do not replicate the usual clinical scenario, such as exclusion of patients with technically difficult studies, as well as cessation of antianginal therapy before the test. The latter may have an important influence on this analysis; in one comparison of dobutamine and exercise echocardiography, the sensitivity of dobutamine stress was significantly less than that obtained with bicycle exercise in patients who mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 10 were treated with beta receptor blockers, or who failed to complete the dobutamine protocol because of the development of side effects. Interestingly, among the patients with coronary disease in whom both tests were positive, the extent of ischemia was reliably greater with exercise than with dobutamine, reflecting the greater cardiac workload imposed by exercise. This more extensive ischemia may lead the observer to be more confident in the results of exercise than dobutamine stress testing, despite the image quality being better with dobutamine. The advantages of pharmacologic approaches are feasibility, better image quality, and ability to image the heart during stepwise increments of stress as well as at peak stress. These are balanced by a number of considerations that favor the use of exercise stress in those who can perform it. Exercise stress testing provides a greater level of stress on the heart, renders electrocardiographic data useful (the results of which are less useful with pharmacologic stressors), and gives results regarding functional capacity and data about stress that are readily extrapolated to everyday life. Exercise also offers important prognostic 328 TABLE 14-11 -- Sensitivity and Specific Myocardial CAD Multivessel, Infarction, Patients, CAD, Diameter, n (% all n (% all Study N n % CAD) CAD) EXERCI Picano et 55 34 >70 18 (53) 6 (18) 76 al[265] Hoffman 66 50 >70 21 (42) 0 (0) 80 et al[81] Cohen et 52 37 >70 21 (57) 11 (30) 78 al[76] Beleslin et 136 119 >50 11 (9) 41 (34) 80 al[79] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 10 Marangelli 60 35 >75 19 (54) — 89 et al[123] Marwick 86 56 >50 34 (61) 0 (0) 88 et al[77] Dagianti 60 25 >70 15 (60) 0 (0) 76 et al[219] Rallidis et 85 85 >70 40 (47) 42 (49) 77 al[266] CAD, coronary artery disease. 329 data. Based on these considerations, exercise echocardiography appears to offer more data than the nonexercise approaches, and we limit the use of exercise-simulating techniques to patients who are unable to perform maximal exercise. However, the new techniques that are adjunctive to stress echocardiography (for example, contrast, tissue Doppler, and acoustic quantification echocardiography) are more easily performed in the stationary patient and may lead to an increase in the number of nonexercise studies in the future. Stress Electrocardiography In the current medical-economic climate, much attention is being paid to using less expensive diagnostic and therapeutic methodologies. Because stress electrocardiography is substantially less expensive than stress imaging tests, it might be considered as an alternative to stress echocardiography. In this respect, it is important to differentiate between the stress electrocardiographic component of the pharmacologic tests and mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 10 the exercise electrocardiogram. The latter is an option only if the patient can exercise maximally, and in this situation, both dobutamine and dipyridamole stress echocardiography are as sensitive as or more sensitive than the exercise electrocardiography. Nonetheless, the discussion suggests that if the patient can exercise, the choice should be between the exercise echocardiogram and the exercise electrocardiogram. If the use of nonexercise stress is restricted to patients who cannot exercise, there is little to recommend the use of the pharmacologic stress electrocardiogram, which has poor sensitivity for the diagnosis of coronary artery disease, even if the standard exercise electrocardiographic criteria are altered for use with nonexercise approaches. Although this test should not be performed in isolation, the presence and characteristics of ischemic electrocardiographic changes add useful information about the severity and prognostic implications of an abnormal stress echocardiogram.[206] TABLE 14-12 -- Comparison of Pharmacologic Stress Echocardiography Coronary Arte Sensitivity, % Patients, NUC Study N Stress Dose ECHOCARDIOGRAPHY IMA Nguyen et 25 Adenosine 0.14 60 90 al[267] mg/kg/min Amanullah 40 Adenosine 0.14 74 94 et al[268] mg/kg/min Marwick 97 Adenosine 0.18 58 86 et al[99] mg/kg/min Marwick 217 Dobutamine 40 µg 72 76 et al[99] Forster et 21 Dobutamine 40 µg + 75 83 al[269] atropine Gunalp et 19 Dobutamine 30 µg 70 90 al[270] Senior et 61 Dobutamine 40 µg 93 95 al[216] Ho et al[271] 54 Dobutamine 40 µg 93 98 Huang et 93 Dobutamine 40 µg 93 90 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 10 al[126] Santoro et 60 Dobutamine 40 µg 61 91 al[272] San 102 Dobutamine 40 µg + 78 87 Roman et atropine al[273] Perin et al 25 Dipyridamole 0.56 58 95 [274] mg/kg Simonetti 35 Dipyridamole 0.84 86 91 et al[232] mg/kg Santoro et 60 Dipyridamole 0.84 55 97 al[272] mg/kg San 102 Dipyridamole 0.84 81 87 Roman et mg/kg al[273] Pharmacologic Stress Echocardiography versus Perfusion Scintigraphy Thallium (or technetium MIBI) imaging has the advantage of being the most widely used imaging technique for the noninvasive diagnosis of coronary artery disease and is technically easier to perform and interpret than is stress echocardiography. However, nuclear imaging has disadvantages pertaining to specificity, cost, and inconvenience to the patient. As there is a substantial variation in the reported accuracy of both stress echocardiography and nuclear imaging, based on variations in the population studied, the relative accuracies of each test can only be addressed by direct comparison in the same patient population. The relative abilities of the tests to deal with the diagnosis of coronary disease, identification of viable myocardium, and prognostic assessment are discussed separately. Bearing in mind the preceding discussion regarding the selection of patients for nonexercise stress, this discussion is confined to patients who are for some reason unable to exercise. Diagnosis of Coronary Artery Disease Several studies focusing on the comparison of stress echocardiography and scintigraphy using dipyridamole, adenosine, dobutamine, or atrial pacing stress for the diagnosis of coronary disease have been published (Table 14- mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 10 12) . The concordance rates between scintigraphy and echocardiography for the presence or absence of disease range from 80% to 90% in most studies. There are several pertinent points in the interpretation of this literature. First, it is important to have a reference standard (coronary angiography) to judge which test is "wrong" if the results are discordant, despite the inherent selection bias that this design produces toward studying patients with more severe disease, as well as the imperfections of using angiography as the arbiter of disease. Second, because both techniques may be technically demanding and require 330 considerable interpretive skill, studies coming from centers with expertise in one or the other are unlikely to be meaningful. The corollary of this observation is that for the choice even to be considered routine practice, high-quality nuclear and echocardiographic laboratories should be available; if a center has expertise in only one methodology, the alternative should not be considered. Simply put, good scintigraphy is always better than poor stress echocardiography and good stress echocardiography is always better than poor scintigraphy. Using dobutamine or pacing stress, the sensitivities of both tests for the identification of coronary artery disease are comparable, with most studies showing slightly greater sensitivity with scintigraphy (see Table 14-12) . This difference is most evident in patients with single-vessel disease,[207] a finding that might be expected from the identification of flow heterogeneity with perfusion imaging, which is an earlier event in the ischemic cascade than regional dysfunction, identified by echocardiography. For the same reason, antianginal therapy influences the results of echocardiography because it prevents the development of ischemia[115] but does not influence the results of perfusion scintigraphy.[208] On the other hand, the better spatial resolution of echocardiography and the ability to categorize wall motion independently in each segment (contrasting with the relative flow comparisons used in myocardial perfusion imaging) may compensate for its requirement of ischemia. Thus, the similarities in the sensitivity of echocardiography and scintigraphy reflect the balance between the underlying physiology of the tests and their imaging characteristics. In contrast, studies with adenosine and dipyridamole have shown vasodilator stress echocardiography to be significantly |
less sensitive than perfusion scintigraphy.[209] This mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 10 Figure 14-14 (Figure Not Available) Prognostic content of single photon emission computed tomography (201 TI SPECT) and stress echocardiography scans. The correlation with outcome of the extent of perfusion defect (PDS) and wall motion abnormality (WMS) appears comparable in this exercise stress study. (From Olmos LI, et al: Circulation 1998;98:2679–2686.) difference is most marked in patients with single vessel coronary disease and reflects failure to develop coronary steal in the absence of extensive coronary disease. This difference in sensitivity is less prominent in patients with multivessel disease. With either dobutamine or vasodilator stress, the specificities of stress echocardiography and perfusion scintigraphy are also comparable, with most series showing a small benefit for echocardiography. Whereas the high sensitivity of myocardial perfusion imaging with SPECT may have been gained at the cost of a sacrifice in specificity, two important sources of false-positive results are patients with left bundle branch block and patients with left ventricular hypertrophy. The influence of left bundle branch block has been investigated in a small number of patients,[210] among whom stress echocardiography produced more favorable results for specificity, although insufficient numbers of patients have been studied to reliably address sensitivity. Patients with hypertension and left ventricular hypertrophy are prone to false-positive SPECT results, probably owing to small vessel disease. Stress echocardiography, especially with dobutamine stress, appears to offer greater levels of accuracy.[211] Prognostic Assessment Stress myocardial perfusion scintigraphy is widely used for risk stratification of patients undergoing vascular surgery, patients with chronic coronary disease, and patients who have had a myocardial infarction. Unfortunately, although a substantial amount of literature regarding the individual predictive abilities of echocardiography and 331 TABLE 14-13 -- Comparison of Nuclear and Stress Echocardiographic T (Evidenced by Improvement of Regional Left Ventric Sensitivity, % Dobutamine mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 10 Thallium Protocol, THALLIUM DOBUTAMINE Study Technique µg/kg/min SPECT ECHOCARDIOGRA Marzullo et al Rest- Low-dose, 86 82 [275] redistribution 10 Charney et al Rest- Low-dose, 95 71 [276] redistribution 10 Kostopoulos et Rest- Low-dose, 90 87 al[277] redistribution 10 Qureshi et al[278] Rest- High-dose, 90 74 redistribution 40 Nagueh et al[279] Rest- High-dose, 91 68 redistribution 40 Senior et al[280] Stress Low-dose, 92 87 (dobutamine)- 10 rest/NTG Arnese et al[281] Stress Low-dose, 89 74 (dobutamine) 10 reinjection Perrone-Filardi Stress Low-dose, 100 79 et al[282] (dobutamine) 10 reinjection Bax et al[283] Stress Low-dose, 93 85 (dobutamine) 10 reinjection Haque et al[284] Stress Low-dose, 100 94 (exercise) 20 reinjection Vanoverschelde Stress High-dose, 72 88 et al[285] (exercise) 40 reinjection Elsasser et al[286] Stress High-dose, 87 95 (dobutamine) 40 reinjection SPECT, single photon emission computed tomography. * Average ejection fraction 38%. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 10 perfusion imaging is available, comparative data are sparse. In patients undergoing surgery for vascular disease, dipyridamole stress thallium imaging has been shown to have a negative predictive value of more than 90% in most studies.[130] The occurrence of unexpected cardiac events in some patients is probably due to intracoronary thrombus formation on nonsignificant stenoses (which do not cause abnormal perfusion results). The predictive value of ischemia at scintigraphy ranges from 30% to 50%, this result being attributable to positive perfusion studies in the context of mild (prognostically benign) coronary disease and false- positive results. Overall, these results are comparable to those of pharmacologic stress echocardiography (see Table 14-7) . There are few comparative studies between stress echocardiography and SPECT. The group of Pierard[135] compared the ability of dobutamine stress echocardiography and dobutamine technetium-99m sestamibi SPECT to predict postoperative cardiac events in 156 patients, among whom the adverse event rate was 5.6%. Both tests were characterized by a high negative predictive value (96% for echocardiography; 97% for SPECT). Postoperative cardiac events were predicted by previous cardiac symptoms, a Detsky score of 15 or greater (RR, 3.0), a positive dobutamine echocardiogram (RR, 3.7), and a positive dobutamine SPECT scan (RR, 7.4). In contrast, work by Pasquet et al[212] suggests that the specificity of stress echocardiography exceeded that of SPECT for the prediction of subsequent events. In patients with chronic stable coronary disease and after myocardial infarction, the relative prognostic roles of stress echocardiography and myocardial perfusion scintigraphy appear comparable (Fig. 14-14) (Figure Not Available) . Ischemia may be difficult to identify within segments having abnormal resting function, and this is a source of discrepancy from the findings of perfusion scintigraphy. Because the territory is supplied by the infarct-related artery, the analysis of sensitivity and specificity does not permit discrimination of which test is correct. Preliminary data comparing dipyridamole stress echocardiography and MIBI-SPECT in patients after recent myocardial infarction have shown the finding of ischemia at echocardiography (and not at scintigraphy) to be predictive of subsequent hard events.[213] Diagnosis of Viable Myocardium mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 10 Positron emission tomography, thallium reinjection techniques, and dobutamine echocardiography have all been shown to reliably identify viable myocardium. A significant evidence base has been accumulated regarding the comparison of these variables (Table 14-13) . In one of the initial studies of patients after thrombolysis, dobutamine responsiveness and spontaneous improvement at follow-up were detected in stunned myocardium (normal flow with reduced function), and no dobutamine response correlated with failure to improve at follow-up was seen in infarcted tissue (reduced flow and reduced fluorodeoxyglucose activity). Hibernating tissue (reduced flow with preserved fluorodeoxyglucose activity) was responsive to dobutamine but failed to improve at follow-up, although not all patients in this category underwent myocardial revascularization. The majority of the comparative studies show SPECT techniques to be more sensitive but of lower specificity for the prediction of functional recovery. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/127.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Consequences of Special Characteristics In addition to the effects noted earlier, there are other differences in intravascular ultrasound owing to the use of high frequencies and size constraints. The strength of backscattered ultrasound relative to the incident ultrasound strength is called the backscattering coefficient. This coefficient is determined not only by the composition of the tissue but also by the frequency of the ultrasound. The backscattering coefficient increases with higher frequencies for virtually all tissues, but the rate of increase is different for each tissue, depending on the microscopic structure.[4] In particular, the strength of the backscattered signal from fibrous tissue increases at a rate greater than that of the other tissues in the arterial wall.[5] A fibrous plaque may have strong echogenicity compared with other tissues at 10 MHz, but it still may be less than calcified tissue. At 30 MHz, however, the strength of the signal from fibrous tissue may be equal to or even greater than that from calcified tissue (Fig. 15-7) . Strong echo alone cannot be used to identify the presence TABLE 15-2 -- Comparison of Characteristics of Systems Nonuniform Ring Type of System Resolution Rotation Down Electronic Good No Yes Cable, direct Very good Yes Yes Cable, mirror Very good Yes No Motor, direct Very good No Yes Figure 15-7 Calcified and fibrous tissue can have very similar echo intensities. This clinical intracoronary image shows an area of dense fibrosis with some calcification. The area of fibrosis extends from 10 to 4 o'clock, but the area from 11 to 1 o'clock, which has the brightest echo mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 intensity, also has the least shadowing. This finding indicates that there is calcification in the plaque in all areas except 11 to 1 o'clock. Note the "halo" surrounding the catheter, owing to ring-down artifact. of calcium in the wall of the vessel, because fibrous tissue may mimic this. Calcified tissue can be distinguished by the additional presence of "shadowing," a profound weakening of signal strength distal to the calcified tissue, owing to the intense attenuation caused by the calcification. Fibrous tissue does not cause this same degree of attenuation, regardless of the intensity of the backscattered signal. Thus, if we see a very bright echo without shadowing, we should suspect that it is fibrous tissue, whereas a bright structure with shadowing should be identified as calcification. It should be noted, however, that the actual classifications are not so clear- cut. Fibrous tissue may have microscopic calcifications, which also cause shadowing. Size constraints lead to other practical issues as well. Intravascular ultrasound catheters need a guidewire for placement, and of the several different types that have been developed, the simplest and least flexible is a fixed guidewire at the tip of the catheter. This type of guidewire does not interfere with the imaging function, but it cannot be used for the exchange of catheters over it. A much more adaptable approach is a removable guidewire, but this approach poses the problem of where to place the guide in the already tight constraints of space at the tip of the catheter. For catheters with electronic beam steering, the center of the catheter is free for use by a guidewire because there is no motor or drive cable. For mechanical systems, there is a space problem, which can be solved in one of two ways. The first solution is to have a channel on the outside of the imaging portion of the catheter through which the guidewire can pass. This approach leaves the imaging portion relatively unchanged, but the guidewire is present in the imaging field, causing a bright echo. The second solution is to use the same channel for the guidewire and an imaging core consisting of the transducer and drive cable, alternately withdrawing one to 345 allow passage of the other. This approach has the advantage of a concentric design with no echo from an adjacent guidewire. Because the imaging core mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 and the guidewire do not have to occupy the tip at the same time, the tip size can be much smaller. For this reason, this design enables the use of the smallest catheters now available. One final consideration is the need to prepare the catheter. All the mechanical designs must be flushed with fluid before use to provide sound transmission from the transducer to the blood; the presence of even microscopic bubbles can adversely affect image quality. The various designs also differ in how easy they are to flush, depending on the size of the catheter and the size of the flushing channel. This consideration is not applicable with electronically steered systems, because the blood itself provides the contact with the transducer. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/132.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company 340 Chapter 15 - Principles of Intravascular Ultrasound David T. Linker MD Intravascular ultrasound is a relatively new technique for imaging a vascular structure from a catheter placed within that structure.[1] The basic physical principles are the same as those for other ultrasound techniques, but the physical constraints and characteristics of a catheter-based imaging technique lead to solutions different from those normally employed in other forms of ultrasound examination. This chapter examines the ways in which the constraints and characteristics of intravascular ultrasound dictate certain forms of design solutions and their consequences on the resultant capabilities of the systems used. The practical consequences for clinical application and future development are also outlined. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/130.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 8 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium |
to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Special Ultrasound Characteristics The principles governing all types of ultrasound imaging are the same, whether the transducers are outside the body, as in transthoracic ultrasound, or within the body, as in transesophageal or intravascular ultrasound. The major differences are transducer size, the distance to the structure being imaged, and the intervening tissues (Table 15-1) . For intravascular ultrasound, these parameters are significantly different. The transducer itself must be very small so that it can be placed inside a catheter, which is inside the arteries or veins. Typical catheter sizes range from less than 1 up to 2.6 mm in diameter. The distance to the structures being imaged is very short, and there is an enveloping layer of fluid (blood) surrounding the transducer at all times. This homogeneous layer of fluid TABLE 15-1 -- Comparison of Intravascular Ultrasound with Other Ultrasound Techniques Transducer Technique Size (cm) Depth (cm) Intervening Tissues Transthoracic >2 ˜3–20 Skin, fat, muscle Transesophageal <1.2 ˜2–20 Esophagus, atrium Intravascular <0.26 ˜0.05–4 Blood is also the main tissue between the transducer and the structures of interest. In transthoracic echocardiography there is little constraint on the size of the transducer, other than convenience and the size of the interspace between ribs. The distance between the transducer and the structures of interest can be much larger, up to tens of centimeters. The intervening tissues are very heterogeneous, including skin, subcutaneous tissues, fat, and muscle. The connection between the transducer and the body must be improved by use of ultrasound gel. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 8 Transesophageal echocardiography has some of the constraints of intravascular ultrasound but not all. The transducer must be small but not as small as that for intravascular ultrasound. Typical sizes are 10 to 12 mm in diameter. The distances to the structures imaged are short, but they still range from 2 to 20 cm. The contact is through a structure with both fluid and air, and therefore variable, and the structures through which sound must pass are almost the same as for transthoracic ultrasound, except for the skin. In summary, the special characteristics of intravascular ultrasound are a very small transducer size, a very short distance from the transducer to the tissues being imaged, and a relatively homogeneous medium between the transducer and the structure being imaged. To understand the consequences of these characteristics and constraints, we must review some details of the physics of ultrasound imaging. Resolution/Attenuation Most imaging transducers are used both for transmission and for reception of the ultrasound energy. For transmission there is a spatial pattern of signal strength, and for reception there is a spatial pattern of sensitivity. These patterns are often similar in form, and taken together they are referred to as the beam pattern of the transducer. A narrow beam leads to improvement of lateral resolution of the image, whereas a wider beam yields lower resolution. This beam pattern is primarily determined by the shape of the transducer and its frequency. The 341 pattern is similar to the diffraction pattern resulting from light traveling through a single small slit. This "single-slit diffraction," which is covered in basic optics, results in a bright central band and less bright alternating bands on either side of the main band, because of interference. A similar pattern results with a single ultrasound transducer: a single main "lobe" of sensitivity and smaller side lobes, owing to interference. For a transducer of given shape and size, the width of the main lobe becomes narrower if the frequency of the transducer is increased, thereby improving lateral resolution. If the frequency is lowered, the main lobe becomes wider, degrading lateral resolution. Increasing the diameter of the transducer creates a narrower main lobe and improves resolution, whereas decreasing the diameter increases the width of the main lobe. These two mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 8 effects of frequency and diameter are closely related. In fact, for two transducers of different size but the same shape, the product of the frequency of emitted sound and the transducer diameter determines the beam pattern (Fig. 15-1) . If we reduce the transducer size and wish to maintain the same lateral resolution, we must increase the frequency proportionately. The main constraint on increasing frequency in diagnostic ultrasound is poor tissue penetration because of attenuation (reduction of the signal strength). Attenuation is increased with higher frequencies and with higher depth. Attenuation also is a function of the tissues through which the sound passes, and it is increased by varying tissue composition, so a uniform tissue such as blood reduces attenuation significantly. Because large distances increase attenuation, the short distance in intravascular ultrasound is also an advantage. Because of these factors, higher frequencies can be used for intravascular ultrasound: up to 40 MHz in some coronary instruments used clinically today, and 20 to 30 MHz for peripheral vascular studies, without encountering prohibitive attenuation of the ultrasound signal strength. The frequency of the transmitted ultrasound can be increased to match the smaller transducer size, improving lateral resolution. Resolution in the direction Figure 15-1 Simulated beam profiles for four transducer size and frequency combinations. Each profile has a central main lobe and may have side lobes as well. Each profile represents the result obtained with a given frequency-diameter product, with the other variables held constant. Moving from A to B represents reduction of the frequency or the transducer diameter by half. Each additional step is another halving of the frequency-diameter product, so that A represents a frequency-diameter product eight times higher than D. of the beam (axial) is also increased, because shorter pulse lengths can be used at higher frequencies. Short Imaging Distance The other effect of very short distances is that imaging is performed very close to the surface of the transducer itself. Imaging close to the transducer face can be unfavorable because of two physical effects: ring-down and near-field artifact. When the transducer is electrically excited to generate the pulse of sound, it "rings" for a short time, much like a bell. This vibration generates electric mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 8 signals similar to, but much stronger than, the signals generated by returning ultrasound. As a result, if we use the same transducer for transmission and reception of the ultrasound signal, which is the case in most systems, the received signal is buried in the ring-down signal (Fig. 15- 2) . This signal creates a limit on the shortest distance from the transducer within which we can generate a useful image. This period of ringing can be shortened by damping the transducer, which has an effect similar to placing a gloved hand on the ringing bell. The problem with this approach is that it reduces both the transmitted ultrasound energy and the sensitivity to received ultrasound signals. Increasing the frequency of the transducer also reduces the ringing time, but it can never completely eliminate it. The other effect is near-field distortion. If the source of the reflected ultrasound is a long distance from the transducer, each wavefront arrives at roughly the same time across the entire face of the transducer, and the resultant signal is the sum of all the received signal (Fig. 15-3) . If the source of the reflected ultrasound is a very short distance in front of the transducer, there is interference of the wavefronts across the face of the transducer, causing loss of signal and distortions in the image. The distance at which this occurs is a function of the frequency and diameter of the transducer. The range of distances that are affected is much larger than that affected by ring down. These two effects combine to make imaging close to the transducer undesirable. Beam Steering To create a two-dimensional image, ultrasonic pulses must be transmitted and received in various directions. There are two fundamental ways of doing this, and the constraints of size and the length of the catheter affect how these methods can be used. The first method is mechanical motion of the transducer element (or elements) to point it (or them) in the different directions. This method can use a rocking motion, as is used in most mechanical ultrasound systems today, or a rotary motion, which was more common in earlier transthoracic systems. Rocking motion is difficult to reproduce at the end of a long catheter, so it has not been used so far for intravascular ultrasound. Rotation of the element is a uniform motion and therefore easier to produce. All mechanical systems used for intravascular ultrasound so far use this technique. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 8 342 Figure 15-2 Transducer ring down is demonstrated using an actual signal from a clinical 30-MHz intravascular ultrasound probe. The region labeled Ringing shows the signal caused by excitation of the transducer to create the ultrasound pulse. The area labeled Catheter shows returning ultrasound signals, in this case very strong signals from the housing of the catheter. The areas labeled Blood and Tissue show the returning signal from blood and adventitia, respectively. The most direct way to cause the rotary motion of the transducer would be to use a small motor at the tip of the catheter (Fig. 15-4) , but it has been difficult to develop such a small motor with sufficient power. In spite of this, one group has made such a catheter for use in larger vessels. The more common method of causing the transducer to rotate is to have the drive motor outside the body and to use a flexible cable to transmit the torque to the transducer end of the catheter. With this sort of design a significant problem is nonuniformity of rotation of the transducer end of the catheter, because the position is measured at the motor end of the catheter. If the drive cable binds, either through a manufacturing defect or because of sharp bends in the catheter, there is a hesitation of rotation of the distal, transducer end, whereas the proximal, motor end continues to turn.[2] When this Figure 15-3 The cause of near-field artifacts is the difference in timing of arrival of wavefronts across the transducer. If the echo source is far away from the transducer face (left), the wavefronts arrive roughly at the same time all across the transducer face. If the echo source is close to the transducer (right), different parts of the transducer receive different phases of the wavefronts, possibly even parts of other wavefronts. The result is decreased and variable signal strength, causing distortion. happens, several pulses are transmitted in the same direction but are displayed as if they are in different directions, causing a blur in the image (Fig. 15-5) . When the rotation is finally resumed, the speed is much faster than Figure 15-4 Schematic examples of three different types of catheter construction. Cable mirror and motor direct are examples of mechanically steered designs, using a flexible cable or a micromotor to cause rotation. One uses a mirror to direct the beam in differing mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 8 directions, reducing near-field and ring-down artifacts, whereas the other uses a transducer pointed directly outward. Either of these can use a micromotor or a drive cable to provide torque. The electronically steered catheter has no moving parts and a large number of smaller transducers mounted on the surface. Only a few transducers are shown here, for clarity. 343 Figure 15-5 Illustration of how nonuniform rotation causes distortion of images from a mechanical system. Beams are sent out and received in uniformly spaced directions to create an image. If the transducer is delayed in its rotation because of a mechanical problem, the motor continues to turn and pulses continue to be sent out, but they will go in the same, or almost the same, direction (beams 1 to 5, left). When the transducer starts to rotate again, it rotates much faster, skipping some regions (beams 6 to 10). The display, however, distributes the beams equally, causing distortion (right). normal and |
the image is compressed. This process can occur at one part of the image or at several (Fig. 15-6) . The construction of the transducer end can also vary. There are two fundamental types of transducer orientation. The simplest to understand is the one with the transducer pointed directly out of the catheter toward the vessel wall. The actual direction of the transducer is usually slightly forward, so that internal reflections within the catheter cause less of a problem. This design has the advantage of simplicity, but there are difficulties stemming from the proximity of the transducer to the structures being imaged. Because the same transducer is used to generate and receive the signals, and there is a very short distance from the transducer to the outside of the catheter, ring down causes a bright halo near the transducer, although this is often blanked out on the screen. Near-field distortion can also be a problem close to the transducer. These two artifacts can be troublesome if the structures of interest are adjacent to the catheter, as they can be in small vessels or in tight stenoses. Figure 15-6 Clinical examples of nonuniform rotation distortion on intracoronary images. A, There is distortion due to nonuniform rotation in one region, similar to what is illustrated in Figure 15-5 . Note that the "smeared" portion from 3 to 4 o'clock represents when the transducer was not rotating fast enough, whereas the compressed region from 5 to 6 o'clock represents when the transducer was rotating too fast. A clue to this artifact is the size of the speckle, which mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 8 becomes larger when the transducer is rotating too slowly and smaller when it is rotating too fast. B, Demonstration of what happens when the rotation of the transducer is slowed in several different directions as it rotates, at about 12, 2, 4, 7, and 10 o'clock. The alternative transducer orientation deals with the problems of near-field artifact and ring down directly by increasing the effective distance between the transducer and the outside of the catheter. This increase in distance is achieved by directing the transducer toward an internal rotating mirror, which then directs the ultrasound outward. Although slightly more complex, this type of design results in less or no ring-down effect at the surface of the catheter and reduced near-field distortion. The other technique for steering the beam is based on electronic combination of the signals from multiple small transducers. These signals can be arranged in a linear phased array, with all the elements potentially contributing to the image formation, or a curvilinear array, in which only some of the elements are used at one time. Because an intravascular device images in all directions, a linear phased array would not be able to steer the beam in all those directions, so the curvilinear array is the one that has been applied. As a result of the constraint of size, it is difficult or 344 impossible for each of the elements of the array to be wired separately, as is the case in the usual array system. Specialized electronics at the tip of the catheter are necessary in order to switch sequentially between the individual transducer elements; therefore, elements cannot be used simultaneously, and several sequentially acquired signals from adjacent transducers must be added together electronically after they have been received in order to create the "beam" signal. This technique is called synthesized aperture, because the equivalent of a simultaneous signal from the entire transducer (aperture) is created (synthesized) by adding the individual signals together. As a result of the need to send the beams out sequentially, the frame rate of image generation is reduced. Also, because the array is curved, some of the elements at the sides of the beam direction contribute little to the imaging, resulting in a smaller effective transducer diameter, reducing effective resolution.[3] Electronic systems share some, but not all, of the problems of mechanical mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 8 systems. The transducer elements are on the surface of the catheter, so they are even closer than in the direct, rotating transducer designs, which means that the ring-down effect and near-field distortion are even more problematic for these systems than for mechanical systems. Because there are no moving parts, however, there is no problem with nonuniform rotation, and the images are stable no matter how much the catheter is bent (Table 15-2) . MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/131.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Practical Issues Unless we understand the limitations and variations of generation of the intravascular ultrasound image, we may misinterpret what is seen. What we see is primarily generated by the differences in acoustic properties between different tissues rather than the absolute value of those properties. An example of this is the media of the artery, which we can see quite clearly as an echolucent zone if there is intimal thickening, but which disappears completely if the intima is of normal thickness. It is reasonable to ask why the intima is not always visible. The answer to this is not clear, but there are two hypotheses. The first is that the intima must exceed a certain thickness, similar to the resolution limit, before it becomes visible. Once it exceeds this resolution limit, it is clearly visible. The problem with this explanation is that a plane reflector should be visible, even if it is smaller than the resolution limit, because the latter refers to resolving two sources of reflection, not one. An alternative explanation is that the normal intima has acoustic properties that are close to those of blood and media, and therefore are not visible, whereas thickened and abnormal intima has different properties and is visible. An issue discussed previously in this chapter is that of Figure 15-8 Altered appearance of calcification using different imaging systems. The clinical intracoronary image (A) shows intense shadowing owing to calcium from 2 to 3 o'clock, imaged with a mechanical system. B, Much less intense shadowing is visualized when using an electronically steered system, from 9 to 11 o'clock. the relative intensity of echoes from structures and their relationship to the frequency of ultrasound. Although calcium may have a much stronger echo than fibrous tissue at the frequencies of ultrasound used for transthoracic and transesophageal imaging, the relationship may be reversed at the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 frequencies used for intravascular ultrasound. Thus, the brightness of the generated echo may not be sufficient to identify calcium, and other findings, such as the presence of shadowing, should be used (see Fig. 15- 7) . The appearance of pathologic structures can also be influenced by the type of ultrasound instrument used and the settings of the instrument. These factors influence the range of gray values that can be accurately represented, and they can in some cases completely alter the appearance. Shadowing caused by calcification can be less apparent with curvilinear array systems than with systems that use a mechanically rotating transducer (Fig. 15-8) , for reasons that are not entirely clear. If we use the same criteria to-diagnose calcification in both situations, we may misinterpret the images. Similarly, the ability to see thickened media or lipid-rich plaque may be altered by the instrument gain settings and the type of instrument. Numerous distortions in the image can occur.[6] The most obvious cause, mentioned earlier, is nonuniform rotation with a mechanical catheter system. The visual distortions may be obvious or may be mistaken for abnormalities of the vessel contour and, therefore, pathology. These distortions may also affect any measurements that can be performed, so interpretation of vessel and lesion size should be made with great caution in the presence of such artifacts. The degree of distortion is greater the more eccentric the position of the catheter, so if the catheter is concentric with the vessel and the disease is also concentric, cautious interpretation may be possible. Another source of alterations in measurement is angulation of the catheter relative to the vessel. This type of problem is more difficult than problems of angulation with other forms of ultrasonic examination in which the operator has both direct control and awareness of the orientation of the transducer. In intravascular ultrasound the transducer moves freely within the vessel. It is not possible to determine the orientation of the vessel relative to the catheter from the images themselves, nor from 346 manipulation of the catheter. Angulation of the catheter relative to the wall can introduce geometric distortion owing to the oblique plane of imaging.[7] This distortion can lead to misinterpretation of the wall pathology or the dimensions of the vessel or lesion. In general, however, the actual mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 magnitude of these distortions is minimal. As an example, a 10-degree angulation can cause less than a 2% increase in luminal area; 20-degree angulation causes about a 6% change. Quantitative evaluation of lesions is also affected by the imaging medium surrounding the catheter because the distances on ultrasound examination are determined by time-of-flight of the ultrasound, which in turn is determined by the speed of ultrasound in the intervening medium.[7] The speed of ultrasound in solids and liquids is predominantly governed by the specific gravity and compressibility, the former being the main variable in liquids. In blood, the main variable determinants of specific gravity are protein content and red cell content. Both change specific gravity, and as a result the time-of-flight of the ultrasound pulse, and the calculated measurements change (see Chapter 9) . This change can be as much as a 5% difference in the clinical range of proteins and red cell counts.[8] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/133.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Future Directions The clinical application of intravascular ultrasound depends in large part on being able to identify clinical situations in which the information obtainable with the technique would lead to better or more specific treatment. So far, the best example of this is using intravascular ultrasound to assess the placement of vascular stents. Such observation has demonstrated that many stents that appear to be properly placed on the basis of angiographic images show poor apposition to the arterial wall on intravascular ultrasound images.[9] [10] The use of additional balloon inflations to improve the ultrasound appearance has reduced the incidence of subacute thrombosis of the stents, even though the patients received less intense anticoagulation than is otherwise customary.[11] As a result, the use of intravascular ultrasound has become routine whenever there is any question about stent placement. In addition, intravascular ultrasound is frequently used to help evaluate lesions with difficult or hard to interpret angiographic appearance. It seems likely that more specialized intravascular ultrasound probes will be developed. Smaller size is one possible direction, and there are already reports of imaging guidewires.[12] Combination with interventional devices is an obvious direction of development and combined imaging/balloon catheters[13] and imaging/atherectomy catheters [14] have already been produced. Other possibilities likely to be developed include forward- looking devices, which have already been reported by two groups.[15] [16] [17] [18] Also, the advantages of ultrasound guidance of lasers[18] [19] [20] [21] [22] have spurred interest in combined laser/imaging catheters. Another general trend is toward increasing transducer frequencies, which result in improved resolution, both in the lateral and in the axial directions. In addition to the formidable technologic difficulties of |
dealing with higher frequencies, there is the physical difficulty of increased backscatter from mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 blood. Increased backscatter results from the marked increase in relative backscatter from blood at higher frequencies compared with all other tissues, which translates into decreased contrast between blood and arterial tissues. Because of this, there have been studies using signal processing techniques to reduce the relative intensity of the blood signal relative to tissue, thereby improving contrast at higher frequencies.[23] [24] Although it is possible to correlate the visual appearance of plaque on the intercoronary ultrasound image with histology,[25] [26] there have been numerous attempts to improve discrimination and reproducibility by automating this process of discrimination. The two general approaches have been to base the processing on the images as they are presented to the viewer, or to use the raw ultrasound signal before it is processed into an image. The former example has the advantage of being easier to implement, requiring only a video digitizer, which is currently easily available. Analyzing the raw signal is much more complicated, requiring modification of the ultrasound instrument as well as specialized digitization hardware to sample the signal at the high frequencies observed. Nonetheless, reasonable results have been achieved using both techniques. An automated analysis of digitized images correlated well with both histology and visual analysis.[27] In another study, the normalized backscatter power and slope were examined in a limited number of samples, and they showed some discrimination of different tissue types.[28] A limiting factor of all of these studies is the need for a standard, because the characteristics of different instruments as well as different catheters can vary, requiring some measurement to normalize the results. For studies based on video digitization, this measurement is normally based on something that is easily visible in the image, and most frequently this has been the adventitia. Because the only parameter being measured is brightness of the ultrasound image, the results are normalized to the brightness of adventitia. For raw ultrasound signal studies, the benchmark has been the reflection from a perfect reflector, which is either a steel or plastic block. This method is clearly impractical in the clinical setting because it requires very careful measurements with micromanipulators to position the reflector. A recently proposed alternative is to use backscatter from the flowing blood within the artery as a standard.[29] In addition to being readily available, the results are less variable than the backscatter from adventitia. Overall, although there have been some intriguing results to date regarding automated analysis for tissue identification, as well as improved tissue identification, the ultimate limits of discrimination of mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 intravascular ultrasound are still unclear, and unambiguous identification may be possible only in very limited situations. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26070721/1031/134.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company 349 Chapter 16 - Intravascular Ultrasound Histologic Correlation and Clinical Applications Katsuhiro Kitamura MD Paul G. Yock MD Peter J. Fitzgerald MD, PhD More than 10 years have passed since intravascular ultrasound (IVUS) was introduced into the clinical setting, bringing about a new era for the assessment and treatment of vascular pathology. Moreover, it has provided a method to directly examine atherosclerosis and other vascular disease processes. The ability to image the vascular wall as well as its lumen has changed the focus of the assessment of vascular disease by clinicians. Although pathologists have long recognized that measurement of lumen dimensions often poorly reflects the extent and importance of arterial disease,[1] [2] [3] IVUS has the ability in vivo to measure both lumen and vessel size.[4] [5] This information brought forth by IVUS has also brought new insights into coronary interventions by direct examination of their effects on atherosclerotic plaque and the vascular wall. With increasing experience and continuing advances in image quality and catheter design, IVUS has become the standard for the assessment of vascular disease. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/136.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Background Angiography: A Shadow of the Truth The introduction of coronary angiography to assess coronary atherosclerosis by Sones in 1958[6] focused attention on the vascular lumen; however, several investigators[7] [8] [9] [10] [11] have subsequently demonstrated that a particular coronary lesion involved in an acute coronary syndrome is not related to its angiographic severity. Pathologic reports have shown that the underlying mechanism of coronary occlusion is thrombus formation precipitated by the rupture of a lipid-laden atherosclerotic plaque, rather than the progression of a previously severe coronary stenosis.[12] [13] [14] [15] [16] [17] [18] Furthermore, it has become apparent that narrowing of vascular lumen is a late event in the development of atherosclerosis. Glagov et al[19] demonstrated that vessels compensate for the development of atherosclerosis by increasing their cross-sectional area to accommodate the plaque burden. Luminal narrowing does not occur until this compensatory mechanism fails. On average, angiographically apparent atherosclerosis occurs only when greater than 40% of the vessel area is occupied by plaque.[20] Thus, angiography, which generates a silhouette of the vessel lumen and no direct information about the vascular wall composition, underestimates the severity[21] and extent[22] of atherosclerosis and offers little information about the characteristics of obstructive plaque. Although angiography provides a road map, IVUS may provide a clinically applicable means to augment the road map by imaging the arterial wall as well as its lumen in vivo. The History of Intravascular Ultrasound The development of IVUS has been made possible by the advances in computerization and electronics and, in particular, the miniaturization of ultrasound transducers. Although catheter-based ultrasound was shown to be feasible in 1956 by Ciezynski, these initial attempts to mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 350 develop IVUS systems were aimed at measuring the dimensions of cardiac chambers. [23] The first real-time, two-dimensional intracardiac images were produced by Bom et al[24] using a 5.6-MHz, 32-element phased array transducer mounted on a 3.2-mm catheter, but the development and widespread clinical application of transcutaneous echocardiography overshadowed the progress in intravascular cardiac imaging. It was not until catheters were further miniaturized that the assessment of atherosclerotic plaque became practical.[25] [26] [27] [28] [29] The first real-time, two-dimensional images from human peripheral vessels were recorded in 1988,[30] followed by the first in vivo imaging of human coronary vessels in 1989.[31] [32] Since that time, advances in catheter design and image quality have allowed the introduction of ultrasound catheters less than 1 mm in diameter that are capable of accurately assessing lumen and vessel dimensions as well as plaque morphology. In 1990, three-dimensional IVUS reconstruction was first described by Burrell et al,[33] and it has dramatically progressed by advances of catheters, pullback devices, and sophisticated computer algorithms. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/137.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Basic Principles Catheter Design Two basic approaches to catheter design have been developed. The first approach involves the use of a single piezoelectric crystal with mechanical rotation of the ultrasound beam to achieve circumferential imaging. The second approach involves a solid-state, multielement transducer (Fig. 16- 1) . These catheters are delivered into the vascular lumen over a guidewire to enable their safe delivery to the region of interest. Both systems are fundamentally different and have their own unique strengths and weaknesses. A mechanical catheter has a flexible drive cable, traveling the whole length of the catheter, which rotates its single transducer on the distal tip at a speed of 1600 to 1800 rpm. Because the maximum delivery of acoustic power is larger than a solid-state system, the penetration Figure 16-1 Diagram of the two basic IVUS imaging catheter configurations. and resolution of the surrounding tissue becomes larger, resulting in better image quality. One problem associated with this type of catheter is nonuniform rotational distortion, which is characterized by portions of stretched or compacted images and is caused by kinking or compression of the ultrasound catheter. This artifact is problematic in vessel curvature of greater than 40 degrees and may cause absolute errors for diameter and area measurement by more than 20%.[35] Solid type catheters have 64 multiple imaging elements, arranged cylindrically at the distal tip, which visualize cross-sectional images perpendicular to catheter axis. This type of catheter does not experience mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 nonuniform rotational distortion, which is an important advantage In addition, the over-the-wire design makes the catheter relatively easy to use and manipulate in the coronary arteries. The multielement design, however, produces ring down. This artifact, seen as a bright ring surrounding the catheter, is generated by continued vibration of the piezoelectric crystals after cessation of the activating electrical impulse. Although this artifact can be electronically subtracted out by eliminating all early signals detected by the catheter, this masking may prevent the detection of structures close to the catheter surface. With respect to image quality, transducers, made from small parts of elements have relatively weak acoustic power, leading to an ambiguous image. The size of both types of catheters has continually decreased to diameters less than 1 mm, which allows for compatibility with 6-F guiding catheter platforms. Imaging frequencies have also increased, now greater than 40 MHz, providing substantially higher resolution for delineating subtle plaque variations in the vessel. Typical ultrasound images are shown in Figure 16-2 . It can be easily recognized that a higher frequency catheter can provide higher resolution at the expense of increased signal strength in blood and decreased signal penetration in tissue. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/138.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 7 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Image Interpretation The Normal Artery The ultrasound appearance of an organ or tissue depends on the acoustic properties of its components, specifically the degree of acoustic impedance difference between its layers. From the ultrasound point of view, normal arteries are mainly composed of collagen and elastin, which are highly echo reflective, and smooth muscle cells, which are relatively sonolucent. The arterial adventitia, which is mainly composed of collagen and elastin, is highly echo reflective, producing bright signals on IVUS. The media of arteries varies according to the respective anatomic location. Large central arteries, such as the aorta and iliac arteries, have an elastic media, which is also highly echo reflective, making the differentiation of media, adventitia, and intima indistinct, especially when the adventitial collagen is densely packed.[36] [37] [38] Typically in elastic arteries, the media is as bright as the surrounding tissue.[28] However, medium size arteries, such as the coronary 351 Figure 16-2 Ultrasound images obtained by 30-MHz (A), 40-MHz |
(B), and 50-MHz (C) catheters. Higher frequency catheters can provide improved resolution, but signal strength of blood increases as signal penetration decreases. and femoral arteries, have a muscular, echolucent media. The detection of arterial intima depends on its thickness.[39] [40] In normal peripheral muscular arteries, reflections from the intima produce a bright inner layer, which helps to produce a distinctive three-layered appearance[41] [42] (Fig. 16-3) . Siegel et al[43] studied the precise origin of this three-layered mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 7 appearance. These researchers confirmed that the innermost bright layer is produced by the intima and internal elastic lamina, the echolucent middle layer is produced by the media, and the bright outermost layer arises from the adventitia and external elastic membrane. However, in coronary arteries, the intimal thickness may not be sufficient to generate a distinct reflective layer. Fitzgerald et al[39] demonstrated that vessels with a three- layered appearance have a significantly thicker intimal layer than those without ultrasound layering. An intimal thickness of at least 178 µm was required before layering was seen with a 30-MHz transducer. Thus, Figure 16-3 Ultrasound image of mild coronary disease, illustrating the typical three-layered appearance. This appearance is a result of the acoustic difference between the layers of the artery: intima, media, and adventitia. in truly normal coronary arteries without intimal thickening, a layered appearance is not seen. Because the "normal" appearance of coronary arteries was first described in patients with diffuse intimal thickening, a three-layered appearance was considered to be normal. Assessment of Atherosclerosis Atherosclerosis is a diffuse vascular disease process initially characterized by intimal thickening. In the early phases, lipid and macrophages accumulate within the intima, then, as the disease progresses, collagen is added by vascular smooth muscle cells.[44] [45] [46] As the production of collagen and accumulation of lipid continues, calcium may also be deposited and the media may thin.[47] The amount of lipid, collagen, and calcium within individual plaques varies widely. Plaque composition is related to the clinical course of coronary atherosclerosis. Fibrous 352 plaques tend to be stable and slowly progressive, with a clinical presentation of stable angina. Lipid rich plaques are less stable and may rupture, producing an acute, unstable ischemic syndrome.[12] [13] [14] [48] , [49] IVUS allows the quantification of the extent of atherosclerosis and an assessment of the composition of the plaque. In muscular arteries the echolucent media provides a separation between the thickened intima and the adventitia, which allows the cross-sectional area of the plaque to be mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 7 clearly delineated. The plaque area should be measured using a leading edge technique, outlining the blood-intima and media-adventitia boundaries. The media-adventitia border is selected because this boundary corresponds to a true anatomic boundary compared with the outline of the plaque, which does not always correspond to the plaque-media boundary. Signal attenuation at the outline of a plaque may produce dropout in the image, masking the true plaque-media boundary. A large plaque burden may also be associated with thinning of the media, making the separation of plaque from adventitia difficult. [28] [47] , [50] However, this boundary is usually apparent in adjacent proximal or distal cross sections. Regions of calcification within the plaque are highly echo reflective. Calcification generates bright echoes (more intense than the surrounding adventitia) associated with acoustic shadowing and reverberations (Fig. 16- 4) .[29] , [51] [52] This acoustic shadowing obscures the media-adventitia border and makes the assessment of the plaque burden difficult, especially when the calcification is extensive and superficial.[28] The reliability of ultrasound in detecting plaque calcification is pretty high. In a histologic comparison study, Di Mario et al[51] reported that calcium deposits were detected by IVUS with 97% accuracy. In vivo studies have also confirmed that IVUS often detects calcification not visible by angiography.[53] [54] Mintz et al[55] reported that calcification was present in 48% of target lesions by fluoroscopy and 76% of lesions by IVUS (P < .001) in patients with coronary interventions. Calcification was more likely to be visible by ultrasound only if it occupied less than 90 degrees of the vessel circumference and/or was less than 5 mm in length. These researchers also reported that calcium was detected in 72% of target lesions in 1442 patients and lesions with an ultrasound plaque burden greater than 0.75 or an angiographic Figure 16-4 Examples of calcified plaques. Deep and superficial calcium with acoustic shadows (A and B) and circumferential calcification with reverberations ("napkin-ring" appearance, C) are shown. diameter stenosis greater than 0.25 had a prevalence of calcium of at least 65%. [56] Fibrous plaque is also echo reflective, although less so than calcium. It produces relatively bright echoes, often of a similar intensity to the adventitia.[28] [29] [42] [51] However, the intensity of echoes from fibrous plaque is variable. This variation may, in part, reflect machine gain settings, but it mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 7 is also likely to be related to the collagen content of the plaque. Dense fibrous plaque can produce echoes that are brighter than the adventitia and can even cause acoustic shadowing, but they cannot produce the reverberations typical of calcification. Lipid is a poor reflector of ultrasound. Therefore, predominantly lipid-rich plaques, fibrofatty or fatty plaques, are often echolucent and less intense than the surrounding adventitia. Lipid pools can also be detected within plaques as echolucent regions without internal structure.[28] [29] The accuracy of IVUS in detecting lipid plaque has been reported to be as high as 78%.[29] In practice, however, echolucent regions must be cautiously interpreted. Artificial echolucency can be produced by ultrasound systems with limited dynamic range. When the dynamic range of the system is low, weak signals are not displayed, creating an image that mimics "lipid lakes" within plaque. The detection of thrombus is also difficult by IVUS because of the acoustic properties of thrombus, which are weakly echo reflective, variable, and often similar to blood or soft atherosclerotic plaque. At 20 to 30 MHz, blood has a fine, variably speckled appearance. This backscatter from blood is often valuable in the interpretation of IVUS images, allowing the discrimination of the inner plaque margin. The echogenicity of blood in vivo is mainly determined by the flow rate. At low flow rates, red blood cells aggregate, increasing the strength of the backscatter. Regions of slow blood flow, such as around dissections or within aneurysms, produce a brighter ultrasound image. The ultrasound appearance of thrombus varies with its composition. Platelet-rich thrombi have a very low echogenicity (similar to saline in vitro), whereas thrombi rich in red blood cells have a much greater echogenicity and demonstrate a uniformly speckled appearance.[57] [58] The echolucency of platelet-rich thrombi may explain the frequent failure of IVUS to detect thrombus in patients 353 Figure 16-5 An example of in-stent thrombus. A large amount of homogeneous echo patterns is observed inside stent struts (arrows). mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 7 with unstable angina.[59] [60] In vivo, thrombus often has a diffuse, ill- defined, homogeneous appearance (Fig. 16-5) . The sensitivity for detecting thrombus by IVUS has been reported between 36% and 80%.[60] [61] [62] Validation of Intravascular Ultrasound Measurements Numerous in vitro studies have validated IVUS measurements using histology as the gold standard.[25] [27] [28] [29] , [63] [64] Nishimura et al[65] reported an excellent (r = 0.98) correlation between lumen area measured by IVUS and histologic measurements in 130 fresh arterial segments. In vitro measurement of atherosclerotic plaque thickness has also been shown to be accurate (r = 0.91), [27] although in some studies plaque thickness was consistently smaller by histology, possibly owing to tissue shrinkage during processing. [28] IVUS measurements have been compared with angiographic measurements in a variety of studies. Nissen et al[66] reported, using normal human arteries, high correlation of diameter measurements between ultrasound and angiography (r = 0.98). The correlation between angiography and IVUS in diseased vessels, however, is not as close, especially when the lesion is eccentric.[67] [68] Following balloon angioplasty, the correlation between ultrasound lumen area and histology is good (r = 0.88),[69] but the correlation between angiography and IVUS is poor (r = 0.26),[5] [54] [70] , [71] These differences reflect the limitations of angiography in quantifying the complex, irregular lumen, which is typical following balloon angioplasty.[72] Many studies have also compared ultrasound assessment of lesion severity by cross-sectional area with traditional quantitative angiography.[54] [66] [73] [74] [75] [76] Nissen et al[67] reported that the cross-sectional lumen area by ultrasound has only a moderate correlation (r = 0.63) with the angiographic lumen area, which was supported by Tobis et al.[54] The reason for lack of correlation is because lesion severity by IVUS is calculated as a ratio of lumen area to vessel area, whereas for quantitative angiography it is based on the minimal lumen diameter within the lesion and the reference segment. Angiographically normal segments are often diagnosed as diseased by ultrasound. [22] Typically, reference segment plaque occupies 35% to 40% of the vessel cross-sectional area. The ultrasound assessment of lesion severity is affected by the remodeling phenomenon[77] [78] [79] therefore, the vessel size at the lesion may not be representative of the nondiseased vessel size. Lesion Morphology mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 7 In addition to these issues of quantification, IVUS and angiography also provide different views of plaque morphology. Fitzgerald et al[76] compared lesion eccentricity by ultrasound with that by angiography. They found 77% of plaques were judged to be eccentric by ultrasound, but only 33% were eccentric by angiography. Additionally, many of the angiographically eccentric plaques were found to be concentric by ultrasound. The accuracy of the detection of morphologic features of plaque remains less certain. Histologic studies have demonstrated that IVUS can detect endothelial tears. Van der Lugt et al[80] reported that the sensitivity of IVUS in detecting morphologic features for each vascular specimen was high for dissection and media rupture (79% and 76%, respectively), but it was low for plaque rupture (37%). The ability of ultrasound to detect spontaneous plaque ruptures, which are often microscopic, is poor.[81] Ge et al[82] performed IVUS on patients with angina and compared groups with disrupted and nondisrupted plaques by IVUS findings. They found that disrupted plaque was related to unstable angina and concluded that IVUS can identify plaque rupture and vulnerable plaques. Yamagishi et al[11] reported that large eccentric plaques, containing an echolucent zone by IVUS, can be at increased risk for instability even though the lumen area is preserved at the time of initial study. They also showed that among 12 coronary sites with an acute occlusion at follow-up, 10 sites contained the echolucent zones. Inter- and Intraobserver Variability of Intravascular Ultrasound Measurements The limited image quality of early IVUS systems often made the interpretation of in vivo images difficult. Despite these limitations, early reports indicated that the inter- and intraobserver correlation of measurements was greater than 95%.[29] [64] [83] In one study, Blessing et al[84] assessed the inter- and intraobserver variability in 100 Palmaz-Schatz stent cases. The result showed that interobserver correlation ranged from 0.92 to 0.97 and intraobserver correlation ranged from 0.94 to 0.97 for measuring reference and minimal stent areas. These studies have clearly shown that the IVUS analysis of selected frames is highly reproducible. However, the variability introduced by selection of frames to be analyzed 354 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 7 is another problem. Pathology reports indicated that lesion morphologic characteristics were typically constant only over a region 100 to 200 µm in length.[81] The characterization of a plaque may depend on which section is analyzed, and it is common practice to assess a lesion at the minimal lumen area, which may not be representative of the plaque as a whole within the target segment. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/139.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 10 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Clinical Applications of |
Intravascular Ultrasound Safety Clinical use of IVUS has been emphasized as a safe procedure, [54] [64] , [67] [85] [86] [87] but the studies cited involved only a small number of patients. Coronary artery spasm was reported to occur, but only rarely was it found to be severe.[88] Hausmann et al[89] reported safety information from 2207 patients undergoing IVUS, including 505 cardiac transplant recipients. In 3.9% of patients, complications occurred that might have been related to the performance of the ultrasound. Sixty-three patients (2.9%) had coronary artery spasm during performance of the ultrasound, which did not lead to further complications. Major procedural complications were more frequent in patients with unstable angina or acute myocardial infarction (2.1%) compared with stable patients (0.8%, P < .01) and more frequently in association with coronary interventions (1.9%) than for other indications (0%, P < .001). Bocksch et al[90] reported that IVUS imaging was done in 103 patients with acute myocardial infarction and showed a remarkable abrupt closure rate of 3.9%. These studies are not comparable because patient characteristics were so different from those of Hausmann's report, but Bocksch emphasized that IVUS should be performed by experienced investigators. Batkoff and Linker[86] reported safety data from 718 IVUS cases. Eight (1.1%) complications occurred, including spasm, vessel dissections, and guidewire entrapment, but no cases resulted in critical outcomes. No differences in frequency of complications among participating institutions were reported (P = .232). In order to perform IVUS safely, it is important to ensure adequate anticoagulation during the procedure. It is our practice to administer 5000 to 10,000 U of IV heparin before performing an IVUS interrogation as well as nitroglycerin before IVUS to standardize measurements. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 10 Detection of Angiographically Silent Disease One of the most basic insights derived from IVUS is the ubiquitous nature of coronary atherosclerosis. Patients with angiographic "discrete" stenoses were found to have significant plaque burden throughout the coronary tree by IVUS. In fact, Mintz et al[22] reported that reference segment cross- sectional narrowing was 51% ± 13%, and only 6.8% of angiographically "normal" reference segments were normal by IVUS. Hausmann et al[91] found that patients with familial hypercholesterolemia had extensive coronary plaques by IVUS, even if angiography showed only minimal narrowing (Fig. 16-6) . This undetected plaque is not visible by angiography because the lumen size is preserved by arterial remodeling, despite significant intimal thickening. [19] [77] [78] [79] [92] , [93] However, such plaques may be of clinical significance. Vasospastic angina and acute coronary syndromes can occur in patients with coronary arteries that are normal by angiography.[11] [94] IVUS also aids in the assessment of lesions that are not well displayed by angiography and may change therapeutic strategy.[95] [96] Angiographic interpretation of lesions may be difficult because of overlapping branches or extreme vessel tortuosity. Bruchhauser et al[96] reviewed cases with ambiguous angiographic appearances using IVUS and, as a result, changed therapy in 21 of 31 patients, thereby eliminating interventions in 19 patients, with excellent clinical results. The accurate assessment of ostial lesions may also be difficult by angiography. Ge et al[97] reported finding plaques in 31 of 92 angiographically "normal" left main coronary arteries. In this study, the average diameter stenosis was 19.3%, with an area stenosis greater than 50% detected in four patients. Assessing the severity of ostial right and ostial left anterior descending lesions is often difficult by angiography; however, IVUS can offer another venue for interrogation and may assist in more careful assessment of these clinical situations. Guidance of Coronary Interventions One of the most widely investigated and applied uses of IVUS is to guide percutaneous coronary interventions. In addition to balloon angioplasty, a variety of new interventional devices, including stents and directional and rotational coronary atherectomy, are currently available to treat coronary stenoses. IVUS has provided new insights into the mechanisms of action of these devices. These insights have led to more appropriate device selection based on the ultrasound appearance of lesions. Additionally, IVUS has mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 10 influenced the way in which operators gauge procedural success. Balloon Angioplasty Andreas Gruentzig[98] speculated that balloon angioplasty compresses atherosclerotic plaque, thus increasing lumen diameter. Early pathologic reports from fatalities following percutaneous transluminal coronary angioplasty (PTCA) reported extensive plaque dissection.[99] It was not until the introduction of IVUS, however, that the mechanism of successful balloon angioplasty could be investigated directly in living patients. Ultrasound studies have demonstrated that lumen area doubled after angioplasty. Three basic mechanisms of this lumen enlargement have been described, including tearing of the plaque, stretching of the vessel wall, and a redistribution of plaque at the treatment site.[69] [100] [101] [102] [103] [104] [105] [106] [107] [108] The efficiency of PTCA seems to depend on a controlled 355 Figure 16-6 Typical example of angiographically silent disease. The angiogram shows no evidence of disease, but at A, B, and C, corresponding IVUS images show mild intimal thickness. disruption of the plaque. Dissections typically occur at the thinnest region of the plaque, at the junction of the plaque and normal vessel wall, or between the media and adventitia.[106] [109] [110] The GUIDE I study[76] found that plaque fracture or dissection was detected by ultrasound in 49% of lesions imaged following PTCA. The study by van der Lugt et al[110] showed that dissections were detected in 63% of whole cases and were generally seen at the thinnest region of the plaque on both histologic sections (92%) and IVUS cross sections (93%). Angiography clearly underestimates the frequency of dissection following PTCA.[111] [112] Typical IVUS images after balloon angioplasty are presented in Figure 16-7 . Dissections appear to be of therapeutic importance. Botas et al[104] demonstrated that vessel distensibility and compliance were returned to normal by balloon angioplasty. Schroeder et al[111] suggested that substantial coronary dissections after PTCA, which do not diminish antegrade blood flow, do not lead to an increase in acute or long-term events. A significant portion of luminal gain may be within these plaque fractures.[113] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 10 Dissections after PTCA vary in severity from limited intimal surface tears to full-thickness dissections, extending into the adventitia. The site of these dissections can often be predicted by ultrasound. In an in vitro and in vivo study, van der Lugt et al [110] reported that plaque fracture after angioplasty occurred at the thinnest region of the plaque, regardless of the preinterventional plaque characteristics. Fitzgerald et al[114] showed the close association between lesion calcification and dissection in vivo. Additionally, in this study, calcified lesions had larger dissection flaps. Direct ultrasound data also suggest that stretching and compression or displacement of plaque are important mechanisms of balloon angioplasty. Vessel area has been reported to increase following balloon angioplasty. [101] , [102] [115] Marsico et al[115] reported that a 2.4-mm2 increase in lumen area of coronary arteries following balloon angioplasty was associated with a 1.6-mm2 increase in total vessel area. It has been suggested that plaque area reduction is a result of plaque compression; however, atherosclerotic plaque is relatively incompressible. A possible explanation is that plaque is redistributed to each side of the lesion rather than physically compressed by balloon angioplasty. Baptista et al[108] indicated that plaque compression or redistribution accounted for 57% of the lumen enlargement following coronary balloon angioplasty. The precise mechanism of balloon angioplasty in a particular case depends on the mechanical properties of individual plaques[101] and may explain the variation in effects seen in various studies.[102] [105] [116] , [117] Stents IVUS has made a significant contribution to the safe and effective deployment of coronary stents. Two types of stents are currently available, demonstrating distinctive ultrasound appearances. For stents with a slotted- tube 356 Figure 16-7 Ultrasound images of dissection after balloon angioplasty. design (e.g., Palmaz-Schatz, Multilink), the images show distinct points corresponding to the struts of the stent encountered in cross section by the beam (Fig. 16-8A) . Coil stents (e.g., Gianturco-Roubin, Wiktor) are mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 10 composed of stainless steel wire arranged in a sinusoidal coil. The image of the stent shows a combination of points and short arcs, derived from the struts at any given cross section within the stent being either orthogonal or oblique to the imaging plane (see Fig. 16-8B) . The use of IVUS to guide stent deployment was pioneered by Colombo et al.[120] A major clinical problem with the use of stents was the 3% to 6% incidence of subacute stent thrombosis or hemorrhagic complications from the use of anticoagulants. Colombo's group recognized that most stent- related complications were due to inadequate deployment despite an angiographically satisfactory appearance.[36] [118] [119] This work led to the routine use of high-pressure inflation (greater than 12 atm) for stent deployment, which has lowered the rate of subacute thrombosis to approximately 1%.[120] The Multicenter Ultrasound Stenting in Coronaries (MUSIC) study[121] demonstrated that IVUS-guided stent deployment could be safely performed with aspirin alone. In this study, the rate of subacute thrombosis at 1 month was only 1.3% and Figure 16-8 Ultrasound images of different stent echo signatures. A, A typical cross-sectional view of the slotted-tube design. B, A view from coil design stent. Variation of its echo patterns comes from the struts at any given cross section within the stent being either orthogonal (solid arrow) or oblique (open arrow) to the imaging plane. 357 the 6-month restenosis rate was 9.7%. Despite the use of high-pressure deployment, ultrasound still shows, in a significant portion of cases, that the struts are not as well expanded as the angiogram suggests. In the Can Routine Ultrasound Influence Stent Expansion (CRUISE) study,[122] 36% of the IVUS-guided group received additional PTCA because of insufficient stent expansion by IVUS, resulting in an increased minimal stent area from 6.25 to 7.14 mm.2 Figure 16-9 illustrates successful stent delivery following high-pressure deployment by angiography, but the stent is not yet well expanded by ultrasound. Several randomized trials have been published to assess whether complete expansion with IVUS guidance can produce a clinical benefit after stenting. The CRUISE study compared angiography-guided with IVUS-guided stenting.[122] There were significant differences between groups for poststent mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 10 minimal stent area (7.78 versus 7.06 mm2 ; P < .001) and 9-month target vessel revascularization (8.5% versus 15.3%; P < .05). The RESIST (REStenosis after Ivus guided STenting) study[123] compared stent deployment with and without additional ballooning according to IVUS criteria. The group with IVUS guidance had significantly larger minimal stent area at 6-month follow-up (4.47 versus 5.36 mm2 ; P < .03), but the rate of restenosis was almost the same between the two groups (29% versus 23%). Although final results have not been published, the AVID trial [124] [125] compared angiography-guided stenting with IVUS-guided stenting. There was a significant difference between both groups regarding final minimal stent area (7.54 versus 6.94 mm2 ; P < .01) and 12-month target lesion revascularization (7.9% versus 14.6%; P < .04) for vessels less than 3.25 mm by angiography. Lower 12-month target lesion revascularization rates were seen in vessels with a distal reference diameter of 2.5 mm by angiography and in vessels with greater than 70% preprocedure stenosis by angiography, saphenous vein grafts. Directional Coronary Atherectomy IVUS has also provided insights into the mechanism of directional coronary atherectomy (DCA). Based on Figure 16-9 Angiogram after stent deployment in the mid right coronary artery shows an acceptable result (A), but the initial IVUS image (B) reveals underexpansion. IVUS image after further dilation with bigger ballon (C) demonstrates substantial improvement in minimal stent area. angiographic studies alone, it has been unclear how much of the beneficial effect of directional atherectomy is due to plaque removal and how much is due to lesion dilation by the atherectomy catheter (Fig. 16-10) . Ultrasound has revealed that about 40% of increased lumen area is due to vessel wall stretching and more than 60% is due to plaque removal.[115] [116] [126] , [127] Lesion morphology influences the outcome of directional atherectomy. Softer, more echolucent plaques are more effectively treated with directional atherectomy than fibrocalcific plaque.[128] Popma et al[129] found that the residual plaque area was greater in calcified than noncalcified lesions, especially in lesions with an arc of calcium that extended for more than 90 degrees of the lesion circumference. The |
current cutting capabilities of the DCA device depend on not only the presence of calcium in a lesion but also the location of the calcium relative to the lumen. A superficial rim of calcium at the lumen border generally prevents any tissue removal. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 10 Ultrasound has significant potential to optimize the performance of directional atherectomy. The angiographic appearance of a lesion reveals little about the volume or distribution of atherosclerotic plaque. Several studies have reported the retrieval of media and adventitia by atherectomy, [130] [131] which may lead to increased rates of intimal proliferation.[131] IVUS provides detailed information about the orientation of plaque and the residual plaque burden. The CAVEAT study failed to show any restenosis benefit for DCA versus PTCA,[132] but additional studies have compared IVUS-guided atherectomy and PTCA. The Optimal Atherectomy Restenosis Study (OARS) [133] was a prospective, four-center registry demonstrating that IVUS-guided DCA resulted in high rates of procedural success, with 2.5% in-hospital major complication. The rates of restenosis and target lesion revascularization at 6 months were 29% and 18%, respectively.[134] The Adjunctive Balloon Angioplasty After Coronary Arthrectomy Study (ABACAS) was another multicenter trial[135] that showed that IVUS-guided DCA followed by balloon angioplasty resulted in lower residual plaque mass compared with DCA alone (42.6% versus 45.6%; P < .001), with 358 Figure 16-10 Images of IVUS-guided directional coronary atherectomy (DCA). The lumen area is increased following serial atherectomy without dissections. low complication rate (2.7% versus 3.6%; P = ns). Moussa et al[136] have reported that stenting after DCA (81% cases were IVUS guided) produced a lower restenosis rate (11% at 6 months) and target lesion revascularization rate (7% at 18 months). DESIRE is a multicenter randomized trial that compared stenting with or without DCA under IVUS guidance. [137] It showed that the acute lumen gain was greater in patients who underwent stenting after DCA compared with those who underwent stenting alone (7.2 versus 5.7 mm2 ; P = .02), resulting in a larger minimal luminal area after the procedure (8.6 versus 7.2 mm2 ; P = .03).[137] Follow- up data are forthcoming. Radiation Therapy Recently, intracoronary radiation has emerged as a potential antiproliferative therapy to prevent restenosis after angioplasty or stenting. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 10 [138] [139] [140] Many animal models and clinical trials have revealed that low- dose ionizing radiation reduces the incidence of neointimal formation and positive vessel remodeling.[141] [142] IVUS can play a valuable role to elucidate the response following intracoronary radiation therapy. Sabate et al[143] demonstrated in 21 patients, investigated by three-dimensional IVUS analysis and treated with PTCA followed by radiation therapy, that both the mean external elastic membrane volume and plaque volume increased significantly, but the luminal volume remained unchanged in the β-irradiated segments. IVUS also has clarified several important mechanisms of findings specific to radiation therapy. Edge effect, which is not specific to radiation therapy, is a phenomenon of restenosis at the stent margins. Albiero et al[144] [145] reported in a study of 32 P radioactive β-emitting stents that the incidence of edge effect was 42%, and it remained unchanged even after deployment of radioactive stents with a higher activity level (12 to 21 µCi). The mechanisms of edge effect are now hypothesized to be due to the combination of low-dose radiation and injuries in the segments adjacent to the irradiated site.[143] [144] The edge effect for catheter-based radiation therapy has been described as geographic miss,[146] causing neointimal growth of non- or poorly irradiated adjacent segments. It is the most important issue for preventing edge phenomenon. Intracoronary radiation may also prevent normal healing processes after balloon injury, called unhealed dissection, although nearly all angiographic dissections heal within 6 months after nonradiated angioplasty.[52] Kay et al [147] reported, based on the data from the BERT 1.5 study, that 16 dissections were recognized among 22 cases by IVUS after intervention, and at 6 months follow-up 8 unhealed dissections were seen by IVUS. No relationship between the existence of unhealed dissection and prescribed radiation dose was found. Meerkin et al[148] found 7 of 16 dissections partially healed but still remained at follow-up, yet there was no correlation with poor outcomes. Another important finding by IVUS is late stent malapposition. This phenomenon was first reported by Kozuma et al[149] after new stent deployment followed by 32 P β-radiation. They speculated that positive vessel remodeling and inhibition of neointimal formation by radiation were the primary mechanism. IVUS is the only method currently available to elucidate this specific phenomenon. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 10 Three-Dimensional Reconstruction 359 Although coronary angiography provides the longitudinal information of the vessel lumen shape, conventional two-dimensional IVUS cannot provide such information, which has been a big limitation. Also, the lumen and vessel parameters are measured manually, which is very time consuming and suffers from high inter- and intraob-server variability.[150] Three-dimensional IVUS, however, combines wall and lumen characteristics of single planes with the longitudinal extension of the vessel, providing quantitative analysis of the coronary vessel morphology in an objective and reproducible manner through automated contour detection techniques. The three-dimensional reconstruction of a vessel from two- dimensional images may provide a greater appreciation of the distribution of plaque and other morphologic features. In order to reconstruct a three-dimensional image from a series of two- dimensional pictures, information is required about the longitudinal relationship of the images. This information is usually provided by performing a pullback at a known speed (0.5 or 1.0 mm per second) and assuming that in each time interval the transducer moves a known distance. The video image signal is digitized and each pixel is assigned a unique position in a three-dimensional grid with the x- and y-axis derived from the two-dimensional image and the z-axis derived from the timing sequence of the frame. Such three-dimensional pixels are known as voxels. To perform three-dimensional reconstruction with IVUS, several corrections must be made. For cyclic changes in vascular dimensions that create image artifacts (sawtoothed appearance), an ECG-gated three- dimensional IVUS system has been developed.[151] [152] The other corrections include catheter movement during cardiac contraction and respiratory movement, curved path of the transducer, and axial IVUS image rotation. Slager et Figure 16-11 A longitudinal three-dimensional reconstruction of the left anterior descending artery (LAD) from a series of cross-sectional images during pullback at 0.5 mm per second. A fibrofatty plaque and superficial calcium are seen in the mid-LAD (arrowheads). The trajectory of the intravascular ultrasound pullback is assumed to be straight (center dark bank). IM, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 10 intermediate branch; LCx, left circumflex coronary artery; LM, left main coronary artery. al[153] developed a new technique for correcting these artifacts. They investigated the feasibility of a new three-dimensional reconstruction model by fusion of angiography and IVUS (ANGUS). This system can reconstruct the three-dimensional contour of lumen and vessel along a spatial trajectory of IVUS pullback by combining the data of biplane angiography. High correlation for geometric measurements (r = 0.84 to 0.97) was observed between three-dimensional and biplane angiographic images by this system. Figure 16-11 illustrates a longitudinal view of a pullback from distal left anterior descending to left main coronary artery. The spatial relationship among plaque, calcification, and vessel wall can be easily recognized. In addition, computer-assisted automated vessel quantification is possible from these three-dimensional images. Several algorithms have been developed to trace automatically.[154] [155] Three-dimensional IVUS has been used for the creation of dose-volume histograms for interventional radiation therapy for restenosis[156] [157] [158] and to control intimal hyperplasia after PTCA followed by brachytherapy.[143] [159] In addition, it may serve as a valuable tool in the assessment of the regression and progression of arteriosclerosis. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/140.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Future Directions Tissue Characterization By IVUS, several in vitro and in vivo studies have tried to identify plaque components in coronary artery lesions with visual analysis of the gray scale images or quantitative videodensitometry analysis.[160] [161] [162] These gray scale IVUS images, however, cannot accurately distinguish among plaque components (fibrous tissue, fibrofatty tissue, and various stages of thrombus). 360 Analysis of the unprocessed backscattered radiofrequency ultrasound signal has been conducted, which may convey more specific information relating to the intrinsic architecture of the plaque substance and permit a more reliable means for intravascular plaque characterization.[163] The internal backscatter from plaque, whether assessed by its peak amplitude or frequency, combined with time averaging methods, has been shown to distinguish plaque types.[164] Vulnerable plaque with lipid pool beneath thin fibrous cap, responsible for acute coronary syndromes and myocardial infarction, generally cannot be identified by the current level of image quality.[51] Several investigators have reported the usefulness of frequency or backscatter analysis in detecting vulnerable plaque.[165] [166] Komiyama et al[165] reported on in vitro study in which radiofrequency signal analysis could detect plaques with lipid core with higher sensitivity and specificity compared with gray scale analysis. Ultrasound frequency and backscatter analysis may be useful to detect plaques at risk of spontaneous rupture or complication with percutaneous mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 interventions and also provide information for atherosclerotic plaque and thrombus characterization as well as transplant vasculopathy.[167] [168] Sonotherapy IVUS has been used for therapeutic purposes. Several investigators have reported biomechanical effects of ultrasound for prohibiting migration and adhesion of smooth muscle cells,[169] [170] which can be applied for the prevention of neointimal hyperplasia after coronary intervention. A system for intracoronary sonotherapy treatment (URX, PharmaSonics Inc.) has been developed, and favorable effects on neointimal hyperplasia in vivo have been reported using a porcine stent injury model.[171] This system is composed of ultrasonic transducers, generating a peak intensity of 100 W/cm2 at a center frequency of 700 kHz. At 7 days, smooth muscle cell proliferation assessed by bromodeoxyuridine histology preparation was significantly reduced in the sonotherapy group compared with the sham group (24.1% versus 31.2%; P < .05). The catheters have been further miniaturized for coronary use and investigated (Fig. 16-12) . Post et al[172] found, also in a porcine model, that sonotherapy significantly decreased the intimal hyperplasia after stenting compared with the control group. In this study, sonotherapy was associated with slight increase in mild vessel wall injury, but endothelialization was complete at 180 days. Intracoronary sonotherapy may be a good modality to inhibit restenosis, and it may also offer treatment advantages when compared with intracoronary brachytherapy. The sonotherapy system does not require the use of radioisotopes, thus negating the need for shielding and oncologists' support, thereby facilitating procedural "ease of use." Ultrasound has been reported to enhance drug delivery as well as gene transfection, suggesting that sonotherapy may be augmented further with a pharmacologic approach.[173] [174] [175] Therapeutic catheter-based sonotherapy Figure 16-12 (color plate.) A schematic view of a sonotherapy catheter (URX IST, PharmaSonics Inc.). This catheter is compatible with an 8F guiding catheter and peak intensity of 100 W/cm2 at a center frequency of 1 MHz with 5 minutes dwell time. is currently under clinical investigation as a tool to prevent restenosis. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 Drug-Eluting Stent Because coronary stent use has become widespread for reducing restenosis after intervention, stents have been proposed as means for local drug delivery. Recently, several drugs with antiproliferative properties have been reported to reduce intimal hyperplasia after balloon angioplasty or stent implantation. Rapamycin, an immuno-suppressive agent with antiproliferative properties, has been reported to inhibit intimal thickening after balloon angioplasty in animal study[176] or after stent implantation in clinical study.[177] Paclitaxel, a microtubule-stabilizing compound with potent antitumor activity, has also been reported to prevent intimal hyperplasia after intervention.[178] [179] These drugs showed dramatic neointimal inhibition in long-term and short-term findings, but excessive or too-fast drug elution provoked incomplete intimal coverage over the stent struts. Although the optimal dose and the elution rate of the drug have yet to be determined, |
incomplete apposition (which has been observed in 6% to 30%[180] [181] ) may prevent effective tissue drug delivery and increase the risk of strut thrombosis by retarding endothelialization. IVUS can detect incomplete apposition easily and maximize drug delivery to the arterial wall. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/141.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Summary IVUS provides a new window for viewing the vascular system. It allows the characterization and quantification 361 of the vascular wall as well as its lumen. This advantage has provided a new understanding of the pathology of atherosclerosis and provided insights into the mechanisms and outcomes of percutaneous coronary interventions. Because IVUS, unlike angiography, can detect stent underexpansion, additional PTCA to optimize stent deployment may translate into better long-term clinical results. Moreover, for brachytherapy, IVUS can provide precise information about mechanisms and appropriate dosing for therapy. IVUS is now being investigated to detect vulnerable plaques (tissue characterization), thereby contributing to "lesion-specific" therapy. In view of IVUS as a therapeutic modality, the use of sonotherapy is just beginning. The unique information provided by IVUS promises to lead to continuing advances in the understanding and treatment of vascular disease. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/142.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Section 4 - Valvular Heart Disease 367 Chapter 17 - Quantitation of Valvular Regurgitation Beyond Color Flow Mapping Sheila K. Heinle MD Echocardiography is an essential tool in the diagnosis and management of patients with valvular regurgitation. Cardiac chamber size and function are assessed by two-dimensional echocardiography, and severity of regurgitation is semiquantitatively assessed by Doppler color flow mapping of jet area as mild, moderate, or severe. However, more precise quantitation of valvular regurgitation may be necessary for early detection of hemodynamically significant valvular regurgitation before development of left ventricular dysfunction.[1] [2] Furthermore, since valve repair is associated with low mortality rates, some investigators now suggest that minimally symptomatic patients in whom significant valvular regurgitation is identified be considered as candidates for valve repair procedures.[3] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Limitations of Doppler Color Flow Mapping Doppler color flow mapping provides real time visualization of regurgitant flow signals. Although Doppler color flow images are derived from autocorrelation techniques that provide mathematical estimates of mean velocities along each scan line, this technique is most commonly applied qualitatively to assess the presence and spatial distribution of the flow disturbance due to valvular regurgitation. Numerous studies have demonstrated concordance in results of color flow mapping and other methods for evaluating regurgitant severity of aortic or mitral regurgitation. For mitral regurgitation, initial studies compared depth of jet penetration into the left atrium[4] 368 and maximal jet area with angiographic severity. Improved correlation was observed when mitral regurgitant jet area was corrected for left atrial area.[5] In patients with aortic insufficiency, measurement of the aortic regurgitant jet height relative to the left ventricular outflow tract height was a better predictor of angiographic grade than the maximal length and area of the regurgitant jet.[6] Criteria based on regurgitant jet size also have been proposed to assess the severity of tricuspid and pulmonic regurgitation.[7] Although maximal jet area correlates well with the semiquantitative angiographic grade of severity, however, only limited correlation is observed with quantitative measures of regurgitant volume (r = 0.55) and fraction (r = 0.62).[8] In addition, maximal jet area is not predictive of hemodynamic abnormalities such as an elevated pulmonary wedge pressure or reduced forward stroke volume. This lack of correlation is related to several factors, including jet geometry, physiologic variability, and instrument settings.[9] In any image plane, regurgitant jet area depends on the geometry and mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 direction of the jet.[10] Doppler color flow mapping of free regurgitant jets that are unbounded by surrounding structures may lead to overestimation of severity due to entrainment of adjacent fluid by the high-velocity jet.[11] In contrast, the area of an eccentric jet is only 40% of the area of a free jet with the same regurgitant fraction.[10] Eccentric jets are influenced by adjacent constraining surfaces,[12] so that area measurements correlate poorly with regurgitant volume.[13] It also is important to note that the color flow map of a regurgitant jet represents the spatial distribution of velocities and is not a direct measure of volume flow rate.[14] Although color Doppler jet area increases with regurgitant volume, this relationship is not linear because it is highly influenced by driving pressure,[15] compliance of the receiving chamber,[16] and the size and shape of the regurgitant orifice.[17] Further, evaluation of regurgitant jet area depends on the echocardiographic approach, transducer frequency, and other instrument parameters. Specific factors influencing regurgitant jet size include ultrasonographic system variability, gain settings, pulse repetition frequency, transducer frequency, and tissue priority algorithm. [18] Thus, estimates of regurgitant severity often are greater when measured by transesophageal compared with transthoracic echocardiography. [9] In addition, measurements of color Doppler jet area are subject to substantial intraobserver[19] and day-to-day[20] variability. A superimposed change in loading conditions or hemodynamics between examinations further confounds evaluation of color Doppler jet area.[21] For example, acute severe mitral regurgitation may be underestimated by color Doppler imaging because of increased heart rate, decreased systemic blood pressure, and a rapid rise in pressure in the noncompliant left atrium.[22] Thus, despite the clinical utility of color Doppler flow mapping for evaluation of patients with known or suspected valvular regurgitation, this qualitative measure of regurgitant severity is not ideal. Efforts to derive more quantitative and clinically applicable measures of regurgitant severity are ongoing. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/145.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Volumetric Methods Regurgitant fraction can be calculated from the difference between flow rates determined at two separate intracardiac sites using the continuity equation. Total stroke volume is measured as antegrade flow across the regurgitant valve, whereas net forward stroke volume is measured as antegrade flow across a competent valve.[23] The combined use of two- dimensional echocardiography with conventional pulsed-wave Doppler and continuous wave Doppler allows the estimate of volumetric flow across any of the cardiac valves using the following equation: SV = CSA × TVI (1) where SV is stroke volume, CSA is cross-sectional area of the annulus, and TVI is time velocity integral measured as the area under the Doppler spectral velocity curve. Volumetric quantification of intracardiac flow using the continuity equation is based on the following assumptions: a constant cross-sectional valve area, a flat velocity profile, and a circular flow area. Although mitral and tricuspid annuli are nearly circular, optimal accuracy requires consideration of their elliptical shape by modifying the equation for stroke volume using an elliptical cross-sectional area: CSA = π(D1 ·D2 )/4 (2) where D and D are annular diameters measured in two orthogonal views. 1 2 [24] When the cross-sectional area is presumed to be circular, for example, in the left ventricular outflow tract, cross-sectional area is calculated as CSA = πr2 (3) mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 To quantitate mitral regurgitant volume (RV), net forward stroke volume (SV) is measured from the aortic annulus and subtracted from the total stroke volume measured at the mitral annulus, as follows: RV = Total SV − Forward SV (4) Total stroke volume can also be obtained by subtracting end-systolic from end-diastolic volume obtained by two-dimensional echocardiography.[25] Regurgitant fraction (RF) is then calculated from the ratio of regurgitant volume to total stroke volume: RF = RV/Total SV (5) Good correlation has been observed between volumetric and angiographic regurgitant fractions for isolated mitral or aortic regurgitation (r = 0.91).[26] Although correlation with angiographic grading is poor, the limitations of using qualitative angiography as a reference standard for assessing the severity of valvular regurgitation have been well documented. [27] The volumetric method is usually applied to left-sided regurgitant lesions, although it is theoretically possible to substitute flow across a competent pulmonary or tricuspid valve for aortic flow in patients with concomitant aortic insufficiency. 369 Figure 17-1 Two-dimensional echocardiogram (left) and Doppler spectral velocity envelope (right) demonstrating proper positioning of the Doppler sample volume at the mitral annulus for accurate time-velocity integral measurement to calculate stroke volume. (Courtesy of Brad Roberts, RDCS.) Although the volumetric method has been validated in a large series of patients with valvular regurgitation, overestimation of mitral regurgitation is a potential limitation of this approach.[28] Improper positioning of the Doppler sample volume may result in overestimation of the mitral time- velocity integral because of the increase in velocity from the annulus to the tip of the leaflets.[29] However, this potential limitation can be avoided by meticulous positioning of the sample volume at the level of the mitral annulus so that diameter and flow velocity are measured at the same anatomic site (Fig. 17-1) . [28] Aortic flow may be underestimated if there is a nonparallel intercept angle between the ultrasound beam and the direction mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 of blood flow.[30] Again, this limitation is minimized by careful patient positioning and use of multiple ultrasonographic windows with meticulous adjustment of transducer position to obtain the highest velocity signal. Perhaps the most common source of error in Doppler flow calculations is inaccuracy in the measurement of mitral or aortic annulus cross-sectional area. [31] Because the two-dimensional echocardiographic diameters are squared in order to calculate an elliptical or circular cross-sectional area, small errors in diameter measurement result in large errors in cross- sectional area. Moreover, the assumption of a constant maximal flow area using the pulsed Doppler volumetric method does not acknowledge the temporal changes in flow area during the cardiac cycle and contributes to overestimation of regurgitant flow. Errors in diameter measurement can be minimized by using an ultrasonographic window that provides a perpendicular intercept angle between the anatomic structure and the ultrasound beam, by careful attention to gain and other instrument settings, and by averaging several beats. When combined, these potential sources of error may contribute to reported regurgitant fractions up to 20% in normal subjects.[26] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/146.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 6 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Indirect Markers of Regurgitation Severity Although indirect markers of regurgitation severity do |
not provide quantitative estimates of regurgitant volume, they provide valuable information regarding the hemodynamic impact of the regurgitant lesion on atrial pressure and left ventricular end-diastolic pressure.[32] Mitral Regurgitation Pulmonary Venous Patterns Pulsed Doppler sampling of the pulmonary vein results in a spectral envelope that consists of three distinct waves. A systolic antegrade wave followed by a smaller diastolic antegrade wave represent pulmonary venous inflow during ventricular systole and diastole, respectively. Following the electrocardiographic P wave, there is a small negative wave that represents atrial reversal during atrial contraction. With increasing mitral regurgitation severity, the systolic phase of pulmonary inflow progressively decreases, with eventual reversal of flow in systole when severe mitral regurgitation is present (Fig. 17-2) . [33] Several studies have examined the value of reversal of systolic pulmonary venous flow as a marker of severe mitral regurgitation (Fig. 17-3) .[33] [34] There is an inverse correlation between the ratio of systolic to diastolic pulmonary venous flow velocity time integrals and the mitral regurgitant fraction in patients with normal left ventricular systolic function (ejection fraction > 45%).[35] In patients with left ventricular systolic dysfunction, a normal pulmonary venous systolic flow pattern indicates a small (<0.3 cm2 ) regurgitant orifice area.[34] Conversely, pulmonary vein systolic flow reversal predicts a large (>0.3 cm2 ) regurgitant orifice, consistent with severe regurgitation. However, blunted systolic flow is much less predictive, as it may be associated with a broad spectrum of regurgitant severity, ranging from trivial to severe regurgitation (Fig. 17-4) . mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 6 To optimize the sensitivity of pulmonary venous systolic flow reversal as an indirect marker of mitral regurgitation severity, it is important to sample both right and left pulmonary veins, since jet direction can influence the pulmonary venous flow pattern.[36] Discordant flow patterns have been observed in the right and left pulmonary veins, with systolic flow reversal demonstrated more 370 Figure 17-2 Summary of the relationship between left atrial pressure hemodynamic and pulmonary venous flow Doppler profiles in 2+, 3+, and 4+ mitral regurgitation (MR). As MR increases, the v wave and v-y descent increase, and the a wave and x-y descent decrease, which is coincident with decreased pulmonary venous systolic (S) flow, increased diastolic (D) flow, and reversed systolic flow (RSF) in 4+ MR. AR, atrial reversed flow velocity. (From Klein AL, Stewart WJ, Bartlett J, et al: J Am Coll Cardiol 1992;20:1345–1352. Reprinted with permission from the American College of Cardiology.) Figure 17-3 Reversal of systolic flow by pulsed Doppler sampling of the pulmonary vein during transesophageal echocardiography in a patient with severe mitral regurgitation. 371 Figure 17-4 Regurgitant orifice area and regurgitant stroke volume in three different pulmonary venous flow patterns. Open triangles, normal flow; open circles, blunted flow; solid circles, reversed patterns. Dashed lines indicate regurgitant orifice area of 0.3 cm2 . (From Pu M, Griffin BP, Vandervoort PM, et al: J Am Soc Echocardiogr 1999;12:736–743.) often in the right pulmonary vein.[33] [34] Other limitations of this indirect method include the influence of other factors on pulmonary venous flow pattern, in addition to left ventricular systolic and diastolic function, including atrial fibrillation, mitral stenosis, ventricular loading conditions, left atrial compliance, and left atrial contractile function.[37] [38] In an effort to account for these other factors, it has been proposed that the systolic component of the pulmonary inflow pattern be expressed as a percentage of mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 6 the total (systolic and diastolic) velocity time integral and then corrected for left atrial filling volume measured from single-plane transthoracic echocardiography. This approach correlated well with Doppler-derived regurgitant fraction[39] however, it remains unclear whether this combined method can be used reliably in patients with acute severe mitral regurgitation, patients with eccentric jets, or patients in atrial fibrillation. Peak E Wave Velocity Early diastolic mitral inflow is represented by the E wave velocity, which is directly related to the pressure gradient between the left atrium and the left ventricle at the time of mitral valve opening. The added regurgitant volume in mitral regurgitation increases the initial atrial-to-ventricular pressure gradient, thus increasing the peak E wave velocity.[40] A recent retrospective study showed a modest positive predictive value (75%) for an E velocity greater than 1.2 m per second for identifying patients with severe chronic mitral regurgitation. This relationship was independent of other variables such as heart rate, age, and restrictive left ventricular diastolic function.[41] However, increased mitral inflow velocity has also been observed in patients with severe aortic regurgitation.[42] Moreover, the predictive value of this marker has not been tested in patients with acute mitral regurgitation. Therefore, although peak E wave velocity may be a simple screening method for hemodynamically significant mitral regurgitation, it should be not used in isolation to judge regurgitant severity. Aortic Regurgitation Pressure Half-Time The pressure half-time index represents the time for the peak gradient across the aortic valve in diastole to decay to half of its initial value. Doppler velocity and catheterization pressure half-times have been demonstrated to be linearly related (r = 0.91), with Doppler pressure half- time inversely related to the angiographic grade of aortic regurgitation.[43] Patients with severe aortic regurgitation have a shortened pressure half-time because of the rapid rate of decline in aortic diastolic pressure and rise in left ventricular diastolic pressure, resulting in rapid equalization of aortic and left ventricular pressures (Fig. 17-5) . A Doppler pressure half-time of 400 msec separates mild (1+, 2+) from significant (3+, 4+) aortic regurgitation by angiographic grading with a specificity of 92% and positive predictive value of 90%.[43] Aortic regurgitant severity may be overestimated, however, if the left ventricular end-diastolic pressure is mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 6 elevated because of depressed left ventricular systolic function resulting in a significant overlap in pressure half-times between patients with mild, moderate, and severe regurgitation.[43] In addition, other factors such as stroke volume, aortic and left ventricular compliance, and systemic vascular resistance influence the pressure half-time.[44] Pressure half-time is most useful as an additional method to classify and monitor progression of chronic aortic regurgitation when color flow Doppler methods are discrepant. [45] Deceleration Slope With increased severity of aortic regurgitation, the diastolic aortic pressure falls rapidly while left ventricular filling pressure rises rapidly, resulting in a steeper deceleration slope on a continuous wave Doppler echocardiogram. Although deceleration slope and pressure half-time both are measured from the continuous wave Doppler curve, deceleration slope is not dependent on the initial pressure gradient. Deceleration slope has been reported to be a better index of regurgitant severity than pressure half- time, demonstrating a close correlation with angiographic grade of regurgitation even in patients with associated aortic stenosis, mitral valve disease, or low cardiac output.[46] A deceleration slope greater than 3 m/sec2 suggests severe aortic regurgitation. Unfortunately, a deceleration slope less than 3 m/sec2 can be seen with mild, moderate, or severe regurgitation. [46] [47] Left ventricular compliance influences the reliability of deceleration slope as an index of aortic regurgitant severity, since a steep slope can be observed in a patient with only mild aortic 372 Figure 17-5 (color plate.) Color Doppler image (A) and continuous wave Doppler image (B) demonstrate severe aortic regurgitation with a pressure half-time of 49 msec and deceleration slope of 18 m per second2 resulting from rapid equalization of pressure between the aorta and left ventricle. (Courtesy of Brad Roberts, RDCS.) regurgitation but a stiff left ventricle. As with pressure half-time, deceleration slope is influenced by systemic vascular resistance.[44] Thus, pressure half-time and deceleration slope are unreliable methods to assess changes in aortic regurgitation severity in response to vasodilators. However, these approaches may be helpful in assessing whether aortic regurgitation is chronic and well-compensated (flat slope), as compared mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 6 with the steep slope in patients with acute, decompensated regurgitation. Diastolic Flow Reversal Severe aortic regurgitation is associated with diastolic reversal of flow in the aorta (Fig. 17-6) [48] as well as Figure 17-6 Diastolic flow reversal demonstrated by pulsed Doppler interrogation of the descending aorta in the same patient shown in Figure 17-5 with severe aortic regurgitation. (Courtesy of Brad Roberts, RDCS.) systolic augmentation of flow within the central aorta.[49] Pandiastolic reversal of flow in the superior abdominal aorta using pulsed Doppler echocardiography from a subcostal window is highly specific and sensitive for predicting severe aortic regurgitation.[50] It is possible to calculate aortic regurgitant fraction from the ratio of reversed to forward flow in the aortic arch using M-mode measurements to account for the systolic and diastolic changes in aortic diameter.[49] However, diastolic flow reversal in the aorta is directly related to aortic compliance, as well as to regurgitant volume. Abnormal diastolic flow patterns can be observed in subjects with abnormal compliance in the proximal aorta or in patients with left to right shunt from the aorta 373 (such as a patent ductus arteriosus).[49] Compared with the ascending aorta, pulsed Doppler interrogation of the descending aorta has been reported to more reliably reflect severity of aortic regurgitation, owing, in part, to the more uniform velocity profiles more distally in the aorta.[51] Other Indirect Markers High left ventricular diastolic pressure associated with severe acute aortic regurgitation results in echocardiographic findings such as premature closure of the mitral valve or diastolic mitral regurgitation.[52] However, these markers of severe aortic regurgitation are poorly sensitive, being present in fewer than half of the patients with this condition.[42] [52] Increased E/A ratio was reported to be more sensitive for severe symptomatic aortic regurgitation, with greater sensitivity than pressure half-time, M-mode, or color flow mapping for predicting regurgitant severity. [42] [52] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 6 Tricuspid Regurgitation A reliable marker of severe tricuspid regurgitation is systolic reversal of flow in the hepatic veins and venae cavae (Fig. 17-7) .[53] Another index of severe tricuspid regurgitation is an associated annular diameter greater than 34 mm or greater than 21 mm/m.[28] Intracardiac Pressure Gradients Continuous wave Doppler echocardiography can be utilized to measure instantaneous and mean pressure gradients to assess the hemodynamic effects of regurgitant valvular lesions by using the modified Bernoulli equation. Left atrial pressure can be derived from the mitral regurgitant Doppler signal by subtracting the peak gradient from systolic blood pressure.[54] Similarly, left ventricular end-diastolic pressure can be calculated from the diastolic blood pressure and the aortic regurgitant end- diastolic pressure gradient.[47] [55] However, Doppler consistently overestimates left ventricular end-diastolic pressure because of suboptimal angulation of the interrogating ultrasound beam, resulting in underestimation of the peak velocity and gradient. [47] Therefore, the main limitation of this technique is suboptimal angulation and the inability to obtain a complete high-quality Doppler spectral envelope. When there is a rapid rise in left atrial pressure (V wave), the mitral regurgitant jet may appear asymmetric and cut off in late systole (Fig. 17-8) . Although right ventricular systolic pressure can be estimated from continuous wave Doppler interrogation of flow across a regurgitant tricuspid valve, [54] it is of little value in assessing the severity of tricuspid regurgitation, since increased regurgitant severity results in increased right atrial pressure and decreased peak tricuspid velocity and pressure gradient. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/147.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 8 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Quantitative Analysis of the Proximal Flow Convergence Region Principle of Conservation of Mass Accelerating laminar flow patterns have been observed proximal to stenotic, regurgitant, and shunt orifices by Doppler color flow mapping by transthoracic and transesophageal echocardiography.[56] [57] [58] [59] [60] Regurgitant flow rate can be calculated from these laminar flow patterns based on the conservation of mass, which assumes that fluid converges uniformly and radially toward a restrictive orifice, forming a series of concentric isovelocity layers. These isovelocity surfaces are hemispheric for orifices that are small relative to the region of acceleration.[61] Compared to the turbulent downstream jet, this more predictable pattern of flow in the proximal flow convergence |
region makes quantitation of regurgitant severity possible. By Doppler color flow mapping, the radius (r) of the isovelocity surface is measured as the distance from the orifice to the point of color aliasing (Fig. 17-9) . Instantaneous flow rate can be calculated as the product of the aliasing velocity V at any of these hemispheric contours A times the surface area (2πr2 ) of that shell: Peak flow rate = VA (2πr2 ) (6) This calculation is based on the conservation of mass, which assumes that the accelerating flow through each isovelocity surface equals flow through the regurgitant orifice, since all flow through the isovelocity surface must pass through the orifice.[57] It is also assumed that the isovelocity hemispheric shells in the proximal flow convergence region demonstrate increasing velocity and decreasing surface area as the regurgitant orifice is approached. Each shell is associated with a particular velocity relative to its surface area. In theory, the proximal isovelocity surface area (PISA) derived from this zone of accelerating laminar flow is less dependent on mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 8 instrument[62] and hemodynamic factors that influence the spatial extent of the regurgitant jet in the receiving chamber. Furthermore, unlike the volumetric method, the PISA method has the practical advantage of being independent of other associated regurgitant lesions. Initial in vitro and animal studies have demonstrated the validity of the hemispheric assumption for proximal isovelocity surfaces of small planar orifices relative to the acceleration zone.[57] [59] [63] There have been several clinical studies in patients with mitral or tricuspid regurgitation validating the PISA method using two-dimensional and quantitative Doppler techniques[64] [65] or color Doppler flow mapping.[66] The cause of mitral regurgitation did not affect the correlation of proximal flow acceleration estimates with angiography and quantitative Doppler calculations.[67] The PISA method was less useful in patients with aortic regurgitation in whom the Doppler beam angle exceeded 30 degrees.[66] By multiplane transesophageal echocardiography, comparison of flow rate calculations from the proximal convergence zone with angiographic grades of mitral regurgitation revealed that the proximal flow convergence method better distinguished severe from mild regurgitation than color Doppler area 374 Figure 17-7 (color plate.) Systolic flow reversal in the hepatic veins demonstrated by M-mode (A) and pulsed Doppler images (B) in a patient with severe tricuspid regurgitation. (Courtesy of Brad Roberts, RDCS.) 375 Figure 17-8 Continuous wave Doppler with V wave cut-off sign in severe mitral regurgitation (A) with simultaneous hemodynamic tracings (B) demonstrating the pressure relationship that causes the alteration in the deceleration slope of the time-velocity signal (arrows). Note the dark signal intensity of the Doppler signal. In the same patient, increased E wave velocity in A is additional evidence for severe mitral regurgitation. (Courtesy of Rick Nishimura, MD.) and ratio of systolic to diastolic pulmonary venous flow velocities.[68] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 8 Technical Considerations The accuracy of the proximal flow convergence method is highly dependent on precise measurement of the PISA Figure 17-9 (color plate.) Color Doppler image of a patient with severe tricuspid regurgitation illustrating the proximal flow convergence zone with the hemispheric blue-to-yellow aliasing contour (blue-yellow interface or Nyquist limit) on the ventricular side of the tricuspid leaflets. (Courtesy of Brad Roberts, RDCS.) radius, which requires high-resolution imaging and zoom magnification.[63] Furthermore, the proximal flow convergence region is not optimally visualized in all patients with regurgitant lesions, particularly in those with mild regurgitation. [66] [67] , [69] [70] Regurgitant Flow Rate and Aliasing Velocity Adequate visualization of proximal flow acceleration thus depends on the severity of regurgitation and the aliasing velocity. Patients with very mild mitral regurgitation (regurgitant flow rate less than 20 m per second or regurgitant stroke volume less than 4.5 mL) do not have a visible proximal acceleration zone at the typical Nyquist velocity (VN ) of 49 to 58 cm per second.[67] Because flow rate is underestimated unless the Nyquist velocity is much less than the orifice velocity, the hemispheric assumption for calculating regurgitant flow rate cannot be used with larger Nyquist velocities.[61] In in vitro models, the measured radius is always higher at lower aliasing velocities for a given flow rate (Fig. 17-10) . [69] Thus, the hemispheric model is most accurate with larger volume flow rates or with lower aliasing velocities. To improve accuracy, the aliasing velocity can be optimized to better define the hemispheric contour. [71] [72] Regurgitant flow rate is systematically overestimated furthest from the orifice and underestimated closest to the orifice because of progressive flattening of the flow convergence region (Fig. 17-11) . Therefore, the hemielliptical model may more accurately reflect flow rates closer to the orifice.[69] In the hemielliptical PISA method, radii from the orifice to the aliasing boundary are measured from long-axis (minor) and short-axis (major) views. This method correlates well with actual volume flow rates under mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 8 376 Figure 17-10 (color plate.) In this patient with severe mitral regurgitation, the radius of the proximal flow convergence zone appears larger at a lower aliasing velocity of 22 cm per second (A) compared with an aliasing velocity of 33 cm per second (B). (Courtesy of Brad Roberts, RDCS.) both constant and pulsatile flow conditions. When a flattened proximal convergence zone exists near the orifice, with a major-to-minor axis ratio greater than 2.0, the hemispheric model underestimates the actual volume flow rate by more than 50%. [69] Based on in vitro models, correction factors have been proposed to adjust for errors in flow rates calculated by the PISA method. [61] Orifice Size and Shape The initial assumption that fluid converges toward an orifice in concentric hemispheric shells applies to an infinitesimally small orifice but cannot be applied to the finite orifice size of regurgitant orifices. In vitro models have demonstrated that the velocity distribution is independent of orifice size if measured at least two orifice diameters from the orifice, in situations in which the hemispheric assumption is valid.[61] In the clinical setting, a discrete Figure 17-11 Diagram of flow converging toward a finite orifice (bottom) showing the streamlines (dotted lines) and the consecutive isovelocity contours (solid lines), illustrating progressive contour flattening as the orifice is approached. (From Vandervoort PM, Thoreau DH, Rivera JM, et al: J Am Coll Cardiol 1993;22:535–541. Reprinted with permission from the American College of Cardiology.) circular regurgitant orifice is rarely seen. Moreover, irregular or multiple orifices may make application of the PISA method more difficult. It has been proposed, however, that the PISA method can be consistently applied with irregular or multiple orifices if the measurements are obtained at greater distances (at least two orifice diameters) from the orifice.[59] [63] These studies conclude that measurements obtained far from the regurgitant orifice eliminate the influence of orifice size and shape. Other studies have demonstrated that orifice shape does not influence the accuracy of flow rate calculations if the aliasing velocity is small (<5%) relative to the orifice velocity.[61] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 8 Surrounding Geometry In the setting of nonplanar surrounding geometry, the isovelocity shells cannot develop as full hemispheres and are effectively truncated as the orifice is approached.[56] [73] Distortion of the flow field is most pronounced when the constraining wall is positioned close to the regurgitant orifice, resulting in overestimation of the calculated flow rates. This situation can be observed with regurgitation caused by a posterior mitral leaflet flail (Fig. 17-12) . [74] Therefore, in the setting of mitral valve prolapse or flail, the following correction factor adjusts the calculated flow rate for the proximal flow convergence angle (α) (Fig. 17-13) : 2π(α/180) (7) Effective Regurgitant Orifice Area Experimental[75] [76] and clinical studies[77] have indicated that the effective regurgitant orifice area (EROA) provides unique quantitative information about the severity of regurgitation and is less influenced by hemodynamic variables than regurgitant volume and fraction.[75] [78] EROA 377 Figure 17-12 (color plate.) Posterior mitral leaflet flail (left) is demonstrated on transesophageal echocardiography with proximal flow convergence and a severe eccentric jet of regurgitation by color Doppler imaging (right) (see also color plate). was initially calculated by the PISA method in an in vitro model using the following equation: EROA = (2πr2 V )/V = Q/V (8) A O O where VA is the velocity at a distance r from the orifice and VO is the orifice velocity obtained by continuous wave Doppler.[79] Thus, in vitro and animal models demonstrated that EROA calculated by the PISA method demonstrated good correlation to actual EROA and to regurgitant stroke volume and fraction (Fig. 17-14) .[79] [80] Alternatively, if mitral regurgitant velocity is assumed to be about 5 m per second and the Nyquist limit is set to 40 cm per second, this equation can be simplified to mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 8 EROA = r2 /2 (9) By comparison to angiographic grades of mitral regurgitation, grade I was associated with an EROA of less Figure 17-13 (color plate.) Flail posterior leaflet by transesophageal echocardiography demonstrating proximal flow convergence with wall constraint because of the proximity of the posterior wall. To adjust for the predictable overestimation caused by this geometric distortion, regurgitant flow rate and orifice area are adjusted by α/180. LA, left atrium; LV, left ventricle. (From Breburda CS, Griffin BP, Pu M, et al: J Am Coll Cardiol 1998;32:432–437. Reprinted with permission from the American College of Cardiology.) than 10 mm2 and grade III with an EROA of greater than 25 mm2 . [79] In subsequent clinical studies, EROA measured by the PISA method correlated well with EROA measured by quantitative Doppler and two- dimensional echocardiographic methods for tricuspid,[81] mitral,[82] and aortic regurgitation.[83] Limitations of EROA calculation by the PISA method include underestimation of aortic EROA in patients with an obtuse (>220-degree) proximal flow convergence angle [83] and overestimation in patients with mitral valve prolapse.[82] Overestimation of EROA in patients with mitral valve prolapse can be explained in part by dynamic changes in the effective orifice area.[84] [85] The PISA method provides instantaneous measurement of regurgitant flow and EROA and thus may not accurately reflect the overall severity of mitral regurgitation over the entire cardiac Figure 17-14 Line plot showing the correlation between effective regurgitant orifice area calculated by the proximal flow convergence method (y-axis) and the Doppler echocardiographic method (x-axis) in the clinical setting of mitral regurgitation. (From Vandervoort PM, Rivera JM, Mele D, et al: Circulation 1993;88:1150–1156.) 378 Figure 17-15 Typical examples of the types of dynamic changes in the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 8 regurgitant orifice area obtained by the electromagnetically determined flow method (EM). The regurgitant orifice size usually increases to maximal size in early to mid-systole (arrow) and decreases in late systole. (From Shiota T, Jones M, Teien DE, et al: J Am Coll Cardiol 1995;26:528–536. Reprinted with permission from the American College of Cardiology.) cycle. Furthermore, the dynamic changes in EROA do not necessarily parallel the changes in regurgitant volume.[84] In late systole, despite continued increase in EROA, there is a decrease in the ventriculoatrial gradient and regurgitant velocity.[53] Experimental and clinical data further support the observation that the mitral regurgitant orifice changes dynamically during systole (Fig. 17-15) .[80] [86] Furthermore, the temporal variation in mitral regurgitant orifice area during systole varies according to the underlying cause.[86] Thus the PISA method of calculating EROA has the potential advantage of identifying the dynamic changes in regurgitant orifice area during the cardiac cycle. Changes in EROA are measured sequentially during the cardiac cycle by color M-mode echocardiography from the zenith of the isovelocity hemisphere.[80] [85] [86] The clinical implications of these data are that the EROA is not completely independent of hemodynamic variables and its changes may explain the beneficial effects of vasodilator therapy on functional mitral regurgitation.[77] In contrast, the existence of dynamic changes in aortic regurgitant orifice area is controversial.[87] [88] Dynamic changes have also been observed in the tricuspid regurgitant orifice area using the proximal flow convergence method.[89] Regurgitant Volume Although the calculation of regurgitant flow rate by the PISA method is relatively simple, requiring only the measurement of the isovelocity radius and aliasing velocity in a single view, it estimates peak, but not mean, flow rate. The measurement of regurgitant volume (RV) may be more accurate and clinically useful because the inclusion of the time velocity integral (TVI) by continuous wave |
Doppler may better reflect regurgitant jet dynamics during the cardiac cycle[64] [90] [91] RV = EROA × TVI (10) When regurgitant volume and flow rate by the PISA method are compared with angiographic grading of mitral regurgitation, PISA-derived regurgitant volume is better than flow rate at distinguishing 4+ mitral regurgitation from the other regurgitant grades.[71] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 8 In addition to the technical considerations that affect the validity of the hemispheric assumption of the PISA method, there are a number of limitations of this method for estimating regurgitant volume and flow rate. Since the PISA method relies on color Doppler to identify the region of proximal flow convergence, it is limited by technical factors that influence the accuracy of color Doppler flow mapping. Of these factors, the angle between the Doppler beam and direction of blood flow is most critical. The angle of the central PISA radius and the ultrasound beam must approach zero for optimal accuracy.[66] Other technical factors to be optimized include wall filter settings, interrogation depth, pulse-repetition frequency, and spatial beam expansion.[92] Furthermore, translational motion of the valve annulus affects the apparent PISA velocity, with overestimation with movement in the same direction[93] and underestimation with movement away from the PISA velocity shift.[94] Moreover, when the entire flow crossing the aliasing boundary does not pass through the restrictive orifice, as in ventricular septal defects,[93] the conservation of mass principle is not strictly applicable. Although attempts have been made to standardize the PISA method to calculate regurgitant flow, the optimal instrument settings for aliasing velocity and its corresponding radius remain unclear.[72] [91] [95] Furthermore, the accuracy of the PISA method is highly dependent on precise measurement of the radius from the orifice. Theoretically, the higher frequency imaging of transesophageal echocardiography provides improved spatial resolution and lower color aliasing velocity, which should improve the accuracy of the radius measurement.[96] Although attempts have been made to better define the radius by high-resolution imaging with zoom magnification, the exact position of the regurgitant orifice may still remain elusive.[70] [97] Errors in measurement of the PISA radius could result in significant errors in the estimation of volume flow. Vandervoort et al[97] propose an automated algorithm to locate the regurgitant orifice from a computer-simulated flow field, but this approach is not widely available. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/148.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Vena Contracta Width Experimental and Clinical Validation The vena contracta width is defined as the narrowest diameter of regurgitant flow immediately downstream from the flow convergence region (Fig. 17-16) . Although, like proximal jet size, it is relatively unaffected by flow rate and driving pressure,[21] [98] vena contracta width is not identical to proximal jet size, since vena contracta width requires measurement of the diameter at the narrowest portion of regurgitant flow between the flow convergence region and the downstream turbulent jet.[99] Furthermore, the vena contracta width more directly reflects 379 Figure 17-16 (color plate.) Transesophageal imaging in the long-axis view demonstrates the vena contracta width as the narrowest extent of regurgitant flow immediately downstream from the flow convergence region in this patient with severe mitral regurgitation. changes in the size of the regurgitant orifice.[100] Unlike proximal jet width, vena contracta width remains accurate in the presence of eccentric jets (Fig. 17-17) . [99] [101] [102] [103] [104] [105] The feasibility of measuring the vena contracta is 92% to 97% in patients with mitral regurgitation with minimal inter-observer variability.[100] [104] [106] Multiplane transesophageal echocardiography was shown to be more accurate than single plane imaging.[106] [107] Thus, the vena contracta method has been proposed to be a simple yet accurate method of assessing mitral regurgitant severity intraoperatively.[107] [108] Furthermore, vena contracta width is more predictive of the severity of mitral regurgitation than color Doppler jet area, left atrial size, and pulmonary venous flow.[104] Since mitral regurgitation worsens in the anteroposterior mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 Figure 17-17 Linear regression plot showing good correlation between vena contracta width in the parasternal long-axis view and regurgitant volume (left) and regurgitant orifice area (right). Solid circles represent eccentric mitral regurgitation jets; open circles central jets. (From Hall SA, Brickner ME, Willett DL, et al: Circulation 1997;95:636–642.) direction of the mitral valve orifice, accurate measurement of the vena contracta is obtained from long-axis views by transthoracic and transesophageal echocardiography. [100] [104] , [106] For mitral regurgitation, a vena contracta width of 5 mm or greater identifies severe mitral regurgitation, and a vena contracta width of 3 mm or less identifies mild mitral regurgitation.[104] In clinical and animal studies of aortic regurgitation, the vena contracta width correlates well with quantitative Doppler and electromagnetic flowmeter measurements, [103] [105] so that a vena contracta width of 6 mm or greater predicts severe aortic regurgitation, whereas mild aortic regurgitation is identified by vena contracta width of less than 5 mm.[105] EROA is estimated from the vena contracta width (VCW) by the following equation: EROA = π(VCW/2)2 (11) The estimated EROA and regurgitant volume flow correlated well with reference measurements by electromagnetic flowmeter (Fig. 17-18) .[103] A vena contracta width of 6.5 mm or greater predicts severe tricuspid regurgitation and correlates with EROA significantly better than visual estimates of jet area, which are influenced by right atrial pressure.[99] Clinical Considerations Accurate measurement of the vena contracta width is critically dependent on imaging with optimized axial resolution. Imaging views with poor lateral resolution result in artifactual widening of the flow signal and overestimation of regurgitant lesion severity. Precise imaging of the vena contracta requires smaller sector angles, high frame-rates, high resolution, appropriate color and tissue priority, and zoom mode magnification. However, the vena contracta width may be difficult to measure with poor acoustic windows, orifice movement, or rapid divergence of the jet beyond the orifice. Vena contracta width is not a direct measurement of regurgitant orifice area and is actually smaller than the anatomic orifice by a factor 380 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 Figure 17-18 Correlation between peak regurgitant flow rates calculated by color Doppler vena contracta and electromagnetic flow meter methods. (From Ishii M, Jones M, Shiota T, et al: Circulation 1997;96:2009–2015.) of 0.8 (coefficient of contraction). There is considerable overlap of actual regurgitant orifice areas in the intermediate mitral regurgitant vena contracta width range between 3 and 5 mm.[104] Therefore, regurgitant lesions in the intermediate vena contracta range may require additional methods of quantitation to more fully assess regurgitant severity.[109] In addition, the vena contracta width as a single measurement does not reflect dynamic changes in the regurgitant orifice during the cardiac cycle. In the presence of an irregular regurgitant orifice, multiple vena contracta width measurements in more than one plane may be necessary to improve accuracy.[103] [106] [109] , [110] Three-dimensional imaging of the vena contracta area accurately measures mitral regurgitant orifice by transesophageal echocardiography intraoperatively and may become the approach of choice as three-dimensional methods become clinically feasible.[108] The value of vena contracta width in the presence of multiple or diffuse regurgitant jets or atrial fibrillation is not known. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/149.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Conservation of Momentum Theoretical Background Based on experimental studies of fluid dynamics of turbulent jet flow, the velocity distribution of the jet in the receiving chamber is best characterized by its momentum, which combines several factors such as flow rate, driving pressure, orifice velocity, and orifice area.[111] In the absence of a pressure gradient within the receiving chamber because of an adjacent wall or counterflow from another orifice, momentum should remain constant within the turbulent jet.[112] The principle of momentum conservation states that the momentum measured anywhere in the downstream jet is the same as the momentum of the jet at its orifice: Momentum = Momentum (12) orifice jet At the orifice, momentum is calculated by the product of jet velocity (Vo ) and flow rate (Q): Momentum = V Q (13) orifice o Thus, the regurgitant orifice flow rate (Q) can be calculated from jet momentum (M) measured anywhere along the extent of the jet, divided by orifice velocity (Vo ), measured by continuous wave Doppler[113] Q = M/V (14) o Methods for Quantitation of Momentum In an in vitro model, when jets are formed through 0.005 to 0.5 cm2 orifices at a driving pressure of 1 to 81 mm Hg, the velocity distribution mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 downstream conforms to a gaussian (bell-shaped) profile with the centerline velocity decaying inversely with distance from the orifice.[113] Jet momentum (M) flux can be calculated across the transverse plane of the jet by integrating flow velocity (v) across the area (A) of the jet in that plane: M = ∫A v2 dA (15) For an axisymmetric jet (circular cross section), momentum can be calculated from a single velocity profile across the jet: M = 2 π∫ ∞v2 rdr (16) 0 where r is the radial distance from the jet centerline to a point at which each velocity is measured. Thus, orifice flow rate can be accurately calculated by dividing momentum by the orifice velocity using equation 14. Effective regurgitant orifice areas then can be calculated by dividing momentum by the square of the orifice velocity: EROA = M/V 2 (17) o An alternative approach, based on data from an in vitro pulsatile model, is to measure only the centerline velocity (V ), which is inversely c proportional to the distance (x) from the orifice[114] V (x) = 7.8√M/x (18) c Then flow rate (Q) can be calculated by recording a single centerline velocity (V ) at a distance x from the orifice as well as orifice velocity c (V ): o Q = V 2 x2 /60.8V (19) c o The flow convergence centerline velocity/distance methods correlated well with reference methods in small mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 381 clinical[115] and animal[116] studies that quantitated mitral and aortic regurgitation. The proposed benefit of the centerline velocity method over the PISA method is that the use of several data points instead of a single velocity data point improves accuracy.[116] Clinical Practice In spite of experimental validation and proposed theoretical advantages of using jet momentum or centerline velocity methods to quantitate valvular regurgitation, these methods are rarely used in the clinical setting for several reasons. First, since it has been reported that free jets are observed in only 60% to 70% of patients with mitral regurgitation,[10] the critical assumption of a free axisymmetric jet may not apply to a significant number of patients with eccentric jets in whom momentum is not conserved because of jet impingement on an adjacent wall or interference from pulmonary venous counterflow. It has been demonstrated that eccentrically directed jets are significantly underestimated by the momentum quantification method.[117] Moreover, application of the centerline velocity profile method requires accurate resolution of velocities within the turbulent jet, which is difficult because aliasing due to high velocities is often seen with mitral regurgitation. The considerable variation in the instantaneous velocity and position of the jet axis during the cardiac cycle requires data averaging using the simplified centerline velocity equation. Finally, the applicability of these methods is not known with varying size and compliance of the receiving chamber. Thus, these practical considerations limit the routine use of these momentum-based methods of quantification in the clinical setting. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/150.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text |
Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Amplitude-Weighted Mean Velocity Amplitude-weighted mean velocity is a nonvolumetric method for calculating the ratio of flow in shunt and regurgitant lesions based on the theory that the amplitude of the recorded Doppler signal is proportional to the number of erythrocytes contributing to the backscattered signal. This approach assumes a hematocrit within the normal range.[118] The amplitude- weighted mean velocity is calculated as the sum of the individual velocities of the erythrocytes within the continuous wave Doppler spectrum multiplied by their respective signal amplitudes.[118] Therefore, the basis of this approach is that each velocity is weighted according to the strength of its signal. Applying this concept over the cardiac cycle, the flow volume during a given time interval is proportional to the time integral of the average weighted mean velocity. Therefore, regurgitant fraction (RF) can be calculated as follows: where the amplitude-weighted mean flow (AWMF) is measured at the regurgitant valve (regurg. valve) and at a competent reference valve (ref. valve). [119] The advantages of this method are that measurement of valvular surface areas is not necessary and its accuracy is not impaired in the presence of mitral valve prolapse. Regurgitant fraction calculated by the amplitude- weighted mean velocity method has been shown to correlate with ventriculographic[118] [120] and quantitative Doppler and two-dimensional echocardiographic findings.[119] There are technical considerations that limit the amplitude-weighted mean velocity method for calculation of regurgitant severity, however. These include the requirements that the continuous wave Doppler beam be of adequate width to include the entire area of the regurgitant signal (for example, the entire mitral annulus). In addition, the beam must be directed mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 properly to avoid inclusion of adjacent flows, and the transducer must be maintained in the same position throughout the recording period to avoid translational motion from one valve to another. Furthermore, determination of the amplitude-weighted mean velocity varies with instrument gain settings and the effect of depth on signal strength. Thus, the ratio of amplitude-weighted mean velocity from the mitral valves to that from the aortic valves may not yield a value of 1.0, even in the absence of valvular regurgitation.[119] In addition to requiring a normal hematocrit, this method is applicable only in the setting of isolated regurgitant lesions, since separation of erythrocytes from blood plasma may falsely elevate the signal amplitude recorded from stenotic lesions.[118] Because the amplitude-weighted mean velocity is dimensionless, its measurement does not represent a physiologic variable and does not allow calculation of regurgitant volume or regurgitant orifice area. Thus, amplitude-weighted mean velocity may best be used as an adjunctive tool to quantitate valvular regurgitation. Finally, the requirement of special software limits the use of this approach in the clinical setting. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/151.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Three-Dimensional Echocardiography Three-dimensional echocardiography is an evolving technique that has been applied for the assessment of intracardiac anatomy,[121] [122] for quantification of intracardiac volumes, [123] and to better characterize mitral valve morphology by multiplane transesophageal echocardiography.[124] Initial three-dimensional reconstruction of color Doppler flow mapping for shunts and valvular regurgitant jets could only be visualized in gray scale and did not include quantitative information or comparison with actual flow rates.[125] [126] However, more recent in vitro studies have demonstrated that regurgitant flow may be accurately quantitated by three-dimensional reconstruction for bioprosthetic valves[127] and for varying native valve orifice shapes and jet morphologies.[110] In a preliminary clinical study, three-dimensional reconstruction has also been shown to accurately quantitate mitral regurgitant orifice area compared with the proximal flow convergence method intraoperatively in patients undergoing mitral valve repair.[108] Although early attempts to obtain color-coded images from three- dimensional reconstruction required manual digitization of Doppler flow signals,[125] more recent studies 382 have demonstrated three-dimensional reconstruction of Doppler signals in original color coding by using direct digital data, which allows separate visualization of intracardiac flow and cardiac structures.[128] [129] These three- dimensional images reveal the complex geometry of eccentric regurgitant jets in patients with mitral valve prolapse and demonstrate how misleading two-dimensional visual assessment or planimetry of regurgitant jets can be ( Fig. 17-19 and Fig. 17-20 ).[128] , [129] Since recent three-dimensional volumes are measured by an automated segmentation and voxel count procedure, they are independent of manual planimetry or subjective mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 estimation. The technical and hemodynamic factors that influence color Doppler flow imaging also influence three-dimensional Doppler images.[129] However, the main limitation of three-dimensional echocardiography is the need for stable positioning of the transducer during image acquisition or a method to continuously track transducer position relative to cardiac structures. Another limitation is that three-dimensional reconstruction is time consuming, and the presence of irregular heart rhythms such as atrial fibrillation can significantly prolong the process. Furthermore, the time- related changes of three-dimensional jet Figure 17-19 (color plate.) A, Transesophageal color Doppler images in a patient with a mitral regurgitant jet recorded at different rotational angles (0 and 90 degrees). B, Three-dimensional reconstruction of the central regurgitant jet in a patient with atrioventricular septal defect. (From De Simone R, Glombitza G, Vahl CF, et al: Eur Heart J 1999;20:619–627.) areas and volumes have not yet been characterized. Some of these limitations will be overcome in the future with the advent of real-time three-dimensional echocardiography. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/152.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 5 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Clinical Implications The quantitation of valvular regurgitation is important, not only for the early detection of hemodynamically significant lesions but also for monitoring of therapeutic success. It has been suggested that not all patients respond favorably to vasodilator therapy, and quantitative methods can thus assist in differentiating patients by their response to therapeutic interventions.[130] [131] [132] However, the quantitative assessment of valvular regurgitation is a far more complex issue than the measurement of such variables as regurgitant volume, regurgitant fraction, and regurgitant orifice area. In addition to the anatomy of the regurgitant lesion, its hemodynamic impact should also be taken into account, since symptoms are not necessarily related to regurgitant severity.[32] [133] A semiquantitative index has been proposed that incorporates variables reflecting 383 Figure 17-20 (color plate.) A, Transesophageal color Doppler images show a wall-impinging mitral regurgitant jet at different angles (0 and 90 degrees). None of these conventional views is able to visualize the regurgitant jet entirely. B, Three-dimensional Doppler reconstructions show that the regurgitant jet resembles a spoon. The lower panel shows the convex face of this spoon jet. (From De Simone R, Glombitza G, Vahl CF, et al: Eur Heart J 1999;20:619–627.) 384 TABLE 17-1 -- Calculation of the Mitral Regurgitant Index Characteristic Score Description Jet penetration 0 No jet mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 5 1 Central jet that does not impinge on lateral wall in any view 2 Eccentric jet that extends to the pulmonary vein 3 Eccentric jet that encircles the atrium PISA 0 No PISA visualized 1 PISA ≤0.5 cm radius 2 PISA 0.5–1.0 cm 3 PISA ≥1.0 cm CW jet 0 No jet detected 1 Incomplete jet envelope 2 Complete envelope, jet density 20%–50% of mitral inflow 3 Complete envelope, jet density 50%–70% of mitral inflow Pulmonary 0 <25 mm Hg artery 1 25–30 mm Hg pressure 2 31–45 mm Hg 3 >45 mm Hg Pulmonary venous 0 Systolic flow exceeds diastolic flow by ≥50% flow 1 Systolic flow exceeds diastolic flow by <50% 2 Diastolic flow > systolic flow 3 Systolic flow reversal Left atrial 0 None enlargement 1 Mild 2 Moderate 3 Severe The mitral regurgitant index = total score/number of variables CW, continuous wave Doppler ultrasonography; PISA, proximal isovelocity surface area. From Thomas L, Foster E, Hoffman JIE, et al: J Am Coll Cardiol mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 5 1999;33:2016–2022. the hemodynamic impact as well as characteristics of the regurgitant jet (Table 17-1) .[133] The same regurgitant volume may be associated with changing valve structure and varying degrees of chamber dilation and function. Furthermore, echocardiographic signs of severe chronic regurgitation may not be applicable in the acute setting. Although volumetric and proximal isovelocity surface area methods have been validated both clinically and experimentally, these methods are rarely applied in routine clinical practice because they are time consuming and highly dependent on operator experience. Indirect TABLE 17-2 -- Proposed Doppler Criteria for Identifying Severe Valvular Regurgitation by the Transesophageal Approach Mitral Regurgitation Jet area/left atrium area >40% Regurgitant fraction >40% Vena contracta width >5.5 mm Systolic pulmonary vein flow reversal Present Aortic Regurgitation Vena contracta width >12 mm Pressure half-time of regurgitant flow <350 msec End-diastolic flow velocity in the descending aorta >18 cm/sec Modified from Tribouilloy C, Shen WF, Leborgne L, et al: Éur Heart J 1996;17:272–280. TABLE 17-3 -- Summary of Echocardiographic Methods to Quantify Valvular Regurgitation Method Limitations Doppler color flow Jet area represents velocity not volume and is mapping influenced by driving pressure, receiving chamber compliance, regurgitant orifice size, and instrument factors. Underestimation of severity occurs with eccentric jets. Volumetric Doppler Accurate in experienced hands, yet time consuming. Greatest measurement of mitral or mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 5 aortic cross-sectional area. Requires competent valve to measure forward stroke volume. Pulmonary venous In addition to severe MR, systolic-to-diastolic flow pulmonary flow ratio may be influenced by other variables, such as LV function, LA compliance, atrial fibrillation, mitral stenosis, loading conditions, sampling of left vs. right pulmonary vein. AR pressure half-time Both markers are less reliable when systemic and deceleration slope vascular resistance is altered or in the presence of LV dysfunction with significant overlap of values for varying degrees of AR severity. Aortic diastolic flow Related to regurgitant volume and aortic reversal compliance. Proximal flow Relies on hemispheric geometric assumptions. convergence Requires selection of optimal aliasing velocity and identification of the orifice for precise measurement of the radius. Overestimation of flow is observed with eccentric jets. Vena contracta width Simple and accurate but requires optimal axial resolution and imaging plane for clear definition. Limited with rapidly divergent jets and overlap in lesion severity between 3–5 mm. Momentum Measures flow rate and ROA from a single velocity profile across an axisymmetric jet. Validated in vitro but rarely used clinically. Not applicable to eccentric jets. Amplitude-weighted Nonvolumetric method for calculating ratio of flow mean velocity based on the amplitude of the Doppler signal. Requires special software. Three-dimensional Reveals the complex geometry of regurgitant echocardiography lesions. Requires stable positioning of transducer and patient during image acquisition, which may be time consuming. AR, aortic regurgitation; LA, left atrium; LV, left ventricle; MR, mitral regurgitation; ROA, regurgitation orifice area. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 5 markers are affected by other variables and should not be used in isolation to determine regurgitant severity (Table 17-2) . Although there are many proposed echocardiographic methods to quantify valvular regurgitation (Table 17-3) , the main limitation has been the lack of a true gold standard for comparison.[27] [134] The challenge to future investigations in this area is to develop |
a better gold standard for quantifying valvular regurgitation by extracting more reproducible yet accurate spatial, temporal, and velocity information from color Doppler imaging. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/153.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 5 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company 389 Chapter 18 - The Role of Echocardiography in the Timing of Surgical Intervention for Chronic Mitral and Aortic Regurgitation David J. Meier MD Carolyn K. Landolfo MD Mark R. Starling MD The optimal timing of surgical intervention in patients with chronic mitral and aortic regurgitation remains controversial and challenging. Historically, mitral and aortic regurgitation have been considered hemodynamically equivalent as conditions of left ventricular (LV) volume overload.[1] Although mitral regurgitation is a condition of primary LV volume overload, aortic regurgitation generates both a pressure and a volume overload on the left ventricle. In both conditions, preload is elevated because of excess volume, resulting in the development of eccentric hypertrophy. In aortic regurgitation, however, afterload is also increased secondary to LV pressure overload, resulting in the development of concomitant concentric hypertrophy. These fundamental hemodynamic differences are responsible for the observed differences between mitral and aortic regurgitation in the natural history of the disease processes, mechanisms for LV systolic dysfunction, response to surgery, and the appropriate timing of surgical intervention. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 5 After a long asymptomatic period, often lasting several years, prolonged mitral or aortic regurgitation inevitably leads to LV pump dysfunction, which is characterized by decreased LV ejection fraction and contractile dysfunction. [2] [3] [4] [5] [6] [7] [8] In assessing LV pump performance in valvular regurgitation, it is important to distinguish between ejection performance and contractile performance of the left ventricle. Left ventricular ejection performance, commonly measured by indices such as ejection fraction and percent fractional shortening, refers to the global pumping capability of the left ventricle. Because LV ejection phase indices are affected by multiple variables, such as contractility, heart rate, preload, and afterload, an abnormal LV ejection fraction does not necessarily imply abnormal contractility. Likewise, LV ejection fraction may be normal, despite significant underlying contractile dysfunction. Left ventricular contractility, on the other hand, refers specifically to the performance of the contractile apparatus of the left ventricle, independent of loading conditions. Although both mitral and aortic regurgitation eventually lead to LV pump dysfunction, the mechanisms underlying decreased LV pump performance differ between the two conditions. Wisenbaugh et al[9] evaluated the hemodynamic characteristics of patients with severe aortic regurgitation (n = 9) and severe mitral regurgitation (n = 8) and compared the findings to those of normal subjects (n = 7) (Fig. 18-1) . Despite a similar volume of regurgitation between the patients with aortic and mitral regurgitation, afterload (end-systolic stress) was found to be significantly increased above control in patients with aortic regurgitation, but not in patients with mitral regurgitation. Conversely, LV contractile dysfunction, measured by the ratio of end-systolic stress to end-systolic volume index, was found to be more depressed in patients with mitral regurgitation than in patients with aortic regurgitation, despite comparable reductions in LV ejection fraction. These data suggest that the mechanism for decreased LV pump performance in aortic regurgitation is afterload excess, in contrast to mitral regurgitation, in which LV contractile dysfunction is the primary mechanism. Because 390 Figure 18-1 The relationship between left ventricular ejection fraction (EF) and end-systolic stress, constructed from the data of Wisenbaugh et al,[9] is illustrated for normal subjects and patients with mitral (MR) or aortic (AR) regurgitation. End-systolic stress or afterload is increased only in the AR group. (From Devlin WH, Starling MR: Cardiol Rev 1994;3:16–28.) mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 5 of the favorable loading conditions in mitral regurgitation, however, ejection phase indices of LV systolic performance often remain normal, thereby masking the severity of LV contractile dysfunction. Although afterload excess is the primary mechanism for LV pump dysfunction in aortic regurgitation, contractile dysfunction also contributes to decreased LV pump performance, but typically as a late manifestation of severe, prolonged regurgitation.[11] These hemodynamic differences between mitral and aortic regurgitation have very important clinical implications, both in terms of disease progression and in response to corrective surgery. Because afterload excess is responsible for the early decline in LV pump performance in aortic regurgitation, the decrease in afterload that follows aortic valve replacement favors improvement in LV systolic performance, even when preoperative LV ejection phase indices are depressed.[12] [13] [14] [15] [16] [17] Later in the course of the disease, however, significant contractile dysfunction also develops, resulting in progressive and potentially irreversible LV failure. In contrast, contractile dysfunction develops relatively early in the natural history of mitral regurgitation, but it may be masked by the favorable preoperative loading conditions and the compensatory activation of the sympathetic nervous system with resultant beta-adrenergic stimulation.[18] [19] [20] [21] [22] [23] [24] Postoperatively, as loading conditions change with elimination of the regurgitant leak into the low-resistance left atrium, this underlying contractile dysfunction becomes unmasked, resulting in a decreased in LV ejection fraction.[5] [6] [7] [16] [25] [26] [27] [28] [29] Patients with mitral regurgitation who have even a mildly depressed LV ejection fraction preoperatively often have severe contractile dysfunction and are, therefore, at risk for significant LV systolic dysfunction, congestive heart failure, and death in the postoperative period.[4] [5] [6] [7] [8] However, in patients with occult contractile dysfunction marked by a mildly elevated end-systolic dimension in the presence of a normal LV ejection fraction, recovery of contractile function often does occur postoperatively.[30] Thus, these data highlight the clinical imperative in mitral regurgitation to identify early, occult, but potentially reversible contractile dysfunction to optimize the long-term results of mitral valve surgery. This is important because there appear to be two populations of patients: those in whom contractility improves and those in whom contractility does not improve following mitral valve surgery. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 5 Therefore, because reduced LV ejection fraction reflects more severe contractile dysfunction in mitral compared with aortic regurgitation, a greater degree of preoperative LV pump dysfunction is tolerated without adverse clinical outcome in aortic regurgitation, provided that the duration of LV pump dysfunction is brief. Prolonged LV pump dysfunction reflects severe contractile dysfunction in both mitral and aortic regurgitation and is associated with an adverse postoperative outcome. The ability to identify contractile dysfunction and correct the regurgitant lesion before contractile dysfunction becomes irreversible is critical to the timing of surgical intervention for both regurgitant valve lesions. Although contractile dysfunction is the mechanism for the early decrease in LV ejection fraction in mitral regurgitation, the type of operation performed also significantly affects the degree of postoperative LV pump dysfunction. [31] [32] [33] [34] [35] [36] [37] [38] [39] [40] [41] LV ejection fraction almost always declines after conventional mitral valve replacement with removal of the submitral apparatus, even when preoperative indices of LV pump performance are normal.[31] [32] [33] [36] [37] This decline of LV ejection fraction has been attributed to an alteration in LV geometry resulting from transection of the chordae tendineae and removal of the papillary muscles. Conversely, LV ejection fraction is not decreased to the same extent after mitral valve reconstruction or mitral valve replacement with preservation of the submitral apparatus.[31] [32] [33] , [40] Therefore, because mitral valve reconstruction preserves LV pump performance and can be performed with a low operative morality rate and low risk for thromboembolism and endocarditis, earlier surgical intervention has been advocated in all patients in whom valve repair is feasible, particularly those with reduced LV pump performance. [42] The major challenge in the management of patients with valvular regurgitation is the ability to identify contractile dysfunction and to correct the regurgitant lesion before irreversible contractile dysfunction develops. The purpose of this chapter is to present the echocardiographic parameters that can be used to guide timing of surgical intervention in aortic and mitral regurgitation. Because LV contractility dysfunction is the most important determinant of survival and postoperative outcome in valvular regurgitation, the primary goal guiding the timing of surgical intervention is assumed to be preservation of contractility. Unfortunately, many noninvasive variables currently used to guide surgical intervention identify patients likely to do poorly after surgery, but they do not pinpoint the onset of occult, reversible contractile dysfunction when timely operative mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 5 intervention would be warranted. [11] [18] , [26] [28] The proposed algorithms presented in this chapter for the evaluation of patients with valvular regurgitation incorporate clinical, hemodynamic, and echocardiographic variables into rational guidelines for 391 appropriate timing of surgical intervention directed toward the long-term preservation of contractility. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/155.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 5 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Pathophysiologic Mechanisms Although LV volume overload is the primary hemodynamic abnormality in mitral regurgitation, both pressure and volume overload exist in aortic regurgitation. [1] Significant elevations in preload caused by increased regurgitant volume in both mitral and aortic regurgitation lead to the development of eccentric hypertrophy, characterized by LV enlargement and increased myocardial mass.[2] [3] [20] The degree of hypertrophy is commensurate with the degree of LV dilation, maintaining the ratio of LV mass to end-diastolic volume within the normal range. In addition to eccentric hypertrophy, increased systolic wall stress (afterload) in aortic regurgitation also leads to the development of concentric hypertrophy.[1] [9] The differences in the compensatory mechanisms of the left ventricle to pure volume overload in mitral regurgitation and both pressure and volume overload in aortic regurgitation account for the observed difference in disease progression, changes in LV pump performance, and response to operation. Mitral Regurgitation Acute Mitral Regurgitation. The pathophysiologic mechanisms underlying mitral regurgitation have been well reviewed by Carabello.[43] [44] Left ventricular ejection fraction increases in acute mitral regurgitation as a result of increased preload and decreased afterload. In acute mitral regurgitation, the left ventricle compensates for the sudden increase in volume by increasing sarcomere diastolic length (preload). Left ventricular end-diastolic volume increases, leading to augmentation of LV stroke work by the Frank-Starling mechanism. In addition to increased preload, systolic ejection of blood through the incompetent mitral valve into the low-impedance left atrium lowers systolic wall stress (afterload). Decreased afterload, in turn, augments ventricular emptying, resulting in reduced end-systolic volume, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 5 increased total stroke volume, and increased ejection fraction. In acute mitral regurgitation, therefore, the left ventricle compensates for the volume overload by emptying more completely. Chronic Compensated Mitral Regurgitation. The transition from the acute to the chronic state of mitral regurgitation is characterized by LV enlargement and compensatory eccentric hypertrophy, resulting in an increase in LV end-diastolic volume and mass. The increase in LV end-diastolic volume enables augmentation of total stroke volume, helping to return forward stroke volume toward the normal range. With the development of eccentric hypertrophy, the radius of the left ventricle increases without a significant change in wall thickness, increasing wall stress into the normal range, in accordance with the law of Laplace. As wall stress increases into the normal range, LV emptying decreases and end- systolic volume increases. In the compensated phase, therefore, the increase in LV end-diastolic volume produced by increased preload and the increase in end-systolic volume result in an ejection fraction that is within the normal range, but less than that of the acute stage. Chronic Decompensated Mitral Regurgitation. As a result of these compensatory mechanisms and the stimulation of the sympathetic nervous system, patients with chronic mitral regurgitation may remain asymptomatic for long periods of time and |
LV ejection phase indices may remain normal, despite underlying contractile dysfunction. Eventually, contractility declines beyond the compensatory capabilities of the left ventricle and the sympathetic nervous system.[24] With LV decompensation, ejection fraction decreases because of an increase in end- systolic volume. Left ventricular end-diastolic pressure increases, resulting in further eccentric hypertrophy and LV dilation. With progressive increases in the radius of the left ventricle, wall stress increases above normal, resulting in a significant increase in end-systolic volume. A vicious cycle thus evolves, leading to a progressive decline in LV pump performance. Response to Operation. In compensated mitral regurgitation, correction of the regurgitant lesion results in a decrease of LV end-diastolic volume and end-diastolic dimension into the normal range. Although postoperative end-systolic stress remains normal, LV ejection fraction decreases in nearly all patients mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 5 after mitral valve replacement with removal of the submitral apparatus.[45] Left ventricular ejection fraction generally remains unchanged in patients with compensated mitral regurgitation who undergo mitral valve reconstruction or mitral valve replacement with preservation of the submitral apparatus.[31] [32] [33] [34] , [40] In decompensated mitral regurgitation, there is marked preoperative LV enlargement, elevation in end-systolic wall stress, and decreased fiber shortening. [45] Postoperatively, the left ventricle remains persistently dilated, end-systolic wall stress increases, and ejection fraction declines significantly. Interestingly, in children and young adults, the early postoperative course of LV systolic dysfunction is similar to that in adults, but the long-term occurrence of LV systolic dysfunction is significantly different. In a recent study by Krishnan et al,[46] long-term postoperative LV systolic dysfunction was found to be rare, but it occasionally occurred. Better clinical postoperative results were associated with a shorter duration of mitral regurgitation. Aortic Regurgitation Acute Aortic Regurgitation. In acute aortic regurgitation, because the normal LV chamber cannot acutely adapt to the large regurgitant volume, forward stroke volume is reduced, resulting in significant elevation in LV end-diastolic pressure.[47] Prolonged regurgitation eventually leads to the development of LV dilation and eccentric hypertrophy.[20] Chronic Compensated Aortic Regurgitation. In the transition from acute to chronic compensated aortic regurgitation, LV dilation and eccentric hypertrophy accommodate a larger end-diastolic volume. [20] [48] The increased LV end-diastolic volume, in turn, allows for 392 increases in both total and forward stroke volume, thereby returning LV filling pressures to normal. These compensatory mechanisms maintain LV ejection fraction and end-systolic volume within the normal range. In addition, vascular adaptation, as measured by total arterial elastance, has been found to occur in response to chronic aortic regurgitation. This LV- mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 5 arterial coupling occurs in a heterogeneous pattern. In some patients it decreases, thereby maximizing LV work and performance, whereas in others it increases, causing "double loading" of the left ventricle and progressive pump dysfunction. [49] Concentric hypertrophy also develops in aortic regurgitation in response to pressure overload.[1] [9] [20] Unlike mitral regurgitation, in which the excess volume is unloaded into the low-impedance left atrium, in aortic regurgitation, the forward and regurgitant volume must be pumped into the higher pressure arterial system, resulting in an increase in end-systolic pressure and wall stress.[50] In accordance with the Laplace relationship, an increased end-systolic wall stress results in concentric hypertrophy, leading to an increase in wall thickness, returning the ratio of cavity radius to wall thickness to within the normal range. Chronic Decompensated Aortic Regurgitation. The transition to decompensated aortic regurgitation is characterized by progressive LV dilation and deterioration in LV pump performance resulting from intrinsic contractile dysfunction.[2] [51] At this stage, the left ventricle has reached its limit of compensation and can no longer increase wall thickness to compensate for increases in preload. The ratio of cavity dimension to wall thickness increases, resulting in elevated end-systolic wall stress and afterload mismatch. Total and forward stroke volumes decrease and end-systolic volume increases, resulting in a decline in ejection fraction and elevation in left-sided filling pressures. Response to Operation. In chronic compensated aortic regurgitation, valve replacement results in a reduction in end-diastolic volume and regression of LV hypertrophy. [16] [17] , [52] [53] [54] [55] [56] [57] Afterload also decreases, resulting in improved LV pump performance, even if LV ejection fraction was reduced preoperatively. In chronic decompensated aortic regurgitation, there is marked LV enlargement, significant elevation in end-systolic wall stress, and decreased LV pump performance.[59] [60] Despite successful valve replacement, LV dilation and hypertrophy persist, end-systolic wall stress remains elevated, and systolic performance remains depressed, indicating the development of irreversible contractile dysfunction. MD Consult L.L.C. http://www.mdconsult.com mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Assessment of Left Ventricular Function in Valvular Regurgitation Although the pathophysiologic mechanisms differ between the two regurgitant valve lesions, LV pump performance is the most important determinant of survival and postoperative outcome in both mitral and aortic regurgitation. As a result, most of the variables used to predict outcome in valvular regurgitation relate to LV ejection phase indices. How, then, is LV systolic performance best evaluated in chronic valvular regurgitation? Ejection Phase Indices. Left ventricular pump performance is often gauged by indices such as ejection fraction and percentage of fractional shortening. These LV ejection phase indices can be altered dramatically, however, by changes in loading conditions, heart rate, and contractility.[18] Alteration in any one of these factors can change LV ejection fraction without necessarily implicating abnormal contractility as the mechanism.[22] Likewise, LV ejection fraction can remain normal, despite markedly impaired contractility. [26] [28] Because mitral and aortic regurgitation are states of altered load, LV ejection phase indices may not accurately assess contractility in these conditions. End-Systolic Indices. To overcome the limitations of LV ejection phase indices in the assessment of contractile state in valvular regurgitation, investigators have alternatively used load-independent variables.[18] [21] [22] [23] [46] Because preload is elevated in valvular regurgitation, preload-independent variables, particularly the end-systolic indices, are commonly employed to assess contractility in mitral and aortic regurgitation.[19] [61] [62] [63] [64] [65] [66] [67] [68] [69] The end- systolic indices have been classified according to those that measure afterload, including end-systolic stress and end-systolic pressure; and those that indicate LV size, including end-systolic volume and end-systolic mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 dimension. The ratio of end-systolic stress (or end-systolic pressure) to end- systolic volume (or end-systolic dimension) are preload-independent indices of contractility that also correct for afterload. The basic principle underlying the use of these indices of contractility is that for a given afterload, a ventricle that can shorten to a smaller end-systolic volume has greater contractility than a ventricle with a larger end-systolic volume. End-Diastolic Indices. End-diastolic indices, including end-diastolic dimension and end-diastolic wall stress (the product of end-diastolic pressure and dimension divided by the wall thickness) have also been used to evaluate LV performance in valvular regurgitaton. [59] [66] Left ventricular end-diastolic dimension increases in valvular regurgitation in response to volume overload. In mitral regurgitation, end-diastolic dimension increases without significant changes in wall thickness, whereas in aortic regurgitation both end-diastolic dimension and wall thickness increase. Progressive increases in end- diastolic dimension and end-diastolic wall stress are suggestive of decompensation in both conditions of valvular regurgitation. Pressure-Volume Relationship. The slope of the LV end-systolic pressure-volume relationship has also been used as a load-independent measure of contractility.[11] [20] [21] , [26] [69] [70] [71] Unfortunately, determination of this slope requires measurement of end- systolic volume at different levels of afterload, typically using pharmacologic stress during cardiac catheterization. In most clinical settings, therefore, the pressure-volume relationship cannot be used as a routine tool for serial assessment of contractility in valvular regurgitation. Importantly, however, it can be used to provide insights into the occurrence of contractile dysfunction that can be translated into better use of ejection phase indices to determine the appropriate timing of surgical intervention, particularly in mitral regurgitation. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/157.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 26 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Chronic Mitral Regurgitation 393 Traditionally, surgery for chronic mitral regurgitation has been delayed until the onset of symptoms. Unfortunately, by the time symptoms have developed, severe irreversible contractile dysfunction may already be present. Contractile dysfunction typically develops during the asymptomatic period when ejection phase indices of LV pump performance remain within the normal range. Because survival is reduced in patients with mitral regurgitation who have irreversible contractile dysfunction, current management strategies have been directed toward the timing of surgery to prevent progression to irreversible contractile dysfunction. Advances in detection of occult contractile dysfunction, better knowledge of the preoperative predictors of surgical outcome, reduction in mortality for mitral valve replacement using chordal-sparing techniques, and advances in mitral valve repair are leading to earlier surgical intervention in this population of patients. Etiology The mitral valve apparatus consists of the annulus, the anterior and posterior leaflets, the chordae tendineae, and the papillary muscles. Mitral regurgitation develops from alterations in one or more components of the mitral apparatus. [72] Causes of chronic mitral regurgitation are listed in Table 18-1 .[73] The most common causes of pure isolated mitral regurgitation include myxomatous degeneration (62%) (Fig. 18-2) , ischemia-related papillary muscle dysfunction (30%), infectious endocarditis (5%), and rheumatic disease (3%).[72] Changing Etiology of Mitral Regurgitation. The spectrum of surgical mitral valve disease has changed significantly mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 26 since the 1970s, with a decline in surgical referral for rheumatic valvular disease and an increase for myxomatous degenerative disease.[74] [75] [76] [77] In one review, TABLE 18-1 -- Causes of Chronic Mitral Regurgitation Mechanism Condition Inflammatory Rheumatic heart disease Systemic lupus erythematosus Takayasu's arteritis Scleroderma Degenerative Myxomatous degeneration of mitral valve leatlets Mitral valve annular calcification Marfan's syndrome Ehlers-Danlos syndrome Pseudoxanthoma elasticum Infectious Bacterial endocarditis Structural Ruptured chordae tendineae Rupture or dysfunction of the papillary muscles Dilation of the mitral valve annulus Hypertrophic cardiomyopathy Paravalvular prosthetic leak Congenital Mitral valve clefts or fenestrations Parachute mitral valve abnormality Adapted from Haffajec CI: Chronic mitral regurgitation. In Dalen JE, Alpert JS (eds): Valvular Heart Disease, 2nd ed. Boston, Little, Brown. 1987, pp 111–119. Figure 18-2 (color plate.) Transesophageal echocardiogram in the longitudinal plane (two-chamber view) from a patient with myxomatous degenerative mitral valve disease who presented with a 3-month history of dyspnea. Demonstrated is mitral valve prolapse (A) with a flail posterior leaflet secondary to a ruptured chordae tendineae, resulting in severe mitral regurgitation (B). rheumatic valvulitis accounted for 46% of all surgically treated cases of mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 26 mitral regurgitation from 1970 through 1974, but only 15% from 1985 through 1989. Conversely, myxomatous degenerative disease accounted for only 37% of cases in the earlier years, but it represented 60% of cases in the latter years.[75] Changes in the etiology of mitral regurgitation have been paralleled by changes in surgical therapy for the disease. The number of valves being repaired has steadily increased, particularly in centers experienced in valve reconstruction. At the Cleveland Clinic, 80% of patients referred for correction of mitral regurgitation in 1988 underwent valve repair (see Chapter 19) .[74] Because of the potential for valve repair, the specific anatomic defect responsible for mitral regurgitation, defined by two- dimensional and transesophageal echocardiography, has become an integral part of the evaluation of patients with mitral regurgitation. The potential to repair myxomatous degenerative valves has been further stratified according to the specific anatomic defect. Because operative mortality and overall complication rates are lower with mitral valve repair procedures,[72] [77] the ability to repair a valve favors earlier surgical intervention to prevent development of occult contractile dysfunction. Natural |
History Importance of Left Ventricular Pump Performance. 394 The natural history of mitral regurgitation is variable and depends on multiple factors, including the volume of regurgitation, LV pump performance, contractile state, and the underlying etiology of the disease.[3] [78] [79] The most important determinant of survival, however, is LV contractile state. Chronic mitral regurgitation represents a state of volume overload in which elevated preload and compensatory eccentric hypertrophy maintain overall LV ejection fraction within the normal range for extended periods of time.[43] [44] In addition, recent evidence suggests that LV pump performance in chronic mitral regurgitation is also maintained by activation of the sympathetic nervous system. Nagatsu and colleagues[24] used a canine model to show that indices of LV ejection and contractile performance could be maintained in the normal or near-normal range by beta-adrenergic stimulation in surgically created chronic mitral regurgitation, despite the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 26 presence of significant underlying contractile dysfunction.[49] This implied that by the time contractile dysfunction is detected in the absence of beta- adrenergic blockade, severe contractile dysfunction is already present. In human subjects, Mehta and colleagues[80] [81] found that the sympathetic nervous system was activated in proportion to the increase in LV end- systolic volume and the reduction in ejection fraction, rather than the severity of mitral regurgitation (Fig. 18-3) . Activation of the sympathetic nervous system was found to increase and was clearly evident at echocardiographic LV end-systolic dimensions of 40 mm or more. Despite the initial compensatory function of beta-adrenergic stimulation in mitral regurgitation, chronic stimulation may have adverse effects on LV contractility. Canine models of surgically created mitral regurgitation have shown that sustained beta-adrenergic blockade resulted in Figure 18-3 The relationship between the extravascular norepinephrine release rates (NE2 ) and echocardiographically determined left ventricular end-systolic dimension (ESD) is shown. Note that sympathetic tone is markedly elevated in mitral regurgitation patients with a left ventricular ESD of greater than 40 mm. (From Mehta RH, Supiano MA, Oral H, et al: Am J Cardiol 2000;86:1193–1197.) improved LV pump performance. This effect was associated with an improvement in cardiocyte contractility secondary to an increased number of contractile elements in isolated cardiocytes.[82] These compensatory mechanisms allow patients to remain asymptomatic for many years. Eventually, a transition phase ensues, during which time insidious contractile dysfunction begins to develop. During this transition phase, however, patients generally remain asymptomatic or are just beginning to develop mild symptoms of fatigue. The development of atrial fibrillation often heralds the onset of this decompensation.[83] [84] By the time patients become overtly symptomatic, with exhaustion, decreased exercise tolerance, and congestive heart failure, severe irreversible contractile dysfunction may have already developed.[3] , [78] It is important to understand that, despite significant and potentially irreversible contractile dysfunction, LV ejection fraction may be reduced to only 40% to 50%. [26] [28] Right heart failure, characterized by congestive hepatomegaly, ascites, and peripheral edema, may develop late in the course of the disease.[77] [85] Medical versus Surgical Therapy. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 26 Overall survival in chronic mitral regurgitation appears to be improved with surgical therapy in patients with normal or reduced LV pump performance. Because the natural history of severe mitral regurgitation has been significantly altered by surgical advances, only a few studies exist that directly compare medical with surgical therapy[86] [87] [88] [89] (Table 18-2) . Rapaport[86] studied the natural history of 70 patients with mitral regurgitation treated medically over a 5- and 10-year period. The survival rate at 5 and 10 years was reported to be 80% and 60%, respectively, for patients with isolated mitral regurgitation. Hammermeister et al[87] reported much lower 5- and 9- to 10-year survival rates for 36 medically treated patients at 55% and 22%, respectively. Survival was significantly improved in the 61 patients who underwent mitral valve replacement, with 5- and 9- to 10-year survival rates of 72% and 63%, respectively. Delahaye et al[89] also reviewed the outcomes of 216 patients with chronic mitral regurgitation. Actuarial survival at 8 years for the surgical group (n = 116) was 74%, compared with 33% for the medical group (n = 54). For mixed mitral regurgitation and stenosis, survival with medical therapy has ranged from 45% to 65% at 5 years and 27% to 32% at 9 to 10 years. Surgery also improves mortality in this subset of patients, with survival rates reported at 61% to 84% at 5 years and 75% at 9 to 10 years. Although survival is reduced in patients with impaired LV pump performance, overall mortality is improved with surgery compared with medical therapy. [87] Therefore, surgery should not be withheld in patients with chronic mitral regurgitation on the basis of reduced LV ejection fraction. Mitral Valve Replacement Importance of Preservation of the Submitral Apparatus. Left ventricular ejection fraction frequently decreases after surgical correction of chronic mitral regurgitation, 395 TABLE 18-2 -- Survival in Chronic Mitral Regurgitation: Comparison Surgical Therapy Medical Therapy Sur mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 26 9- TO 10- 5-YEAR YEAR PATIENTS, SURVIVAL, SURVIVAL, PATIENTS, Study Condition n % % n Rapaport[86] MR 70 80 60 MR/MS 102 65 32 Hammermeister MR 36 55 22 61 et al[87] MR/MS 22 63 27 45 Munoz et al[88] MR/MS 99 45 45 Delahaye et al MR 54 33 116 [89] MR, mitral regurgitation; MS, mitral stenosis. even if preoperative indices of LV pump performance are normal.[16] [25] [29] Traditionally, it was believed that afterload (end-systolic wall stress) was decreased in mitral regurgitation by systolic "unloading" into the low- impedance left atrium. Correction of mitral regurgitation with elimination of the low-resistance leak into the left atrium was thought to acutely increase afterload, resulting in the decrease in LV ejection fraction observed postoperatively.[29] It is now known that for the majority of patients with severe mitral regurgitation, afterload is normal before surgical correction. Furthermore, changes in afterload are not solely responsible for the observed decrease in LV pump performance after surgical correction of mitral regurgitation. Rather, primary contractile dysfunction, resulting from chronic volume overload, and alterations in LV geometry secondary to removal of the submitral apparatus during conventional mitral valve replacement are also responsible for the post-operative decline in LV pump performance. Conventional mitral valve replacement with transection of the chordae tendineae and removal of the subvalvular apparatus almost always results in a postoperative decline Figure 18-4 Preoperative (PRE) and postoperative (POST) left ventricular (LV) ejection fractions depicted for patients undergoing mitral valve replacement with transection (open squares) and preservation (solid circles) of the chordae tendineae. Data for individual mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 26 patients are represented by smaller symbols; mean ± SEM is represented by larger symbols. Mitral valve replacement with transection of the chordae tendineae resulted in a decrease in LV ejection fraction, but mitral valve replacement with chordal preservation did not. (From Rozich JD, Carabello BA, Usher BW, et al: Circulation 1992;86:1718–1726.) in global and regional LV ejection fraction, even when preoperative indices of LV pump performance are normal.[90] LV ejection fraction decreases immediately after removal of the subvalvular apparatus[34] and persists over the long term after excision.[89] For the majority of patients, however, this decline in LV ejection fraction does not occur with mitral valve reconstruction[34] [91] [92] or mitral valve replacement with preservation of the chordae tendineae and papillary muscles [31] [33] , [40] (Fig. 18-4) . In addition to preservation of LV systolic performance, postoperative survival and exercise capacity have been shown to improve in patients who undergo mitral valve replacement with chordal preservation.[37] The mechanisms for preservation of LV pump performance after mitral valve replacement with chordal preservation have been defined by Rozich et al[40] using two-dimensional echocardiography. Disruption of the functional components of the submitral apparatus during conventional mitral valve replacement disturbs the continuity between the mitral annulus and LV wall through the leaflets, chordae tendineae, and papillary muscles, resulting in significant increases in end-systolic volume and 396 end-systolic stress. In addition, the ratio of the LV major axis to minor axis dimension decreases significantly, suggesting a loss of LV geometry with assumption of a more spherical shape.[33] [40] [45] Mitral valve replacement with chordal preservation maintains LV systolic performance by preserving LV geometry, resulting in a smaller LV cavity and a decrease in end- systolic wall stress.[35] Although the decline in LV pump performance after conventional mitral valve replacement can be attributed, at least in part, to disruption of LV geometry after removal of the submitral apparatus, underlying contractile dysfunction secondary to long-standing volume overload is still the major determinant of postoperative LV pump dysfunction. Left ventricular pump performance declines postoperatively in patients with significant preoperative LV enlargement, despite mitral valve replacement with preservation of the submitral apparatus. Wisenbaugh et al[93] demonstrated mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 26 that patients with an end-systolic diameter of greater than 50 mm had a poor long-term outcome after mitral valve replacement, despite chordal preservation. Similar data have been reported by Enriquez-Sarano et al[5] for patients undergoing mitral valve reconstruction, with a decline in postoperative LV ejection fraction demonstrated for patients with a preoperative LV ejection fraction of less than 60%. These data confirm the fact that occult contractile dysfunction secondary to long-standing volume overload is an important mechanism for the observed postoperative decline in LV ejection fraction after correction of mitral regurgitation. Mitral Valve Reconstruction Left Ventricular Systolic Performance. The long-term success of mitral valve reconstruction for mitral regurgitation has been reported in numerous series.[37] [77] [79] , [91] , [94] [95] [96] [97] [98] [99] [100] [101] [102] [103] [104] [105] [106] [107] [108] In addition to preservation of LV geometry, mitral valve reconstruction has been shown to confer additional operative and long-term survival advantages over mitral valve replacement for chronic mitral regurgitation. The reduction in LV pump performance that has been observed after conventional mitral valve replacement has not been observed with mitral valve reconstruction, provided that the preoperative contractile state remains intact (Table 18-3) . TABLE 18-3 -- Preoperative and Postoperative Ejection Fraction: A Comparison of Mitral Valve Repair and Mitral Valve Replacement with Chordal Transection and Preservation Replacement Replacement with Chordal with Chordal Transection, Preservation, Repair, % % % Study PREOP POSTOP PREOP POSTOP PREOP POSTOP Duran et al[91] 47 54 54 47 David et al[33] 63 63 62 51 64 65 David et al[31] 55 48 53 52 Goldman et al[34] 44 49 64 40 Hennein et al[37] 46 31 50 54 Sakai et al[92] 65 68 64 57 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 26 Rozich et al[40] 60 36 63 61 Enriquez-Sarano et al[5] 63 54 69 49 Preop, preoperative; Postop, postoperative. Mortality. Operative mortality and long-term survival rates are also better after mitral valve repair compared with mitral valve replacement (Table 18-4) . Mitral valve reconstruction has been compared to replacement in several studies. The first large retrospective study was reported by Duran et al [91] in 1980 for 562 patients undergoing mitral valve surgery predominantly for rheumatic heart disease. Operative mortality for the 255 patients undergoing mitral valve repair was 1.9% compared with 11.4% for the 307 patients in the replacement group. Survival at 2 years was better for the repair group (98.3%) than for the replacement group (92.9%), largely due to the differences in operative mortality. Only one prospective trial exists comparing mitral valve reconstruction with replacement. Perier[110] studied 400 patients with mitral regurgitation predominantly of rheumatic origin. Patients were divided into four groups of 100 patients each, with one group undergoing mitral valve repair and the remaining three groups treated with valve replacement using different prostheses. The 7-year survival rate was 82% for the repair group versus 56%, 61%, and 60% for the three replacement groups. Yacoub et al[108] reported long-term results for mitral valve reconstruction versus replacement for the "floppy mitral valve syndrome." Survival rates at 5 and 10 years were 91% and 81%, respectively, for the repair group, versus 81% and 39% for the replacement group. In addition to preservation of LV pump performance, therefore, mitral valve reconstruction also confers a survival advantage over mitral valve replacement. Thromboembolism. In addition to the decreased operative mortality and increased long-term survival associated with mitral valve repair, the thromboembolic and hemorrhagic complications associated with mitral valve reconstruction are also significantly decreased compared with mitral valve replacement. Several |
studies have reported that approximately 95% of patients are free from thomboembolic complications at 5 to 10 years after surgery.[111] In contrast, 10% to 35% of patients with mechanical prostheses have thromboembolic events within 5 to 10 years of surgery.[112] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 26 Hemorrhage. Because only a minority of patients who undergo valve reconstruction are maintained on chronic anticoagulation therapy, the incidence of significant bleeding complications is also extremely small,[101] [111] in contrast 397 TABLE 18-4 -- Operative Mortality and Long-Term Survival: Mitral Valve Repair versus Replacement Operative Mortality Long-Term Survival YEARS REPAIR, REPLACEMENT, AFTER REPAIR, REPLACEMENT, Study n (%) n (%) OPERATION % % Duran et 255 1.8 307 11.4 4 96 81 al[91] Yacoub 86 3.1 46 7.0 5 91 62 et al[108] Oliveira 82 4.9 101 5.0 6 88 68 et al[106] Adebo 21 0 44 6.8 5 85 78 and Ross [96] Perier et 100 2.0 100(SE) 13 61(SE) al[110] 100(BS) 12 7 82 60(BS) 100(BP) 12 56(BP) Orszulak 131 6.1 106 7.5 5 92 72 et al[107] Sand et al 48 0 222 4.0 5 76 56 [94] Angell et 112 5.4 72 18.1 5/10 90/75 55/40 al[95] Cohn et 75 4.0 63 3.0 3 94 85 al[97] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 26 Galloway 280 2.0 169(ME) 6.6 5 76 72(ME) et al[101] 975(BP) 8.5 69(BP) Craver et 65 1.5 65 4.6 4 84 82 al[99] Kawachi 43 2.3 48 8.3 5/8 91/91 82/75 et al[103] Enriquez- 151 1.3 175 * 5.7 9 79; EF 71; EF > 60 Sarano et * > 60 al[7] 48; EF 50; EF < 60 < 60 Enriquez- 44 † 6.8 39 † 30.8 10 68 52 Sarano et al[5] BP, bioprosthesis; BS, Björk-Shiley; EF, ejection fraction; ME, mechanical; SE, Starr-Edwards. *Age ≤ 75 years. †Age > 75 years. to relatively frequent episodes of bleeding after valve replacement.[112] Endocarditis. The risk of endocarditis is also decreased after mitral valve repair compared with replacement. In the series of Duran et al,[91] infectious endocarditis occurred at a rate of 0.4% per year after repair and at 2.2% per year after replacement. Late endocarditis after mitral valve reconstruction is negligible, in contrast to the 3% to 6% incidence after mitral valve replacement. [111] Predictors of Postoperative Outcome and Survival As previously stated, patients with mitral chronic regurgitation who have reduced LV pump performance prior to surgery are at risk for a suboptimal postoperative outcome, characterized by persistent LV systolic dysfunction, congestive heart failure, and death. Presumably, operation in such patients mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 12 di 26 is being performed late in the hemodynamic course at a time when severe, irreversible contractile dysfunction has already developed. So, should surgery be performed "prophylactically" in all asymptomatic patients to prevent occult contractile dysfunction? The optimal time for surgery is at the onset of LV contractile dysfunction, justifying the surgical risk, but early enough in the course to be reversible. If it were possible to pinpoint this critical moment in the natural history of chronic mitral regurgitation, then it would be simple to plan the timing of surgery in these patients. Unfortunately, no variable that can be routinely measured in the clinical setting is able to define the precise onset of reversible contractile dysfunction in chronic mitral regurgitation. Several markers, however, have been identified that predict a poor outcome after mitral valve surgery. These variables, in conjunction with those that have recently been identified to predict an optimal outcome, can be used to provide a rational framework for the timing of surgery in this valve disease for the purpose of preservation of contractility. Table 18-5 summarizes the preoperative clinical, hemodynamic, angiographic, and echocardiographic parameters that have been used to predict postoperative outcome in patients with mitral regurgitation. Clinical Predictors. Among 177 surgically treated patients with mitral valve disease, Hammermeister et al[87] found age to be the only independent predictor of survival after mitral valve replacement. Patients older than 61 years had a 5-year survival rate of 40%, compared with 74% in patients 41 to 60 years old and 87% in patients younger than 40 years. In a study by Phillips et al,[8] patient age was also found to predict survival. Patients younger than 60 years at the time of surgery had a 5-year survival rate of 91%, compared with 72% for those 61 years old or older. In several studies by Enriquez- Sarano and colleagues,[5] [7] age was also found to be an important predictor of operative morality in patients undergoing mitral valve surgery. Operative mortality in elderly patients (older than 75 years) was 30.8% for valve replacement and 6.8% for valve repair versus 5.7% for valve replacement and 1.3% for valve repair in patients younger than 75 years of age. In addition to age, Enriquez-Sarano and colleagues[5] [6] [7] also found the following clinical variables to be predictive of overall survival, operative mortality, and postoperative LV ejection fraction in patients undergoing mitral valve replacement or reconstruction: creatinine (no level specified), New York Heart Association (NYHA) functional class greater than II, atrial mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 13 di 26 fibrillation, and concomitant coronary artery disease. Recently, in a study of 576 consecutive postoperative survivors, Dujardin et al[113] found that preoperative LV ejection fraction (<60%) and concomitant 398 TABLE 18-5 -- Surgery for Mitral Valve Regurgitation: Predictors of Mortality and Left Ventricular Dysfunction Predictor Value References Clinical Age > 60 years 8 > 75 years 5 NYHA functional class > Class II 5–7, 114, 116 Atrial fibrillation 5–7 Coronary artery disease 5–7 Hemodynamic Mean pulmonary artery > 20 mm Hg 4 pressure Cardiac index < 2.0 L/m/m2 116 LV end-diastolic pressure > 12 mm Hg 116 Catheterization 8 LV ejection fraction < 50% 19 End-systolic volume index ≥ 30 mL/m2 4 ≥ 50 mL/m2 62 ≥ 60 mL/m2 64 ES stress < 2.6 dyne × 103 /cm2 ES volume index mL/m2 Echocardiography LV ejection fraction < 50% 6 < 60% 7 < 63% 25 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 14 di 26 Fractional shortening < 31% 69 End-diastolic dimension > 70 mm 25 End-systolic dimension > 50 mm 25, 93 > 45 mm 6, 7 ≥ 40 mm 30 End-systolic dimension > 2.6 cm/m2 69 index End-systolic stress index > 195 mm Hg 69 Doppler-derived LV dP/dt < 1343 mm Hg/sec 118 Radionuclide Right ventricular ejection < 30% 119 fraction ES, end systolic; LV, left ventricular; NYHA, New York Heart Association. coronary artery disease were each positively associated with postoperative mortality and congestive heart failure. Ramanthan et al[114] likewise found NYHA functional class to be an important predictor of survival in medically treated patients with mitral regurgitation followed for a 4-year period, with mortality rates of 53% and 44% for class III and class IV patients, respectively. Similarly, in a recent study of 478 patients with organic mitral regurgitation corrected surgically, Tribouilloy et al[115] found preoperative functional class III/IV symptoms to be independently associated with decreased immediate and long-term postoperative survival. The excess mortality associated with NYHA class III/IV as compared to class I/II was demonstrated regardless of LV ejection fraction (Fig. 18-5) . These researchers concluded that surgical intervention should be considered when no or minimal symptoms are present in low operative risk patients. Salomon et al[116] retrospectively analyzed multiple patient-related risk factors to determine survival after mitral valve replacement in 897 patients, 240 with mitral stenosis, 352 with mitral regurgitation, and 305 with mixed stenosis and regurgitation. In addition to patient age of less than 60 years, preoperative NYHA class of III or lower, cardiac index of 2.0 or greater, and LV end-diastolic pressure of 12 or less were also found to predict improved perioperative as well as long-term survival. Similarly, Crawford et al[4] found that a mean preoperative pulmonary artery pressure of 20 mm Hg or greater predicted a reduced LV ejection fraction after mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 15 di 26 mitral valve replacement. Left Ventricular Ejection Fraction. Although it does not identify asymptomatic patients with early contractile dysfunction, LV ejection fraction has been used extensively to predict outcome after surgery. As mentioned earlier, Dujardin et al[113] found, in a study of 576 consecutive postoperative survivors of mitral valve surgery, that Figure 18-5 Overall survival is compared between patients in New York Heart Association (NYHA) class I/II and those in class III/IV who had a preoperative left ventricular ejection fraction (EF) of 60% or greater (A) or less than 60% (B). (From Enriquez-Sarano M, Tajik AJ, Schaff HV, et al: Circulation 1995;91:1022–1028.) 399 Figure 18-6 Postoperative survival following mitral valve surgery on organic mitral regurgitation based on patients' preoperative left ventricular ejection fraction is shown. (From Enriquez-Sarano M, Tajik AJ, Schaff HV, et al: Circulation 1994;90:830–837.) LV ejection fraction of 60% or greater was associated with improved survival (adjusted risk ratio 0.49) and reduced incidence of congestive heart failure (adjusted risk ratio 0.30). In a study by Enriquez-Sarano et al[7] of 409 patients with isolated mitral regurgitation undergoing mitral valve surgery, preoperative LV ejection fraction was found to be the most important predictor of long-term survival. Survival at 10 years was 72% for patients with a mean preoperative LV ejection fraction of 60% or greater, 53% for patients with an ejection fraction in the range of 50% to 60%, but only 32% percent for those with an ejection fraction of less than 50% (Fig. 18-6) . Enriquez-Sarano et al[6] also reviewed the echocardiographic predictors of postoperative LV pump performance in 266 patients undergoing mitral valve replacement for mitral regurgitation. Independent predictors of postoperative LV pump dysfunction (defined as an ejection fraction of less than 50%) included a preoperative LV ejection fraction of less than 50% or an end-systolic dimension of greater than 45 mm. Postoperative LV pump mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 16 di 26 dysfunction (ejection fraction of less than 50%) was associated with an increased mortality rate evidenced by an 8-year survival rate of 38% in patients with decreased postoperative LV ejection fraction, compared with 69% for patients with a postoperative LV ejection fraction of greater than 50%. In a study of 150 patients undergoing mitral valve replacement for isolated mitral regurgitation, Phillips et al[8] also demonstrated the value of preoperative LV ejection fraction in predicting long-term survival. Five- year survival rates for patients with a preoperative LV ejection fraction of 50% or greater, 40% to 49%, and less than 40% were 89%, 71%, and 38%, respectively. These data suggest that by the time LV ejection fraction had decreased to below the lower limits of normal, severe contractile dysfunction had already developed, and recovery was unlikely after surgery. Reduced LV ejection fraction, therefore, identifies patients who are likely to do poorly after surgery, but a normal LV ejection fraction does not distinguish between patients with normal contractility and those with occult early contractile dysfunction, who might benefit from prompt surgical intervention. Crawford et al[4] studied 48 patients with mitral regurgitation and 23 patients with mixed mitral stenosis and regurgitation to determine the role of LV size, pump performance, and clinical status in predicting survival and LV pump performance after mitral valve replacement. Mortality and increased NYHA functional class due to congestive heart failure were significantly higher in patients with mitral regurgitation and a postoperative LV ejection fraction of less than 50% and in patients with mixed stenosis and regurgitation and postoperative LV enlargement, defined by an end- diastolic volume index of greater than 101 mL/m2 . The strongest predictor of postoperative LV ejection fraction was the preoperative ejection fraction. Preoperative predictors of postoperative LV enlargement included an end- systolic volume index of greater than 50 mL/m2 and a mean pulmonary artery pressure of greater than 20 mm Hg. Similarly, Starling[30] studied 15 patients with chronic mitral regurgitation with micromanometer LV pressures and radionuclide angiograms for LV volumes over a range of loading conditions before and 1 year after successful mitral valve surgery. This study demonstrated that LV contractile impairment is reversible in many patients with chronic mitral regurgitation and that the best predictors of this reversibility include a normal preoperative LV ejection fraction and less LV dilation as manifest mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 17 di 26 by end-systolic volume (Fig. 18-7) . Thus, following mitral valve surgery for chronic mitral regurgitation, LV contractility improved in those patients |
with an average preoperative LV ejection fraction of 0.63 ± 0.09 and an end-systolic volume index of 44 ± 12 mL/m2 , whereas it remained abnormal in those patients with an LV ejection fraction of 0.49 ± 0.12 and an end-systolic volume index of 89 ± 28 mL/m2 . This implies that early surgical intervention can preserve LV contractility and portend an excellent long-term outcome in some patients with mitral regurgitation. 400 Figure 18-7 The left ventricular (LV) end-systolic pressure-volume relationship (Ees ) both before and after successful mitral valve surgery uncorrected (A) and corrected (B) for LV size is shown. A substantial increase in contractility occurs on the postoperative study compared with the preoperative study in the majority of patients, although a small group of patients shows either a decline or no change in this contractile index. *P < .05. (From Starling MR: Circulation 1995;92:811–818.) The percentage of fractional shortening has also been used to assess LV pump performance in mitral regurgitation. Zile et al[69] found that a preoperative fractional shortening of less than 31% predicted postoperative congestive heart failure and death after mitral valve replacement in patients with mitral regurgitation. Despite the fact that survival is decreased in patients with reduced LV pump performance, patients with a decreased LV ejection fraction have improved survival with surgery over medical therapy.[87] The 5-year survival rate in patients with a reduced LV ejection fraction (31% to 50%) was 82% with valve repair or replacement, compared with 45% for the medically treated group. The 10-year survival rate was 82% for the repair group, 74% for the replacement group, and less than 20% for medically treated patients. Therefore, despite reduced overall survival in patients with mitral regurgitation and impaired LV pump performance, mitral valve surgery, particularly valve repair, should not be withheld in this subset of patients, as survival is significantly worse with medical therapy alone. End-Systolic Dimension. Using two-dimensional echocardiography, Schuler et al[25] demonstrated the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 18 di 26 importance of the preoperative LV end-systolic dimension as a predictor of postoperative LV pump dysfunction in 16 patients with mitral regurgitation who underwent conventional mitral valve replacement. Group I consisted of those patients with a normal preoperative LV ejection fraction and mild LV enlargement; group II included those patients with a low normal LV ejection fraction and moderate LV enlargement. Postoperatively, at a mean follow-up of 15 months, group I patients demonstrated a significant decrease in mean echocardiographic LV end-diastolic and end-systolic dimension, a slight decline in LV ejection fraction, and regression of LV hypertrophy. In contrast, group II patients had no significant decrease in LV end-diastolic dimension, an increase in end-systolic dimension, and a marked reduction in LV ejection fraction. A preoperative LV end-diastolic dimension of greater than 70 mm, end-systolic dimension of greater than 50 mm, and LV ejection fraction of less than 55% identified the majority of patients with postoperative LV pump dysfunction and lack of regression of LV hypertrophy. Wisenbaugh et al[93] evaluated the outcome of 66 patients after mitral valve replacement with preservation of the submitral apparatus. At a mean follow-up period of 24 months, postoperative death or severe heart failure were predicted by a preoperative echocardiographic end-systolic dimension of 50 mm or greater. A preoperative LV end-systolic dimension of less than 40 mm identified all patients with an excellent postoperative outcome. The importance of echocardiographic end-systolic dimension in predicting adverse postoperative outcome has also been reported by Enriquez-Sarano and associates[6] [7] for an end-systolic dimension of greater than 45 mm and by Zile et al[69] for an end-systolic dimension index of greater than 26 mm/m2 . Similarly, in a recent study by Flemming et al,[117] 27 patients were evaluated with micromanometer LV pressures, radionuclide angiography, and echocardiographic parameters prior to and at 3 and 12 months after mitral valve surgery. They found that the most predictive echocardiographic indicator of early occult LV contractile dysfunction was an end-systolic dimension of 40 mm or more (Fig. 18-8) . This index was also able to predict a unique response to mitral valve surgery that was characterized by a short-term fall in LV pump performance, but a long-term recovery to normal LV pump performance, possibly because of a recovery of LV contractile function. They concluded that this measure may be useful to separate those with and without early occult LV contractile dysfunction and normal LV pump performance and to identify those patients who may mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 19 di 26 benefit from early mitral valve surgery with or without mild symptoms to preserve LV systolic performance. End-Systolic Volume. Borow et al[19] have evaluated the 401 Figure 18-8 Receiver operator characteristic curves were generated using sensitivity and 100-minus specificity for echocardiographic left ventricular (LV) end-systolic dimension (ESD), fractional shortening (FS), and end-diastolic dimension (EDD) to identify contractile dysfunction in mitral regurgitation (MR) patients with a normal LV ejection fraction. An LV ESD of 40 mm or greater was optimal for identifying patients with MR and a normal LV ejection fraction and early occult contractile dysfunction. (From Flemming MA, Oral H, Rothman ED, et al: Am Heart J 2000;140:476–482.) role of the preoperative end-systolic volume index as a predictor of postoperative LV pump performance and survival in chronic mitral regurgitation. Abnormal postoperative LV pump performance was predicted by a preoperative end-systolic volume index of greater than 60 mL/m2 . Furthermore, a preoperative end-systolic volume index of greater than 90 mL/m2 predicted increased postoperative mortality. Specifically, four of five patients with an end-systolic volume index of greater than 60 mL/m2 died in the perioperative period, whereas no patients with an end- systolic volume index of less than 60 mL/m2 died of cardiac failure. All patients with an end-systolic volume index of less than 60 mL/m2 achieved NYHA class I or II postoperatively. In the study by Crawford et al,[4] an end-systolic volume index of 50 mL/m2 or greater was similarly found to predict postoperative LV pump dysfunction. End-Systolic Wall Stress. In addition to an echocardiographic LV end-systolic dimension index of greater than 26 mm/m2 and percentage fractional shortening of less than 31%, Zile et al[57] have also demonstrated that an echocardiographic LV end-systolic wall stress index of greater than 195 mm Hg can be used to predict postoperative congestive heart failure and death after mitral valve replacement for chronic mitral regurgitation. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 20 di 26 End-Systolic Wall Stress/End-Systolic Volume Index. Variables predictive of reversible LV contractile dysfunction have been identified in mitral regurgitation, but such measurements have required complex invasive hemodynamic protocols. In a study of 21 patients with mitral regurgitation, Carabello et al[64] found that the ratio of end-systolic wall stress to end-systolic volume, a preload-independent index of contractility, was the best predictor of outcome after mitral valve replacement for mitral regurgitation. The end-systolic wall stress to end- systolic volume index was 5.6 in normal subjects, 3.3 in patients with a favorable postoperative outcome (NYHA class II or lower), and 2.2 in patients with an unfavorable postoperative outcome, including NYHA class III or IV symptoms or death. The fact that the absolute value of the ratio of LV end-systolic wall stress to end-systolic volume index was lower in patients with a favorable postoperative outcome than in normal subjects suggests that preoperative contractility was abnormal in this subset of patients with mitral regurgitation, but to an extent that did not adversely affect postoperative outcome. A significant decrease in the LV end-systolic wall stress to end-systolic volume index, on the other hand, appeared to identify a patient group with severe, irreversible contractile dysfunction. The LV end-systolic wall stress to end-systolic volume index may, therefore, be useful in identifying patients with early contractile dysfunction in whom timely operative intervention would be warranted. In a subsequent study, Carabello et al [62] further demonstrated that an end- systolic wall stress to end-systolic volume index ratio of 2.6 or less predicted poor surgical outcome, defined as postoperative death or NYHA class III or IV symptoms. Pressure-Volume Relationship. Starling et al[26] have demonstrated that the slope of the end-systolic pressure-volume relationship (chamber elastance), a load-independent measure of contractility, can be used to identify occult reversible contractile dysfunction in patients with mitral regurgitation who have a normal LV ejection fraction. Patients with a normal preoperative LV ejection fraction but impaired contractility (reduced elastance) had an initial decline in ejection fraction in the immediate postoperative period, but it improved within 1 year of surgery. In contrast, patients who had both impaired contractility and a reduced ejection fraction preoperatively had persistent postoperative LV pump dysfunction. These data suggested that the combination of abnormal elastance and normal ejection fraction can identify a patient group in whom contractile dysfunction is present but still mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 21 di 26 reversible. In this particular group of patients, prompt surgical intervention is indicated to avoid progression to irreversible dysfunction. Unfortunately, because measurements of elastance require complex hemodynamic protocols, elastance cannot be used as a routine tool for serial assessment of patients with mitral regurgitation. However, the information gained using elastance has helped to interpret the clinical data used to determine the appropriate timing for surgical intervention in patients with mitral regurgitation. In a preliminary analysis of patients with mitral regurgitation and normal LV ejection fraction, patients with impaired contractility could be separated from those with normal contractility on the basis of echocardiographic indices of LV size and performance.[117] An LV end-systolic dimension of greater than 40 mm approximated a reasonable separation of these patients and may, therefore, represent a reasonable surrogate for the elastance concept in patients with mitral regurgitation. Doppler-Derived dP/dt. The spectral velocity pattern of mitral regurgitation obtained by continuous wave Doppler echocardiography can also be used to assess LV systolic performance in mitral regurgitation. The spectral velocity curve represents the instantaneous pressure difference between the left ventricle and the left atrium. When systolic performance is reduced, the rate of rise of LV 402 Figure 18-9 Spectral Doppler signal of mitral regurgitation from a patient with depressed left ventricular function, demonstrating a slow rate of acceleration to peak regurgitant velocity, reflecting a low dP/dt. The dP/dt is estimated from the time interval (dt) required for the mitral regurgitant velocity to rise from 1 to 3 m per second. In this case, the dP/dt measured 800 mm Hg per second. pressure is decreased, resulting in a concomitant decrease in the rate of increase in the velocity of mitral regurgitation. The slope of the mitral regurgitant velocity curve, designated as dP/dt, is decreased when LV systolic performance is decreased (Fig. 18-9) . Pai et al [118] studied the Doppler-derived index of the rate of LV pressure rise (dP/dt) in 25 patients with mitral regurgitation before and 6.5 weeks after mitral valve surgery. The LV dP/dt was found to be the best independent predictor of postoperative LV ejection fraction. A preoperative dP/dt of 1343 mm Hg mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 22 di 26 per second or less predicted a postoperative ejection fraction of 50% or less. Right Ventricular Ejection Fraction. Hochreiter et al[119] assessed the prognostic importance of right ventricular ejection fraction in 35 medically treated and 21 surgically treated patients with chronic mitral regurgitation. Patients with a right ventricular ejection fraction of 30% or less had a markedly reduced 4-year survival rate (18%) when treated medically compared with those treated surgically (84%). Left Atrial Size. Reed et al[120] studied the role of left atrial size in predicting postoperative outcome in 176 symptomatic patients who underwent mitral valve replacement with a mean follow-up of 3.8 years. An abnormal left atrial size index (defined as the product of the major and minor atrial dimensions measured in the apical four-chamber view) was found to predict postoperative death. The left atrial size index, however, predicted mortality independent of LV systolic performance only in patients with a supernormal LV ejection fraction (>75%). Since patients with an LV ejection fraction in this range have an excellent prognosis, regardless of the left atrial size, this index appears to offer no additional prognostic information to LV systolic performance. Timing of Surgery Before discussing a rational approach to the proper timing of surgical intervention for chronic mitral regurgitation, the following key points should be emphasized: 1. Chronic severe mitral regurgitation leads to a progressive decline in LV pump performance. 2. Patients |
may remain asymptomatic with a normal LV ejection fraction for extended periods of time. 3. Occult contractile dysfunction generally develops at a time when patients remain asymptomatic and LV ejection fraction remains normal, and it may be reversible after surgical intervention. 4. Patients with normal LV ejection fraction and occult reversible contractile dysfunction who undergo mitral valve replacement or reconstruction have a favorable long-term prognosis. 5. Patients with LV pump dysfunction and irreversible contractile dysfunction are at risk for postoperative LV systolic dysfunction, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 23 di 26 death, and congestive heart failure. 6. Although reduced LV pump performance is associated with an overall decrease in long-term survival for patients with mitral regurgitation, survival is improved with surgical therapy compared with medical therapy. 7. Compared with conventional mitral valve replacement, mitral valve reconstruction preserves LV pump performance and reduces mortality and comorbid complications. 8. If feasible, mitral valve reconstruction should be the procedure of choice in patients with reduced preoperative LV pump performance. 9. Long-term postoperative LV pump dysfunction due to mitral regurgitation in children and young adults is rare, but it does occur. However, a shorter duration is associated with improved postoperative results. Since long-term survival in chronic mitral regurgitation is dependent on the contractile state of the left ventricle, the primary goal of surgical intervention should conceptually be to preserve contractility. All symptomatic patients with mitral regurgitation should be referred promptly for valve repair or replacement. It is often difficult for clinicians to justify referral of asymptomatic patients for surgical procedures that have a finite risk for death, even when the risk is small. The immediate operative and postoperative risks, on the one hand, must be balanced by the risk for progression to severe, irreversible contractile dysfunction and, thus, reduced long-term survival. Table 18-6 presents a proposed algorithm for the timing of surgery in patients with chronic mitral regurgitation, based on a system in which points are assigned to the different clinical variables that normally play a role in the decision-making process. The major components of the decision analysis, depicted in part A of the algorithm, include clinical and hemodynamic parameters, LV size and pump performance, and the feasibility of valve repair. The measured components of the algorithm, including LV ejection fraction and end-systolic dimension, were selected on the basis of ease and reproducibility of the measurements using two-dimensional echocardiography. The ability to repair a valve should be determined based on the anatomic and pathologic defects of the valve as defined by transesophageal echocardiography. The feasibility of valve repair, based on the echocardiographic findings, should then be determined in consultation with a surgeon experienced in valve reconstruction. In general, symptomatic patients with congestive heart mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 24 di 26 403 TABLE 18-6 -- Proposed Algorithm for Timing of Surgery in Patients with Mitral Regurgitation Part A: Assign a point score for each of the four designated categories. LV Function and Size EJECTION Clinical * FRACTION, END-SYSTOLIC Feasibility of Valve Points Symptoms % DIMENSION, mm Repair 0 None > 60 < 40 None 1 I/II 50–60 40–45 Possible 2 III/IV < 50 > 45 Definite Part B: Based on the total point score, follow suggested guidelines regarding timing of surgery. Total Points Decision Regarding Surgical Intervention 0–1 Delay surgery; recommend clinical and echocardiographic follow- up at 12 months 2 Borderline; recommend clinical and echocardiographic follow-up at 6 months ≥ 3 Proceed with surgery Part C: Although not essential for decision analysis, additional predictors of adverse outcome, all of which can be measured by two- dimensional echocardiography, can also be used to support decisions. Additional Predictors of Adverse Outcome in Aortic Regurgitation † Value Fractional shortening < 31% End-systolic volume index > 30 mL/m2 End-systolic stress index > 195 mm Hg End-diastolic dimension > 70 mm Doppler dP/dt of mitral regurgitant jet < 1343 mm Hg/sec Right ventricular ejection fraction < 30% mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 25 di 26 *Add one point for age > 60 and coronary artery disease; add three points for history of atrial arrhythmias. †Add two points for each predictor present. failure, decreased exercise tolerance, or atrial arrhythmias should be referred for surgery, regardless of the status of the left ventricle, particularly when mitral valve reconstruction can be performed. Asymptomatic patients with an LV ejection fraction in the low-normal range (<55%) or LV dilation with an end-systolic dimension of greater than 40 mm are likely to have contractile dysfunction and should, therefore, be referred for surgery. Asymptomatic patients with a high-normal LV ejection fraction (>60%) and small (<40 mm) end-systolic dimension can be followed clinically with serial echocardiography every 6 to 12 months for evidence of reduced exercise tolerance, declining LV ejection fraction, or increased end-systolic dimension. Any change from baseline may indicate the onset of contractile dysfunction, and patients should be referred for prompt surgical intervention. Parenthetically, symptoms in patients with chronic mitral regurgitation are sometimes subtle and difficult to elicit. They are normally fatigue, not dyspnea. Based on the outcome data, patients with early symptoms should also undergo surgery even if they do not meet these LV size and performance criteria. Recently, the natural history of chronic mitral regurgitation and its surgical correction were evaluated in children and young adults.[121] Although the early postoperative course of LV pump dysfunction in children parallels the course in adults, children usually demonstrate a late improvement in LV systolic performance. Thus, early surgical intervention in children without symptoms or LV pump dysfunction is not necessary for most children. However, the duration of mitral regurgitation is correlated with outcome; and for those children who will inevitably require mitral valve repair, operative intervention should be entertained prior to the onset of heart failure. Included in the algorithm in Table 18-6 are additional parameters that identify patients at high risk for contractile dysfunction and, therefore, can be used to strengthen decisions for surgical intervention. Although some of these predictors were validated using nonechocardiographic techniques, all parameters included in this part of the algorithm can be measured using two-dimensional echocardiography. Because more detailed measurements mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 26 di 26 and computations are required, most are not included as part of a routine echocardiographic report. These variables are not requisite components of the algorithm and should be considered adjunctive to decision making. Two case studies illustrate how this algorithm can be applied in the clinical setting. The first patient was a 32-year-old aerobics instructor referred for an evaluation of an asymptomatic murmur. Transesophageal echocardiography revealed mitral valve prolapse with a flail posterior leaflet and severe mitral regurgitation. The LV ejection fraction measured 65%, and the end-systolic dimension measured 38 mm. Using step A of the algorithm, this patient would be given a total of 2 points, based on the high feasibility of mitral valve repair. Given the normal LV end-systolic dimension and the high-normal ejection fraction, the possibility of occult contractile dysfunction in this patient was thought to be very small; therefore, surgery was deferred in this patient with follow-up performed 404 every 6 months. At 1-year follow-up, although the patient remained asymptomatic, the LV ejection fraction had decreased to 60% and the end- systolic dimension had increased to 42 mm, suggesting the onset of early contractile dysfunction. This patient was then referred for successful mitral valve reconstruction. The second patient was a 50-year-old woman with a history of rheumatic heart disease who presented with atrial fibrillation. Echocardiography revealed an LV ejection fraction of 55%, mild mitral stenosis with mild leaflet thickening, and severe mitral regurgitation. According to the proposed algorithm, the development of atrial fibrillation and the LV ejection fraction of 55% resulted in a total of 3 points, justifying operative intervention. Mitral valve repair in this particular case of rheumatic mitral regurgitation was considered possible but not definite; hence, this patient was referred for possible valve repair to be followed by valve replacement if reconstruction was unsuccessful. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/158.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 18 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Chronic Aortic Regurgitation Despite significant volume and pressure overload on the left ventricle, patients with aortic regurgitation typically remain asymptomatic for extended periods of time.[122] Symptoms of dyspnea, orthopnea, nocturnal angina, and syncope develop relatively late in the course of the disease. Aortic valve replacement has clearly been shown to prolong survival and improve functional class in patients with severe symptoms.[12] [123] [124] The optimal timing for valve replacement in asymptomatic or minimally symptomatic patients, however, is less concrete. Progression to contractile dysfunction may precede symptom onset; therefore, if symptom onset is used as the sole guide for surgical intervention, a small subset of patients will be at risk for LV dilation and pump dysfunction and, thus, congestive heart failure and death in the postoperative Figure 18-10 The relationship between left ventricular (LV) ejection fraction and total vascular load is shown in aortic regurgitation (AR) patients with normal LV contractility (solid circles) and depressed contractility (open circles). There was a significant difference between the slopes of these two relationships, indicating that in patients with AR and contractile dysfunction, the sensitivity of LV ejection fraction to total vascular load was greater than in patients with preserved contractility. (From Devlin WH, Petrusha J, Briesmiester K, et al: Circulation 1999;99:1027–1033.) period.[14] Fortunately, in contrast to mitral regurgitation, LV pump performance often improves postoperatively in patients with aortic regurgitation, even if depressed preoperatively.[1] [17] [125] , [126] Because afterload excess is primarily responsible for the initial decline in LV pump performance in aortic regurgitation, the decrease in afterload after aortic valve replacement favors postoperative improvements in LV systolic performance in the majority of patients. Although developing relatively late in the natural history of the disease, contractile dysfunction also contributes to LV pump dysfunction in aortic regurgitation and is associated with an mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 18 increased risk for postoperative morbidity and mortality. It is also apparent from one recent study[49] that LV loading conditions have a greater effect on LV pump performance in patients with contractile dysfunction compared with those with preserved LV contractility (Fig. 18-10) . So, should prophylactic aortic valve replacement be performed to preserve LV contractility? The benefits of preserving contractility, on the one hand, must be weighed against the immediate operative risks and the potential for bleeding, thromboembolism, and endocarditis associated with prosthetic valves.[127] [128] Ideally, to justify the surgical risk, the appropriate timing of surgery in patients with aortic regurgitation is at the onset of LV pump dysfunction, yet early enough to avoid the development of irreversible contractile dysfunction. Etiology Aortic regurgitation results from primary pathologic abnormality of the aortic valve leaflets (Fig. 18-11) or of the wall of the aortic root, or a combination of both abnormalities. [129] [130] Aortic root disease accounts for approximately one third of all patients with isolated aortic regurgitation, who ultimately undergo valve replacement. The 405 Figure 18-11 (color plate.) Transesophageal echocardiogram in the longitudinal plane (long-axis view) from a patient who presented with dyspnea on exertion several years after having been treated for aortic valve endocarditis. Demonstrated are focally thickened aortic valve leaflets with prolapse of the leaflets into the left ventricular outflow tract (A), resulting in severe aortic regurgitation (B). etiology of aortic regurgitation, grouped by the mechanism of regurgitation, is given in Table 18-7 . Natural History of Medically Treated Patients The clinical history of patients with chronic aortic regurgitation is characterized by a long asymptomatic phase, often lasting several decades, followed by a symptomatic phase with a relatively rapid progressive deterioration in clinical status.[86] [131] [132] [133] All patients with aortic regurgitation have reduced survival with medical therapy, with approximately 75% of patients alive at 5 years and 50% alive at 10 years after the initial diagnosis has been made.[79] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 18 Asymptomatic Patients. Asymptomatic patients with normal LV pump performance have an excellent |
long-term prognosis.[61] In a study of 77 asymptomatic patients with a normal LV ejection fraction, 90% of patients remained asymptomatic at 3 years; 81% at 5 years; and 75% at 7 years (Fig. 18-12) . The percentage of patients requiring aortic valve replacement was less than 4% per year. Data suggest that vasodilator therapy with nifedipine reduces LV dilation and hypertrophy in asymptomatic patients with aortic regurgitation who have normal LV TABLE 18-7 -- Mechanisms and Etiology of Aortic Regurgitation Mechanism Condition Inflammatory Rheumatic fever Syphilis Systemic lupus erythematosus Ankylosing spondylitis Reiter's syndrome Behçet's syndrome Takayasu's arteritis Methysergide therapy Structural Unicuspid, bicuspid, quadricuspid valves Annular dilation from aortic aneurysm Sinus of Valsalva aneurysm Fenestrated valve Destructive Infectious endocarditis Trauma Aortic dissection Congenital Marfan's syndrome Ventricular septal defect Pseudoxanthoma elasticum Osteogenesis imperfecta Mucopolysaccharidoses Ehlers-Danlos syndrome mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 18 Abnormal loading Hypertension conditions Renal failure Adapted from Alpert JS: Chronic aortic regurgitation. In Dalen JE, Alpert JS (eds): Valvular Heart Disease, 2nd ed. Boston, Little, Brown, 1987, pp 283–318. systolic performance.[133] [134] [135] [136] [137] [138] [139] [140] Furthermore, these beneficial hemodynamic effects have significantly delayed the need for aortic valve replacement in this subset of patients. Because afterload excess is the primary hemodynamic abnormality leading to LV pump dysfunction in chronic aortic regurgitation, the beneficial unloading effects of nifedipine can be anticipated in this setting. Figure 18-12 The clinical course of 77 asymptomatic patients with chronic aortic regurgitation and normal left ventricular (LV) function is presented from the time of initial diagnosis. Clinical end points include onset of symptoms or development of LV pump dysfunction. (From Bonow RO, Rosing DR, McIntosh CL, et al: Circulation 1981;68:509–517.) 406 In contrast to the excellent long-term prognosis of asymptomatic patients with normal LV pump performance, approximately 66% of asymptomatic patients with impaired LV function are likely to require surgery within 2 to 3 years.[13] [129] [130] Symptomatic Patients. Severely symptomatic patients with aortic regurgitation have a poor prognosis with medical therapy.[141] [142] [143] Only 4% of patients with NYHA class III or IV symptoms of congestive heart failure are alive at 10 years. Similarly, patients with both symptomatic congestive heart failure and LV pump dysfunction generally die within 2 years without surgical intervention. Patients with right-sided congestive heart failure have a particularly poor prognosis, with less than 10% of patients alive at 4 years. [144] Natural History of Surgically Treated Patients mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 18 Survival. Although there have been no randomized trials directly comparing medical therapy with surgery, surgical intervention appears to improve survival and functional class in patients with symptomatic aortic regurgitation. Rapaport [86] reported 5- and 10-year survival rates of 75% and 50%, respectively, for medically treated patients with aortic regurgitation. Operative and in- hospital mortality rates for symptomatic patients with chronic aortic regurgitation have ranged from 4% to 10%.[12] [124] [144] [145] Increased operative mortality after aortic valve replacement for aortic regurgitation is associated with advanced functional class (class III or higher), creatinine level greater than 3.0 mg/dL, and atrial fibrillation.[146] [147] Long-term survival after aortic valve replacement for aortic regurgitation is displayed in Table 18-8 . The observed variability in survival with surgery predominantly reflects the year of surgery, improvements in surgical technique in the later years, especially with regard to myocardial preservation using cardioplegic arrest, differences in patient populations, and the presence of concomitant coronary artery disease. Five-year survival rates after aortic valve replacement from studies published in the mid- 1980s have ranged from 82% to 83%.[12] [68] [148] The 10-year survival rate reported in only one of these studies was 65%.[148] Clinical Improvement. Aortic valve replacement results in significant relief of symptoms in the majority of TABLE 18-8 -- Survival After Aortic Valve Replacement for Aortic Regurgitation Survival Rate, % Study Patients, n 3-YEAR 5-YEAR 8- TO 10-YEAR. Hirshfeld et al[147] 88 55 48 48 Roberts et al[154] 26 76 65 58 Forman et al[123] 90 79 — — Clark et al[150] 17 61 — — Greves et al[124] 36 85 85 — Acar et al[144] 126 85 70 49 Louagie et al[148] 114 90 82 65 Bonow et al[12] 80 90 83 — mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 18 Taniguchi et al[168] 62 88 83 — patients.[12] [143] Whereas 70% to 80% of patients will have improvement in functional class, approximately 40% of patients will become completely asymptomatic. In contrast to the situation for chronic mitral regurgitation, the majority of patients with chronic aortic regurgitation demonstrate clinical improvement, despite NYHA class III or IV symptoms of congestive heart failure and a decreased LV ejection fraction.[149] Left Ventricular Pump Performance. Left ventricular pump performance typically improves after aortic valve replacement with correction of the volume and pressure overload.[14] [58] [150] , [151] Patients with normal preoperative LV ejection fraction generally have normal postoperative LV pump performance and an excellent long-term prognosis.[12] [14] [151] Unlike patients with chronic mitral regurgitation, the majority of patients with chronic aortic regurgitation who have a decreased preoperative LV ejection fraction often demonstrate significant improvements in LV pump performance after correction of the volume and pressure overload.[12] [15] [17] [58] , [63] [151] There is, however, a smaller subset of patients who have persistent LV systolic dysfunction postoperatively, suggesting the presence of irreversible contractile dysfunction.[12] [14] [15] [60] This group of patients has an extremely poor prognosis, with death often occurring from progressive congestive heart failure. Predictors of Outcome and Survival Clinical Predictors. Several clinical factors, the majority of which indirectly reflect long- standing volume and pressure overload on the left ventricle, have prognostic significance in chronic aortic regurgitation (Table 18-9) . Heart volume, indicated by the cardiothoracic ratio on the chest radiograph, has been shown to predict long-term survival.[126] [144] [152] In one study, patients with a cardiothoracic ratio of 0.58 or greater had a 5-year survival rate of only 48%, compared with 90% for patients with a ratio of less than 0.58. Earlier studies from the 1970s suggested that an age older than 65 years,[144] [153] electrocardiographic evidence of marked LV hypertrophy,[154] [155] NYHA class III or IV,[126] [154] and elevated systolic blood pressure (>140 mm Hg) or decreased diastolic pressure (<40 mm Hg)[156] identified patients at increased risk for postoperative death. In a recent study by Klodas et al [157] comparing postoperative survival in functional class I or II patients with mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 18 functional class III or IV patients, preoperative 407 TABLE 18-9 -- Surgery for Aortic Regurgitation: Predictors of Mortality and Left Ventricular Dysfunction Predictor Value References Clinical Age > 65 years 144, 153 Cardiothoracic ratio ≥ 0.58 126, 144, 152 NYHA functional class ≥ Class III 126, 153 Poor exercise tolerance < 8 METs 14, 158 Prolonged LV dysfunction > 18 mo 15 Electrocardiographic evidence of LV > 18 mo 147, 156 hypertrophy Hemodynamic LV end-diastolic pressure > 20 mm Hg 144 Cardiac index < 2.5 L/m/m2 123, 124 Catheterization LV ejection fraction < 50% 123 ≤ 45% 124 End-systolic volume index ≥ 60 mL/m2 19 ≤110 mL/m2 62, 168 Peak systolic pressure/End-systolic ≥ 1.72 mm 169 volume index Hg/mL/m2 Echocardiography Percentage fractional shortening < 25% 60 < 28% 66 < 29% 155 End-systolic dimension > 50 mm 66 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 18 > 55 mm 60 > 60 mm 63 End-systolic dimension index > 2.6 cm/m2 59 End-systolic wall stress > 235 mm Hg 66 End-systolic dimension > 80 mm 59, 60 > 72 mm 66 End-diastolic dimension (R) ≥ 3.2 66 End-diastolic wall thickness (th) ≥ 4.0 59 LV, left ventricular; NYHA, New York Heart Association. functional class III or IV symptoms were found to be independent risk factors for increased early and long-term postoperative mortality, suggesting that the onset of symptoms should warrant a rapid consideration of surgery. This is particularly true for women. Hemodynamic Predictors. Hemodynamic predictors of adverse postoperative outcome have also been used to stratify patients prior to aortic valve replacement. The 2-year survival rate in patients with a reduced cardiac index ( 2.5 L/m/m2 ) has been reported to be 72%, compared with 94% for those with a normal index.[144] In two other studies,[123] [124] survival rates at 3 and 5 years in patients with a cardiac index of 2.5 L/m/m2 or less were reported to be 63% and 66%, respectively. Elevated LV end-diastolic pressure of 20 mm Hg or greater has also been associated with increased mortality after aortic valve replacement.[144] Indices of Left Ventricular Systolic Performance in Symptomatic Patients Ejection Phase Indices! Left ventricular pump performance has been shown to be the most important determinant of survival in symptomatic patients with aortic regurgitation. [123] [124] , [153] Forman et al[123] found preoperative LV ejection fraction to be the most important determinant of survival in 90 patients with chronic aortic regurgitation who underwent valve replacement. Patients with an ejection fraction of less than 50% had a poor 3-year survival rate (64%) when compared with those with an LV ejection fraction of 50% or greater (91%). Greves et al[124] similarly demonstrated an adverse outcome mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 18 in patients with a reduced LV ejection fraction secondary to aortic regurgitation, reporting a 5-year survival rate of 54% in patients with an ejection fraction of 45% or less, compared with 87% for those with an ejection fraction of greater than 45%. Duration of Left Ventricular Systolic Dysfunction. In addition to decreased LV pump performance as an important predictor of adverse outcome in chronic aortic regurgitation, Bonow et al[15] have also demonstrated the impact of the duration of preoperative LV pump dysfunction in determining survival (Fig. 18-13) . Despite comparable reductions in LV fractional shortening and similar exercise tolerance, patients with prolonged LV systolic dysfunction (≥18 months) had a survival rate of only 45%, compared with 100% for patients with a more brief (<14 months) duration of LV pump dysfunction. Percentage of Fractional Shortening. Percentage of fractional shortening, an ejection phase index of LV systolic performance derived using two-dimensional or M-mode echocardiography, has also been used to predict postoperative death and LV systolic dysfunction in symptomatic patients with aortic regurgitation. Cunha et al [155] found that the postoperative 5-year survival rate was 100% in patients with a fractional shortening of greater than 35 percent, compared with a rate of 91% for a fractional shortening in the range of 31% to 35%, and a rate of 78% for a fractional shortening of 30% or less. In a study conducted by the National Institutes of Health,[14] a fractional shortening of less than 29% was associated with a 3-year survival rate of 62%, compared with 91% for a fractional shortening of 29% or greater. Similar data have been reported for a fractional shortening of less than 25%[60] and of 28% or less. [66] 408 Figure 18-13 Survival in aortic regurgitation after aortic valve replacement as a function of the duration of left ventricular (LV) dysfunction, demonstrating significantly reduced survival in patients with prolonged (>18 months) LV pump dysfunction. (From Bonow RO, Picone Al, McIntosh CL, et al: Circulation 1985;72:1244–1256.) Exercise Capacity. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 18 Preoperative exercise capacity has been shown to provide additional prognostic information to LV pump performance in aortic regurgitaton.[14] [158] Poor exercise tolerance (defined by the National Institutes of Health protocol, equivalent to approximately 8 metabolic equivalents [METs]) also predicts survival in symptomatic patients with aortic regurgitation. The 3- year survival rate in patients with preserved exercise capacity was 100%, compared with 52% for patients with reduced exercise tolerance. Exercise capacity further stratifies patients with concomitant LV pump dysfunction into low- and high-risk groups. Decreased exercise tolerance in patients with a decreased fractional shortening (<29%) identified a patient subgroup at significantly higher risk for postoperative LV pump dysfunction and death secondary to congestive heart failure (Fig. 18-14) . Survival at 3.5 years was 32% in this particular subgroup of patients. In addition to exercise capacity, the LV ejection fraction response to exercise has been used to evaluate functional reserve in symptomatic patients with aortic regurgitation.[47] [159] [160] [161] [162] [163] [164] [165] [166] [167] The majority of symptomatic patients with aortic regurgitation have an abnormal LV ejection fraction response to exercise; however, no specific level of reduced exercise performance has clearly |
been shown to predict survival or LV pump dysfunction in this patient population. Hence, the LV ejection fraction response to exercise in symptomatic patients provides no prognostic information in addition to resting LV ejection fraction and exercise capacity in determining outcome in chronic aortic regurgitation. The difficulty in assigning a specific cut-off level for exercise performance in aortic regurgitation relates to the fact that ejection phase indices of LV systolic performance are highly dependent on heart rate, preload, afterload, and contractility, all of which are altered during exercise.[18] End-Systolic Dimension. Henry et al[58] prospectively studied 50 patients with symptomatic aortic regurgitation prior to aortic valve replacement to define echocardiographic predictors of adverse postoperative outcome. Left ventricular end-systolic dimension of greater than 55 mm predicted postoperative congestive heart failure and death after aortic valve replacement. The survival rate at 3.5 years was 83% for patients with an end-systolic dimension of less than 55 mm, but only 42% for an end-systolic dimension of greater than 55 mm. Left ventricular end-systolic dimension of greater than 55 mm and a percentage fractional shortening of less than 25% identified a patient group at high risk for adverse outcome, with death occurring in 9 of 13 patients (69%) (Fig. 18-15) . More recently, Carabello et al[63] showed that mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 18 symptomatic patients with impaired LV pump performance and an end- systolic dimension of less than 60 mm have an excellent long-term survival and experience improvement in LV ejection fraction after aortic valve replacement. In patients 409 Figure 18-14 Survival in symptomatic patients with aortic regurgitation and reduced preoperative echocardiographic left ventricular (LV) fractional shortening (<29%) presented as a function of the preoperative exercise capacity. Patients able to complete 22.5 minutes of the National Institutes of Health protocol had significantly improved survival compared with patients with impaired exercise capacity, despite similar reductions in LV function. (From Bonow RO, Rosing DR, Kent KM, et al: Am J Cardiol 1982;50:325– 336.) with a reduced LV ejection fraction preoperatively, an end-systolic dimension of less than 60 mm correlated with a postoperative ejection fraction of 55%. End-Systolic Volume Index. Borow et al[19] studied 41 symptomatic patients with mitral or aortic regurgitation and found that a normal preoperative LV end-systolic volume index predicted normal postoperative LV pump performance and improvement in symptoms to NYHA functional class I or II. For the subset of patients with chronic aortic regurgitation, an end-systolic volume index of 90 mL/m2 or greater identified patients at higher risk for postoperative death and persistent LV pump dysfunction. Similar findings were reported by Carabello et al[62] Figure 18-15 The relationship between preoperative echocardiographic left ventricular (LV) fractional shortening and end-systolic dimension in determining prognosis in symptomatic patients after aortic valve replacement for chronic aortic regurgitation is illustrated. The 97% confidence intervals for normal subjects are indicated by the elliptical area. The high- risk area defined by an LV end-systolic dimension of greater than 55 mm and fractional shortening of less than 25% identifies patients at risk for postoperative death. (From Henry WL, Bonow RO, Borer JS, et al: Circulation 1980;61:471–483.) for an end-systolic volume index of greater than 110 mL/m2 and by Taniguchi et al[168] for an end-systolic volume index of greater than 200 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 12 di 18 mL/m2 . In these two studies, the greater degree of preoperative LV pump dysfunction tolerated without adversely affecting outcome has been attributed to improved surgical techniques in more recent years, particularly with regard to myocardial preservation during cardiopulmonary bypass. End-Diastolic Dimension. Echocardiographic LV end-diastolic dimension has also been used to determine prognosis in aortic regurgitation, but it is less sensitive than end- systolic dimension in predicting postoperative outcome. A preoperative end-diastolic dimension of greater than 80 mm has been shown to identify a subset of patients with severe preoperative LV enlargement at risk for persistent postoperative LV dilation and congestive heart failure.[59] [60] Although it is less useful as a preoperative predictor, a postoperative end- diastolic dimension of greater than 70 mm identified patients at significant risk for postoperative death from congestive heart failure.[60] End-Diastolic Radius–to–Wall Thickness Ratio. The end-diastolic radius–to–wall thickness ratio, measured by two- dimensional echocardiography, has also been used to predict outcome in aortic regurgitation. The ratio of LV dimension reflected in radius (r) to wall thickness (th) at end-diastole is linearly related to the ratio of LV volume to mass and has been used to determine the degree to which mass is appropriate for a given volume. In patients with chronic aortic regurgitation, the degree of LV dilation may exceed the limit of compensatory LV hypertrophy, resulting in significant LV dilation and pump dysfunction and an increase in the r/th ratio. Gaasch et al,[59] in 12 patients with chronic aortic regurgitation who underwent aortic valve replacement, found that a r/th ratio of 4.0 or greater identified all four patients who showed no reduction in LV dimension or mass postoperatively. Similarly, Kumpuris et al [66] demonstrated that a r/th ratio of 3.2 or greater predicted persistent postoperative LV dilation. Pressure-Volume Relationship. 410 The slope of the LV end-systolic pressure-volume relationship is a load- independent measurement of contractility that is commonly employed to assess contractile state in valvular regurgitation. Starling et al[11] have used the slope of the pressure-volume relationship and the circumferential stress- mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 13 di 18 shortening relationship (the ratio of end-systolic stress to ejection fraction) in patients with aortic regurgitation to differentiate reversible from irreversible LV pump dysfunction. As noted previously, although afterload excess is responsible for the early decline in LV pump dysfunction in aortic regurgitation, contractile dysfunction also contributes to pump failure, but late in the course of the disease. Starling et al[11] demonstrated that the severity of preoperative contractile dysfunction determined recovery of LV ejection fraction. LV pump performance recovered postoperatively in the group of patients with less severe contractile dysfunction, in whom afterload excess predominated, but failed to recover in patients with more severe contractile dysfunction. Unfortunately, measurements of the slope of the end-systolic pressure-volume relationship and circumferential stress- shortening relationship require complex, invasive, hemodynamic protocols; therefore, these indices cannot be routinely applied in most clinical settings. However, assessment of contractility using these techniques is important in that it provides the framework for timing of surgery using noninvasive modalities. To simplify the measurement of the end-systolic pressure-volume relationship, the ratio of the peak systolic pressure to end-systolic volume generated from a single point at rest has also been used to demonstrate abnormal contractility in patients with aortic regurgitation.[70] [169] Pirwitz et al[169] found the ratio of peak systolic pressure to end-systolic volume to be the strongest predictor of postoperative outcome in 27 patients with aortic regurgitation and LV dilation with an end-diastolic volume of greater than 60 mL/m2 . A ratio of 1.72 mm Hg/mL/m2 or greater identified all patients with postoperative functional class I or II, whereas a ratio of less than 1.72 identified 31% of patients in class III and 8% (n = 1) of patients who died. Indices of Systolic Left Ventricular Performance in Asymptomatic Patients Ejection Phase Indices. As previously noted, asymptomatic patients with normal LV pump performance have an excellent long-term survival rate, and less than 4% of patients per year require aortic valve replacement.[61] Asymptomatic patients with impaired LV ejection fractions, on the other hand, have a considerably more aggressive clinical course and should be referred for elective aortic valve replacement to avoid progression to irreversible contractile dysfunction. Several investigators have evaluated the LV ejection fraction response mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 14 di 18 during exercise as a way of predicting the onset of resting LV pump dysfunction in asymptomatic patients with aortic regurgitation.[160] [166] [170] Using radionuclide angiographic techniques, Borer et al[160] evaluated 22 asymptomatic patients with aortic regurgitation to assess LV ejection fraction reserve during exercise. Of the 21 patients (95%) with a normal resting LV ejection fraction, 9 patients (43%) had an abnormal LV ejection fraction response to exercise. The authors concluded that exercise-induced LV systolic dysfunction may precede the development of symptoms and abnormal resting LV pump performance and, therefore, may be used to follow patients for clinical deterioration. Although a decrease in LV ejection fraction with exercise may precede the onset of resting LV pump dysfunction in patients with aortic regurgitation, an abnormal exercise response does not necessarily portend a poor surgical or adverse postoperative outcome. End-Systolic Dimension. To predict the subset of asymptomatic patients with aortic regurgitation likely to develop symptoms or require aortic valve replacement, Henry et al [142] studied 37 asymptomatic patients with serial echocardiograms for a mean of 34 months. The need for subsequent operative intervention was best predicted by the preoperative LV end-systolic dimension.[59] Eighty percent of patients with an end-systolic dimension of greater than 55 mm required surgery within the follow-up period, compared with 20% of patients with an end-systolic dimension of less than 55 mm. Left ventricular end-systolic dimension has also been used to predict asymptomatic patients likely to require aortic valve replacement. No patient with an LV end-systolic dimension of 40 mm or less required aortic valve replacement at 4 years, whereas 65% of patients with an end-systolic dimension of greater than 50 mm required surgery within the follow-up period. Pressure-Volume Relationship. The slope of the LV end-systolic pressure-volume relationship has also been used to demonstrate abnormal contractility in asymptomatic patients with aortic regurgitation.[70] [71] [167] [171] Schuler et al[71] studied 14 asymptomatic patients with chronic aortic regurgitation and found that the slope of the end-systolic pressure-volume relationship could be used to identify contractile dysfunction in patients with preserved exercise tolerance and a normal LV ejection fraction. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 15 di 18 Timing of Surgery in Chronic Aortic Regurgitation In considering the timing for surgical intervention in these patients, several facts should be re-emphasized: 1. Chronic aortic regurgitation leads to a progressive decline in LV pump performance secondary to afterload excess. 2. Subclinical LV contractile dysfunction may develop when the LV ejection fraction remains normal, although unlike in patients with mitral regurgitation, LV ejection fraction in aortic regurgitation generally improves after valve replacement. 3. Asymptomatic patients with a normal LV ejection fraction have an excellent long-term prognosis with medical therapy. 4. Asymptomatic patients with normal LV pump performance should be treated with afterload reduction to delay the progression of LV dilation and the need for aortic valve replacement. 5. Valve replacement in symptomatic or asymptomatic patients with mild or moderately depressed LV pump 411 performance improves survival over medically treated patients with aortic regurgitation. 6. Severe preoperative contractile dysfunction is associated with persistent LV dilation and pump dysfunction, often resulting in postoperative congestive heart failure and death. 7. NYHA functional class III and IV symptoms are independently associated with increased early and long-term postoperative death. TABLE 18-10 -- Proposed Algorithm for Timing of Surgery in Patients with Aortic Regurgitation Part A: Assign a point score for each of the four designated categories. LV Function and Size Clinical EJECTION END-SYSTOLIC Exercise Points Symptoms * FRACTION, % DIMENSION, mm Capacity † 0 None > 60 < 45 Preserved 1 I/II 50–60 45–55 2 III/IV < 50 > 55 Decreased mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 16 di 18 Part B: Based on the total point score, follow suggested guidelines regarding timing of surgery. Total Points Decision Regarding Surgical Intervention 0–1 Delay surgery; clinical and echocardiographic follow-up at 12 mo 2 Borderline; recommend clinical and echocardiographic follow-up at 6 mo ≥ 3 Proceed with surgery Part C: Although not a requisite part of the algorithm, these additional predictors of adverse outcome can also be used in decision analysis. These variables marked with a double-dagger (‡) can be measured by two-dimensional echocardiography. Additional Predictors of Adverse Outcome in Aortic Regurgitation ‡ Value Percentage fractional shortening < 29% End-systolic volume index > 60 mL/m2 End-systolic wall stress > 235 mm Hg End-diastolic dimension > 80 mm End-diastolic dimension (radius) (R)/End-diastolic wall ≥ 3.2 thickness (th) *Add one point for age > 65; cardiothoracic ratio 0.58; LV hypertrophy on electrocardiogram. †Preserved = ability to complete at least 8 METs on graded exercise treadmill testing or stable exercise performance; Decreased = inability to complete 8 METs on graded exercise treadmill testing or a decline in exercise performance from an established baseline. ‡Add |
two points for each additional predictor present. In aortic regurgitation, the timing of surgery in both asymptomatic and symptomatic patients is relatively straightforward. In general, the majority of symptomatic patients have improved survival, functional class, and LV pump performance with aortic valve replacement; therefore, they should be referred promptly for aortic valve replacement, regardless of the status of LV ejection fraction. Asymptomatic patients with impaired LV pump mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 17 di 18 performance have a rapidly progressive course and are likely to develop symptoms and require aortic valve replacement within 2 to 3 years. These patients should be referred for elective aortic valve replacement. Asymptomatic patients who have normal exercise tolerance and preserved LV pump performance can be treated medically and followed closely with serial noninvasive assessments of LV ejection fraction. Left ventricular end-systolic dimension and exercise capacity are parameters that can be used to serially assess asymptomatic patients with aortic regurgitation for the development of LV pump dysfunction. A poor or decreasing exercise tolerance, defined as the inability to complete approximately 8 METs on a graded exercise treadmill test or any decline in LV pump performance from a previously established baseline, may signal the onset of LV decompensation. Similarly, patients who develop a progressive increase in end-systolic dimension likely have contractile dysfunction and, therefore, should be referred for surgery. Given that functional class III and IV symptoms are independent predictors of early and long-term postoperative mortality, patients with class II symptoms should be referred for surgical correction before class III or IV symptoms develop. Table 18-10 presents guidelines in the form of an algorithm for timing of surgery in patients with chronic aortic regurgitation based on a system in which points are assigned to different clinical variables. The major components (part A) of this algorithm include hemodynamic variables, including LV ejection fraction, LV size, and exercise capacity. The measured components of the algorithm, including LV ejection fraction and end-systolic dimension, were chosen on the basis of ease and reproducibility of the measurements using two-dimensional echocardiography. Included in this algorithm (part B) are additional parameters, all of which can be measured using two-dimensional echocardiography, that identify patients at high risk for contractile dysfunction. These parameters may, therefore, be used to confirm a decision to proceed with surgery, but they are not considered requisite components of the algorithm. These variables should be considered only supplemental to the decision-making process. The use of this algorithm to gauge the appropriate 412 timing of surgical intervention in aortic regurgitation is illustrated in the following case study. The patient was a 45-year-old construction worker mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 18 di 18 with severe aortic regurgitation secondary to a bicuspid aortic valve. At the time of initial evaluation, the patient was able to complete stage III of a Bruce protocol without symptoms. Echocardiographic LV end-systolic dimension measured 45 mm, and the LV ejection fraction measured 55%. According to the algorithm, the patient would be assigned two points, justifying medical therapy with serial clinical and echocardiographic follow-up. The patient was treated with a vasodilator and followed every 6 months for 1 year, and then yearly thereafter. At 5 years after the initial diagnosis, although the patient remained asymptomatic, echocardiography revealed an increase in the LV end-systolic dimension to 55 mm and a decrease in the LV ejection fraction to 48%, resulting in a total of 3 points. The patient was then referred for successful aortic valve replacement. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/159.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Summary After a long asymptomatic period, often lasting several years, severe, chronic mitral and aortic regurgitation eventually lead to reduced LV pump performance. In aortic regurgitation, decreased LV ejection performance is predominantly caused by afterload excess until late in the course of the disease, when contractile dysfunction supervenes. In contrast, contractile dysfunction occurs early in the course of mitral regurgitation, but it is masked by the favorable preoperative loading conditions. For both conditions, the development of irreversible contractile dysfunction is associated with increased risk for postoperative LV pump dysfunction and death from congestive heart failure. To justify the risk of surgery, the ideal timing for surgical intervention in patients with valvular regurgitation is, therefore, at the onset of contractile dysfunction, yet early enough to prevent the development of irreversible contractile dysfunction. Two-dimensional echocardiography, in conjunction with a thorough history and physical examination, provides an accurate, reproducible, and cost- effective methodology for the serial screening for the development of contractile dysfunction in patients with valvular regurgitation. In this chapter, all of the major predictors of clinical outcome in valvular regurgitation, including those validated from nonechocardiographic methodologies, have been integrated to create the pathophysiologic framework necessary to develop algorithms for timing of surgical intervention using echocardiographic tools. The proposed algorithms for timing of surgery in patients with chronic mitral and aortic regurgitation guide operative intervention to preserve contractility and thereby improve long-term postoperative outcome and minimize unnecessary risk. MD Consult L.L.C. http://www.mdconsult.com mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company 417 Chapter 19 - Echocardiography in Patient Selection, Operative Planning, and Intraoperative Evaluation of Mitral Valve Repair Brian P. Griffin MD William J. Stewart MD The advent of transesophageal echocardiography (TEE) and innovations in ultrasound technology have led to progressive improvement in the outcomes of valve surgery, especially mitral valve repair. Echocardiography has been used extensively in the operating room since the early 1980s. It is an essential element of every valve reconstruction operation. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/162.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 4 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Indications for Intraoperative Echocardiography Intraoperative echocardiography has both diagnostic and monitoring functions that are useful in mitral valve repair and other valve-sparing operations. The diagnostic functions are used before cardiopulmonary bypass (prepump) to determine the mechanism and severity of the mitral valvular dysfunction, identify lesions of other valves, and refine the surgical mission. The diagnostic functions are used after cardiopulmonary bypass (postpump) to determine the success of the surgical mission. Intraoperative echocardiography is essential in performing valve repair, aortic homograft, and pulmonary autograft implantation.[1] In addition to its use in valve surgery, the diagnostic function of intraoperative echocardiography also is used in the surgical management of congenital heart disease, [2] [3] hypertrophic cardiomyopathy,[4] [5] reconstruction of the ascending aorta,[6] [7] and many other surgeries (Table 19-1) . [8] The monitoring function of intraoperative echocardiography is used to determine the hemodynamic status of the patient before and after surgery, for assessing intravascular volume, and ventricular contractility. Perioperative monitoring of left ventricular function is important in patients with impaired contractility who are undergoing any kind of cardiac surgery, including myocardial revascularization, [9] [10] and in those with significant cardiac disease undergoing high-risk noncardiac surgery such as reconstructive surgery of the descending thoracic and abdominal aorta[11] [12] [13] (see Chapter 3) . Intraoperative echocardiography also is used to help position intravascular and intracardiac catheters,[14] , [15] including those used for retrograde cardioplegia via the coronary sinus. When postpump echocardiography detects intracardiac air, [16] [17] this can be cleared by further venting of the cardiac chambers to prevent embolization to the coronary blood vessels[18] 418 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 4 TABLE 19-1 -- Indications for Intraoperative Echocardiography Mitral Disease Assess feasibility and success of mitral repair for mitral regurgitation. Assess feasibility and success of commissurotomy for mitral stenosis. Determine need for mitral surgery in patients undergoing revascularization or aortic surgery. Assess presence of disease of other valves or other cardiac structures. Aortic Disease Assess feasibility and success of aortic valve repair. Assess size of prosthesis. Assess feasibility and success of homograft implantation or Ross procedure. Tricuspid Disease Assess need for and feasibility and success of tricuspid repair. Prosthetic Function Determine presence and site of paravalvular leak. Assess perivalvular tissue for abscesses or infection. Assess site and presence of pannus or thrombus. Revascularization Assess regional wall motion and global left ventricular function before and after revascularization. Determine sequence of graft placement. Detect and assess complications of infarction (ventricular septal defect, mitral regurgitation). Surgery on Aorta Assess size and extent of aneurysm. Determine the mechanism and severity of associated aortic regurgitation. Determine presence and complications of aortic dissection. Determine presence and extent of aortic atheroma. Transplantation/Devices mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 4 Assess left ventricular function and suture lines postoperatively. Assess appropriate sizing, function, and hemodynamic changes with ventricular assist devices. Congenital Heart Surgery Determine connections (ventriculoarterial, atrioventricular). Assess systemic and nonsystemic ventricular size and function. Assess anatomy of shunts and valvular anatomy. Monitoring Assess ventricular volume and function. Monitor drug effects on ventricular function. Diagnose presence and location of ischemia. or the brain.[19] In patients who are difficult to wean off cardiopulmonary bypass or who remain hypotensive in the early postoperative period, echocardiography is a useful diagnostic and monitoring tool.[20] [21] More recent indications for intraoperative echocardiography include use in patient selection and monitoring for alternative surgical approaches such as the use of smaller incisions, port access techniques for cannulation, and off- pump coronary artery grafting without cardiopulmonary bypass. [22] [23] The most frequent indication for intraoperative echocardiography is the postpump assessment of valve reconstruction surgery to determine whether the desired surgical result has been obtained. The availability of online feedback concerning the adequacy of the surgical result has allowed surgeons to become more innovative in repair techniques. Immediately after valve repair and before the chest is closed, the echocardiographer can determine whether the repair is adequate or if there is residual regurgitation or other complications present, requiring further repair or prosthetic implantation. Making this determination before the chest is closed allows the surgeon to perform further surgical procedures during a second run of cardiopulmonary bypass (a "second pump run") to optimize the surgical outcome. This second pump run eliminates the need for another surgical procedure at a later time, which would require another thoracotomy and create an increased mortality risk for the patient. In one study, 11% of patients undergoing valve surgery had inadequate results based on postpump echocardiographic imaging and required further surgery.[24] In our experience, intraoperative echocardiographic findings require a second pump run in 6% of cases.[1] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 4 It is axiomatic that all elective patients undergoing cardiac surgery have a full diagnostic work-up and a definite surgical plan before arriving in the operating room. Despite this, there are findings on the prepump echocardiogram that alter management by refining the preoperative diagnosis and the surgical mission. In our unpublished series of 436 consecutive prepump echocardiograms in patients with various valve problems, the surgical procedure was changed in 40 cases (9.2%). In a series of 154 consecutive patients undergoing valvular surgery, 29 patients (19%) had significant new findings by prepump intraoperative echocardiography. These findings changed the operative plan in 14 patients (9%). The changes were more common in mitral than aortic operations. The most frequent additional finding in this study was an increase in the severity of the valvular regurgitation compared with preoperative studies.[24] Even in patients in |
whom no major change in plan occurred, the prepump echocardiogram provided an updated understanding of the specific valvular anatomy and the mechanism of dysfunction, which helped to refine the surgical technique. These changes result from the improvement in resolution of TEE over preoperative transthoracic echocardiography (TTE) or cardiac catheterization and from changes in hemodynamic conditions or ischemia between the time of preoperative testing and the time of surgery. A 1999 study of 1918 consecutive cases in which intraoperative echocardiography was used showed a very low prevalence (2.5%) of discordant findings by echocardiography compared with operative findings. In only 0.3% of patients were the discrepancies sufficiently severe to warrant a change in the operative procedure. [25] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/163.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 7 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Technique of Intraoperative Echocardiography Intraoperative echocardiography may be performed from either the transesophageal or epicardial imaging windows (Table 19-2) . Transesophageal Echocardiography TEE is the most widely used technique for intraoperative echocardiography. Figure 19-1 illustrates the experience with intraoperative echocardiography at the Cleveland Clinic Foundation from 1984 through 1999. TEE became available in 1987 and progressively supplanted the epicardial route for most studies. Compared with epicardial echocardiography, TEE has the advantage of allowing image acquisition without interfering with the surgical field or procedure. Immediately after induction 419 TABLE 19-2 -- Relative Advantages of Epicardial and Transesophageal Approaches to Intraoperative Echocardiography Epicardial Transesophageal INDICATIONS LVOT gradients; HOCM; All others congenital, aortic atheroma; TEE impossible or nondiagnostic TRANSDUCER 3.5–7.5 MHz transthoracic 3.5–7.5 MHz (standard TTE) sector scan transesophageal ADVANTAGES Excellent images, especially Does not interfere with of LVOT and septum; rapid sterile field; continuous imaging in emergency imaging possible mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 7 DISADVANTAGES Requires plastic covers for May be difficult to sterile preparation of probe; intubate esophagus once interferes with operative patient is draped; field and procedure; imaging occasionally impossible to of posterior structures obtain images (e.g., due to difficult with prosthetic hiatal hernia, air), imaging shadowing; may interfere of anterior structures with hemodynamics; difficult requires >1 person HOCM, hypertrophic obstructive cardiomyopathy; LVOT, left ventricular outflow tract; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography. of anesthesia and endotracheal intubation, the TEE probe is inserted and left in place throughout the operation. Although the technique of intraoperative TEE is similar to its use in the echocardiography laboratory, there are additional potential pitfalls. First, it is occasionally difficult to pass the probe, particularly if the patient has been draped and the ether screen has been positioned. Usually, Figure 19-1 Cleveland Clinic Foundation experience with intraoperative echocardiography from 1984 to 1999. The total number of intraoperative echocardiograms per year is shown (bars). this problem can be overcome using a laryngoscope and direct vision. Inadequate imaging occurs with the transesophageal approach for a number of reasons. Anatomic causes include a hiatal hernia or the presence of an echodense structure such as a mechanical valve prosthesis can cause shadowing of other cardiac structures. With all TEE studies, there is a "blind spot" approximately 2 to 4 cm in size in the middle portion of the ascending aorta caused by interposition of the trachea between the esophagus and the ascending aorta. Interference from electrical apparatus such as electrocautery leads to distortion of two-dimensional imaging and renders spectral and color Doppler signals impossible to interpret. Fortunately, imaging may be resumed once the electrocautery is discontinued. Another potential cause of ultrasonic probe dysfunction in the operating room is the thermistor in the transesophageal probe, which can sense an elevated esophageal temperature and cause the probe to stop mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 7 functioning. This safety feature, designed to minimize the risk of esophageal damage from excess heat buildup in a malfunctioning probe, may deactivate the TEE transducer while the heart is being rewarmed after surgery. Newer probes have a mechanism whereby the probe temperature can be reset to take into account the patient's temperature. Finally, while the heart is on cardiopulmonary bypass, the absence of cardiac motion causes suboptimal images until the heart is filled with blood again and starts to eject during rewarming. Epicardial Echocardiography In epicardial imaging, images of the heart are acquired by placing a standard transthoracic transducer directly on the epicardium. Sterility is maintained using a double plastic sleeve. Intervening air is eliminated by using sterile acoustic gel inside the layers of plastic and by moistening the epicardial surface. An acoustic standoff such as a sterile bag or glove filled with saline is sometimes used if the structures of interest are superficial, in the first centimeter of depth below the probe. Epicardial echocardiography often provides better image quality than TEE of structures such as the ascending aorta, aortic arch, and left ventricular outflow tract, and it is especially accurate in measuring the outflow tract velocities. We use an epicardial approach when images obtained by TEE are inadequate during an open-chest procedure. Similarly, TTE can be used when needed during closed-chest procedures, including most types of noncardiac surgery. In addition, epicardial imaging is needed in infants who are too small for the available TEE probes. In the experience at the Cleveland Clinic Foundation, progressively fewer procedures are performed using an epicardial imaging window. The major current indication for an epicardial approach is in the evaluation of the ascending aorta of patients with suspected ascending atheroma, on the basis of clinical suspicion, calcification on chest x-ray study, or palpation by the surgeon. Identification of the severity and location of atheroma helps the surgical team optimize the location and methods of cannulation, 420 including the use of an alternative cannulation site such as the subclavian artery. In 1987 we described the following four standard imaging windows (Fig. 19-2) to be useful for epicardial imaging:[26] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 7 1. Parasternal equivalent. The transducer is placed on the most anterior portion of the heart, the right ventricular outflow tract. Image planes are similar to those for transthoracic imaging from the left parasternal imaging window. Both long-axis and short-axis views are obtained. The heart is scanned in the short axis from base to apex. By imaging more medially, the tricuspid valve and right ventricle also may be imaged. 2. Aorta-pulmonary sulcus. The transducer is placed in the sulcus between the pulmonary artery and ascending aorta, with the long side of the transducer against the left side of the ascending aorta. This view provides excellent images of the left ventricular outflow tract, aorta, aortic valve, mitral valve, and left atrium. 3. Subcostal equivalent. The transducer is at the most inferior portion of the thoracotomy incision against the most inferior portion of the right ventricular free wall. The four-chamber view is used to evaluate all four chambers, mitral and tricuspid valves, pulmonary artery, and the systemic veins. Angling medially allows imaging of the venae cavae, atria, and atrial septum. Angling superiorly visualizes the right ventricular outflow tract. Angling laterally brings in the left ventricular apex. 4. Aorta-superior vena cava position. The long side of the transducer is placed against the right side of the ascending aorta, pointing inferiorly and to the left, to image the left ventricular outflow tract and the aortic and mitral valves. This view is the best way to determine left ventricular outflow gradients with the continuous wave Doppler beam parallel to flow. The left atrium is also well seen from this view. Figure 19-2 The four standard positions for epicardial transducer placement. (From Cosgrove DM, Stewart WJ: Curr Probl Cardiol 1989;XIV:359–415.) The epicardial window allows excellent imaging of intracardiac structures such as the cardiac valves and myocardium. High-velocity jets may be measured by continuous wave Doppler either with an imaging transducer or a stand-alone, nonimaging transducer. The epicardial window also has some disadvantages: 1. It enters the operative field and interrupts the operation itself. For this mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 7 reason, a more limited time is available for imaging. 2. Imaging of structures in the near field may be difficult unless a good acoustic standoff is achieved. 3. Most surgeons and individuals that are accustomed to scrubbing for surgery are not adept at image acquisition with a hand-held transducer or echocardiographic anatomy, which requires a substantial learning curve. 4. If the probe is applied too heavily against the heart, it may cause arrhythmias or transiently interfere with cardiac filling. Equipment Ideally, an ultrasound machine devoted solely to intraoperative echocardiography should be available. In addition to interfacing with transesophageal and transthoracic transducers, the machine should be capable of recording M-mode and two-dimensional imaging and all Doppler modalities. A facility should be available near the operating room for cleaning and disinfecting the probes. Transthoracic probes from 3.0 to 7.5 MHz may be useful for different purposes, depending on the objectives of the study, using the lower frequency for general cardiac imaging and the higher frequency for infant congenital cases and aortic atheroma investigation. A stand-alone continuous wave Doppler probe should also be available. Sterile sleeves and acoustic gel should be available for epicardial imaging. The ultrasonic machine should have a capability for cineloop display and retrieval to compare prepump with postpump images. Videotapes or digital storage media should be available for archival of each study, an important consideration for medical-legal purposes. Cables should be available to input the electrocardiographic signal from the operating room monitoring system into the ultrasound machine. Many institutions have the capability of transmitting images from the operating room to a remote site such as the echocardiography laboratory in order to allow oversight or second opinions to be obtained in selected cases. Increasingly, digital storage of images is possible, which allows rapid retrieval to demonstrate findings to the surgical personnel and facilitates comparison of the preoperative and postoperative images.[27] Personnel Intraoperative echocardiography is a highly demanding technical field requiring specialized personnel skilled in transesophageal and epicardial imaging. This field requires mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 7 421 familiarity with the phases of cardiac surgery and their effects on hemodynamics as manifested by echo and Doppler studies. The American Society of Echocardiography suggests that those learning TEE be in the phase of developing level 3 experience, which is equivalent to experience in performing at least 300 echocardiographic studies. In busy operating rooms in which a large volume of intraoperative studies are being undertaken, an echo technologist or other ancillary support person, working under the aegis of the echocardiographer, can facilitate and improve the efficiency of acquiring multiple studies, some of which may be needed simultaneously. Intraoperative Echocardiography Examination Intraoperative echocardiography should be performed in a standard comprehensive manner so that the acquisition of critical information is not omitted. It is important to do a complete TEE study, using imaging planes that allow good views of each intracardiac valve and chamber as well as the great vessels.[28] The entire prepump examination should be recorded on videotape or digitally to provide a durable record of the examination, especially as a reference for postpump studies and for medical-legal purposes. In cases in which comparison with postpump findings is likely, storing key images in a cineloop facilitates rapid comparison at the end of the operation. In diagnostic (as opposed to monitoring) studies, the structure of interest to the primary surgical mission should first be examined thoroughly in multiple planes, using imaging and Doppler modalities. If the echo study must thereafter be abbreviated because of pressing demands of the surgical agenda or the need to limit anesthetic and cross-clamp time, the primary concern, the raison d'être of the echo study, has at least been addressed. Other structures of interest should then be examined, including long- and short-axis views of all four chambers, all four valves, and the great vessels. The entire aorta should be examined in all cases. We also advocate a routine intravenous contrast injection to look for intracardiac shunting. The number of times the probe is passed through the gastroesophageal junction |
should be minimized, as should all unnecessary manipulation of the probe, to reduce the risk of mucosal trauma, esophageal tears, and pharyngeal trauma that are reported in a very small percentage of cases.[29] Once the prepump study is completed, a written report of the examination detailing significant findings should be made. Although ultrasound has not mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 7 been demonstrated to cause any significant damage to cardiac structures during prolonged examinations,[29] it is advisable to put the machine on freeze so that no ultrasound energy is transmitted when imaging is not required. After cessation of cardiopulmonary bypass, a second comprehensive examination should be carried out and a second or updated report generated. The intraoperative examination has several aspects that are different from a TEE or TTE study in the outpatient echocardiography laboratory: 1. The echocardiogram is performed simultaneously with the operation; therefore, the room conditions, including the lighting and the space for the machine, may be suboptimal. For example, radiofrequency interference from other machines may mar the quality of images for long periods. 2. The hemodynamic milieu may change quickly, and the echocardiographic appearance may differ from images acquired outside the operating room. Changes in hemodynamics, such as intravascular volume, preload, and afterload, substantially affect the severity of valvular lesions. If necessary, the hemodynamic situation may be manipulated to match "street conditions" in order to determine the true or potential severity of a valvular lesion. 3. The surgeon who requests the intraoperative study may request online interpretation. Care must be maintained to make only diagnoses and conclusions that have been verified by examination from multiple imaging planes under appropriate imaging and hemodynamic conditions. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/164.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 12 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Prepump Intraoperative Echocardiography in Patients Undergoing Valve Repair for Mitral Regurgitation The prepump echocardiogram assessment of mitral regurgitation (Table 19- 3) usually merely confirms findings made previously by preoperative echocardiography or cardiac catheterization. TEE, however, often can improve on the accuracy and resolution of preoperative TTE because of improved resolution of the component structures, the mitral valve and the regurgitant jet. There are four main goals of intraoperative echocardiography in mitral valve disease: 1. To assess the severity of mitral regurgitation and determine the need for mitral valve surgery. 2. To assess the mechanism of mitral regurgitation and determine if a repair rather than prosthetic replacement is feasible and to determine the technique of repair. 3. To determine the presence of other significant valvular 422 disease that may require surgical attention, such as tricuspid regurgitation or aortic valve disease. 4. To assess left and right ventricular function in order to be able to compare with the postpump study. TABLE 19-3 -- Intraoperative Assessment of Repair and Reconstructive Valve Operations Prepump Assess severity of stenosis/regurgitation. Assess mechanism of regurgitation and potential reparability of valve. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 12 Measure dimensions of annulus, chambers, valves. Assess whether lesions other than the primary lesion require surgery. Determine biventricular function. Postpump Assess severity and mechanism of residual regurgitation/stenosis. Detect systolic anterior motion of the mitral valve and left ventricular outflow obstruction. Determine change in severity of other valve lesions. Assess biventricular function. Detect iatrogenic complications. Severity of Mitral Regurgitation The severity of mitral regurgitation is assessed by intraoperative echocardiography in the same manner as the use of echocardiography for other applications in other parts of the hospital (see Chapter 1) .[30] [31] [32] [33] [34] Several have indicated that the intraoperative assessment of mitral regurgitation agrees with the preoperative assessment by contrast ventriculography or TTE.[35] [36] In patients with ischemic mitral regurgitation, agreement between preoperative studies and the intraoperative assessment is less, possibly because of changes in hemodynamics or the degree of ischemia. One study of patients with ischemic mitral regurgitation showed that in 11% of patients the preoperative and intraoperative assessments of mitral regurgitation severity differed by more than one grade, with discordance occurring in both directions.[37] Discordance was more common in patients with clinical instability or those who received thrombolysis. It is important to remember that mitral regurgitation is dynamic and is affected by loading conditions. Reduction of afterload or intravascular volume at the time of the operation may reduce the true severity of the regurgitation. When less mitral regurgitation is found than expected, the intravascular blood volume should be expanded and systemic vascular resistance increased transiently using repeated boluses of IV phenylephrine. The velocity of mitral regurgitation, and therefore display of its jet by color Doppler, depends on the pressure difference between the left atrium and left ventricle, which is higher with hypertension. The size of the jet in the left atrium is also very sensitive to changes in color gain (directly proportional) and pulse repetition frequency (inversely proportional) (see Chapter 17) . mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 12 The transesophageal imaging window has advantages over epicardial imaging in the assessment of mitral regurgitation. A mitral prosthesis or severe mitral calcification causes acoustic shadowing of the regurgitant jet when the transducer is placed anteriorly, such as in epicardial imaging or TTE. Excellent agreement, however, has been reported between the epicardial and transesophageal approaches in assessing mitral regurgitation. [38] Semiquantitation of mitral regurgitation on a scale from 0 to 4+[30] [31] is determined based on a weighted average of several criteria: 1. The size of the left atrial flow disturbance, based on the depth of penetration and area of the regurgitant jet in the left atrial cavity assessed in multiple imaging planes; a multiplane probe facilitates this process, especially in eccentric jets. 2. The geometry of the jet; eccentric jets tends to have a higher regurgitant volume than free jets of the same area.[32] 3. The size of the proximal convergence zone, also called the proximal isovelocity surface area (PISA) technique. More severe regurgitation is associated with a larger radius of the proximal flow convergence.[33] Flow convergence can be used to calculate regurgitant flow, orifice area, and volume (see later). 4. The width of the proximal portion of the regurgitant jet on the left atrial side of the orifice is also useful and may be less load sensitive than mapping of the regurgitant jet in the atrium.[39] 5. The pulmonary venous pulsed Doppler tracing. Severe mitral regurgitation often leads to systolic reversal of flow in the pulmonary veins,[34] which is 69% sensitive and 98% specific in predicting a regurgitant orifice area of greater than 0.3 cm2 .[40] Blunting of pulmonary vein flow is somewhat reliable in predicting severe mitral regurgitation for patients in normal rhythm with normal left ventricular function but is unreliable in patients with severe left ventricular dysfunction or atrial fibrillation. A normal pulmonary vein flow pattern is useful in excluding severe mitral regurgitation and predicting a regurgitant orifice area of less than 0.3 cm2 . Importantly, in patients in which the right and left pulmonary vein flow pattern is discordant (23% of patients), the more abnormal pattern is most predictive of mitral regurgitation severity. 6. Quantification of mitral regurgitant volume (RV) from the difference between Doppler echocardiography measurements of antegrade flow through the mitral and the aortic valves. Regurgitant fraction (RF) is mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 12 the proportion of total mitral flow (MF) that is regurgitant: RF (%) = RV/MF Mitral and aortic valve flow can be assessed by the product of annular cross-sectional area derived from echo and velocity derived from pulsed Doppler measurements at the same site. Mitral cross-sectional area is derived from two orthogonal diameters of the annulus, which is elliptic in shape.[41] This method has not been used routinely because of the time- consuming nature of the measurements required and the ease and general reliability of semiquantitative techniques (see Chapter 17) . Other methods of assessing the severity of mitral regurgitation in the operating room include surgical palpation of the left atrium for the thrill of a mitral regurgitant jet, evaluation of the size of v waves on the left atrial pressure tracing, fluid filling of the arrested left ventricle, and contrast echocardiography. These methods lack sensitivity and are not as reliable or as convenient as color flow Doppler techniques.[36] [42] [43] The size of the regurgitant orifice area can be derived from Doppler echocardiography techniques in the operating room,[44] using either the antegrade flow difference method or the flow convergence method. The maximum regurgitant orifice area is calculated by dividing regurgitant flow rate by the maximum mitral regurgitant flow velocity (V ) obtained from max continuous wave Doppler. The regurgitant orifice area is greater than 0.4 cm2 in severe mitral regurgitation and greater than 0.25 cm2 in moderately severe mitral regurgitation. The flow convergence, or PISA, technique analyzes flow proximal (on the left ventricular side) to the regurgitant orifice, assuming a hemispheric shape.[44] [45] In this area, blood accelerates predictably as it moves toward the 423 regurgitant orifice and forms a series of concentric shells of decreasing area and increasing velocity that are depicted clearly as easily measured hemispheres on the color image because of the color aliasing of the accelerating flow. Because the surface area of a hemiellipse can be calculated from 2πr2 for blood flow moving at velocity v and at a radius r from the regurgitant orifice (Fig. 19-3) , flow rate Q can be calculated as mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 12 follows: Q = 2πr2 v The PISA method provides excellent estimation of regurgitant flow when the flow convergence is centrally located, well away from the walls; however, this method overestimates regurgitant flow when the proximal flow is constrained by the left ventricular wall. Use of appropriate correction factors can compensate for this problem.[46] Automated analysis of digital velocity maps in the echocardiographic machine is feasible and has the potential to further simplify this technique.[47] The PISA method of determining the regurgitant orifice area (ROA) may be simplified without significant loss of accuracy. If the aliasing velocity of the color Doppler is set to approximately 40 cm per second and the mitral regurgitation by continuous wave Doppler (V ) is assumed to be 5 m per second (500 cm max per second), then the formula becomes ROA = (2πr2 v)/Vmax ROA [2(3.14)(r2 )(40 cm/s)]/(500 cm/s) ROA 250 r2 /500 ROA r2 /2 This method has particular merit in the operating room where rapid quantification is often helpful. Mechanism of Mitral Regurgitation Assessment of the cause (Fig. 19-4) and mechanism (Fig. 19-5) of mitral regurgitation is of great importance Figure 19-3 (color plate.) Proximal convergence zone of a patient with severe mitral regurgitation. The hemisphere produced by flow at an aliasing velocity of 51 cm per second is shown (arrow). The radius of the hemisphere is 1 cm. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 12 Figure 19-4 Feasibility of mitral repair by etiology of valve disease at the Cleveland Clinic Foundation. (From Stewart WJ: ACC Heart House Learning Center Highlights 1995;10:2–7.) in determining the suitability of the mitral valve for repair. Mitral valve repair is most likely in patients with mitral regurgitation due to myxomatous degeneration and is least likely in patients with regurgitation due to endocarditis. Repair is now successful in greater than 90% of all patients with myxomatous disease. The probability of repair, however, is affected by the mechanism of regurgitation, especially whether the posterior leaflet, the anterior leaflet, or both leaflets are involved. Repair is most likely with posterior prolapse or flail, whereas bileaflet involvement and isolated anterior leaflet prolapse reduce the likelihood of successful repair substantially.[48] An Organized Approach to Imaging the Mitral Valve To adequately assess the pathophysiologic mechanism responsible for mitral regurgitation, it is essential to perform Figure 19-5 Feasibility of mitral valve repair by mechanism of regurgitation in myxomatous mitral valve disease. (From Stewart WJ: ACC Heart House Learning Center Highlights 1995;10:2–7.) 424 a thorough examination of the mitral valve and mitral apparatus |
and to determine the origin and geometry of the regurgitant jet. The long-axis imaging planes are best for determining which mitral leaflet is involved. Long-axis views of the mitral valve are obtained by imaging from midesophageal TEE planes. Figure 19-6 shows the "multiplane protractor" with all of the multiplane angles superimposed on the mitral valve. Most basilar long-axis views around the entire multiplane sweep allow portions of both leaflets to be examined individually. At approximately 50 to 60 degrees in most patients, the imaging plane parallel to a line between the commissures, is very useful for determining which portion of the anterior or posterior leaflet is involved. Imaging at a multiplane angle of about 135 degrees cuts perpendicular to this intercommissural line. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 12 The short-axis views also are useful for determining which portion of the anterior or posterior leaflet is involved. These views may be obtained from either the transgastric short-axis view or the epicardial parasternal short- axis equivalent view.[49] The posterior leaflet has three divisions or scallops: the medial, middle, and lateral. The anterior leaflet is not segmented but has a central portion known as the bare area between the insertions of the chordae from the anterolateral and posteromedial papillary muscles. In a similar way the posterior leaflet is also supported, about half each by chordae from the anterolateral and posteromedial papillary muscles. The papillary muscles lie below each mitral commissure. The papillary muscles and chordae usually are well visualized from the transgastric long-axis views of the left ventricle using biplane or multiplane probes.[50] In assessing the mitral valve and in providing the results to the surgeon, giving an accurate localization of the abnormality is important. A prospective study of 50 patients used a segmental approach to the mitral valve, breaking each leaflet into three segments, and found that TEE was 96% accurate for localization compared with surgical findings.[51] Other Figure 19-6 The short-axis view of the mitral valve in systole from a transverse transgastric view. The medial and lateral commissures (COMM) and the positions of the medial (MED), middle (MID), and lateral (LAT) scallops of the posterior leaflet are shown. ANT, anterior. (From Stewart WJ; Griffin B, Thomas JD: Am J Cardiol Imaging 1995;9:121–128.) Figure 19-7 Transgastric short-axis view of the mitral valve in a patient with severe prolapse of the middle scallop of the posterior leaflet (arrow). ANT, anterior leaflet. researchers have shown that localization of the defect to the posterior leaflet by TEE is 78% sensitive and 92% specific in myxomatous disease, with accuracy being least when the medial rather than the lateral or middle scallop is involved.[52] Assessment of the mechanism of mitral regurgitation is performed by analyzing the motion of the valve leaflets with two- dimensional echocardiography (Fig. 19-7) and the direction of the regurgitant jet with color flow imaging [53] (Table 19-4) . Three types of leaflet motion (Fig. 19-8) may be associated with mitral regurgitation: (1) excessive motion, as seen with prolapse or flail valve caused by chordal rupture or elongation, (2) restricted motion, as seen in rheumatic disease and papillary muscle infarction, and (3) normal motion, as seen with leaflet perforation and ventricular-annular dilation. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 12 Intraoperative echocardiography has been shown to be highly sensitive and specific in determining the mechanism of mitral regurgitation in patients undergoing mitral TABLE 19-4 -- Determination of the Mechanism of Mitral Regurgitation from Analysis of Jet Direction and Leaflet Mobility Leaflet Motion Jet Direction EXCESSIVE RESTRICTIVE NORMAL Anterior Prolapse/flail of posterior leaflet Posterior Prolapse/flail of Restriction of Apical tethering anterior leaflet posterior > from LV dilation anterior leaflet Central Prolapse/flail of Equal Apical tethering both leaflets restriction of from LV dilation, both leaflets annular dilation Commissural Rupture of commissural chordae or papillary muscle Eccentric origin Leaflet perforation or cleft LV, left ventricular. 425 Figure 19-8 Morphology and echocardiographic appearance of normal, excessive, and restricted motion of the mitral valve, each of which can cause mitral regurgitation. (From Cosgrove DM, Stewart WJ: Curr Probl Cardiol 1989;XIV:359–415.) valve surgery. In a study of 286 patients undergoing mitral valve surgery in whom the echocardiography mechanism was correlated with the surgical findings, echocardiography was highly accurate (86%) in determining the mechanism of mitral regurgitation.[53] Echocardiography was least accurate in ascertaining the mechanism of mitral regurgitation in patients with mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 12 leaflet perforation, bileaflet prolapse, or ventricular-annular dilation. Excessive Leaflet Motion. Excessive leaflet motion occurs with elongation or disruption of any portion of the mitral valve or of the mitral apparatus, including the papillary muscles and chordae. Myxomatous disease, endocarditis, and papillary muscle infarction all can lead to this abnormality. With excessive leaflet motion, the regurgitant jet is directed away from the affected leaflet. Thus, prolapse or flail of the posterior leaflet leads to an anteriorly directed jet (Fig. 19-9) . In bileaflet prolapse, the excessive motion is often asymmetric, and the jet direction is away from the more severely affected leaflet. When the amount of prolapse or flail is completely balanced between both leaflets, a central jet direction occurs. If the chordae to the commissures are ruptured, then a jet originating at the commissures is seen in the transgastric short-axis view. Jets originating at the commissure also are seen in infarction of a papillary muscle, most commonly the posteromedial one.[54] Excess motion with overwhelming mitral regurgitation results when the head of a papillary muscle ruptures in an acute myocardial infarct. This type of rupture may be differentiated from acute chordal rupture by detecting a mass attached to the flail leaflet that is a portion of the muscle and by the appropriate clinical setting (Fig. 19-10) . Precise delineation of which portion of the valve has excess motion is important in planning the surgical repair. Rupture of the posterior chordae is the most common abnormality and is repaired by quadrilateral resection of the posterior leaflet (Fig. 19-11) . Elongation of the chordae is repaired by chordal transfer or by implantation of artificial chordae. Papillary muscle elongation or disruption may be repaired by reimplantation, supporting, or shortening the affected muscle.[48] Postoperative prognosis is best in those with excessive leaflet motion. Restricted Leaflet Motion. This pattern is seen most commonly in rheumatic disease, but it also can occur in regurgitation from ischemic heart disease, the chronic phase of lupus, or acquired valvular disease caused by certain drugs such as ergot derivatives and anorexigenic drugs such as the fen-phen combination (fenfluramine and phentermine). In rheumatic, lupus, and drug-induced diseases, the leaflets are thickened. If both leaflets are equally affected by the pathologic process, the jet direction is central. More commonly in rheumatic disease, the posterior leaflet is more severely affected than the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 12 anterior leaflet, and the relatively normal anterior leaflet "over-rides" the restricted posterior leaflet. The direction of the regurgitant jet in this situation is posterior, toward the affected leaflet. The surgical approach to this condition includes débridement of the valve tissue and chordae, commissurotomy, and annuloplasty. This type of repair is more technically demanding and is less often successful. In ischemic heart disease, the posterior leaflet is typically restricted in motion owing to apical displacement of the posteromedial papillary muscle. The displacement results from ischemia or infarction of this papillary muscle or the muscle to which it is attached and which is usually in the perfusion territory of the right or circumflex coronary artery. The leaflets themselves are normal and are not thickened but fail to coapt adequately (Fig. 19-12) . In extreme cases the leaflets may not touch at all. The surgical approach to this problem usually involves placement of an annuloplasty ring to reduce the size of the mitral annulus and coronary revascularization. Use of a figure- of-eight or Alfieri stitch either alone or in combination with annuloplasty ring also has been used. The Alfieri 426 Figure 19-9 (color plate.) Posterior leaflet prolapse (A) with severe mitral regurgitation (B) before mitral valve repair and no mitral regurgitation after successful mitral valve repair (C). stitch effectively converts the mitral valve into a doubleorifice valve by attaching the leaflets at their midpoint. Surgical treatment of ischemic regurgitation with restricted leaflet motion is less successful in that residual regurgitation is often more significant than after myxomatous valve repair. Figure 19-10 Papillary muscle rupture with resulting severe mitral regurgitation. The rupture portion of muscle is seen prolapsing into the left atrium (arrow). Normal Leaflet Motion. Perforation of the valve leaflet causing mitral regurgitation occurs most commonly because of endocarditis or because of a congenital cleft in the valve. Occasionally it is iatrogenic, after attempted repair. The jet origin is eccentric, arising from the midportion of the leaflets rather than from the coaptation line. The mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 12 Figure 19-11 Quadrilateral resection of the posterior leaflet of the mitral valve with annular ring implantation. (From Cosgrove DM, Stewart WJ: Curr Probl Cardiol 1989;XIV:359–415.) 427 Figure 19-12 Ischemic mitral regurgitation with restricted posterior leaflet motion and posteriorly directed jet of mitral regurgitation. prejet flow acceleration also may be seen away from the coaptation line, along the affected leaflet. Leaflet perforation may be repaired in some instances by suture closure or with pericardial patch.[55] Normal leaflet motion is commonly seen in patients with mitral regurgitation secondary to left ventricular dilation of any cause, such as disease of other valves, dilated cardiomyopathy, or severe ischemic cardiomyopathy. We have previously termed this category ventricular- annular dilation. Ventricular enlargement causes displacement of the mitral coaptation point toward the apex with resultant impaired coaptation. Annular dilation is seen in these patients, but it occurs in proportion to left ventricular dilation, in contrast to myxomatous or rheumatic mitral regurgitation patients whose annulus size is often abnormally large. Annuloplasty with ring insertion is commonly used in the surgical management of these patients. An Alfieri stitch to support the valve also has been used instead of or in addition to the annuloplasty. There has been an upsurge in interest in the surgical management of severe mitral regurgitation in patients with dilated cardiomyopathy. Excellent functional improvement with a relatively low operative mortality has been reported even in selected patients with severe mitral regurgitation and severe left ventricular dysfunction. One study of 248 patients undergoing mitral valve surgery showed that TEE was greater than 90% accurate for definition of the mechanism of regurgitation, localizing the origin of regurgitation, and in detecting a flail segment. TEE was 88% accurate in detecting ruptured chordae. The TEE findings of valve function were highly predictive not only of valve reparability but also of long-term survival, which were independent of age, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 12 di 12 gender, ejection fraction, and coronary artery disease. [56] Other Valve Disease and Biventricular Function During Mitral Repair The severity of aortic and tricuspid valvular disease is assessed by intraoperative TEE using color flow mapping to determine the severity of the dysfunction and the necessity of valve surgery. These decisions should be made preoperatively, but diagnostic information should be refined intraoperatively, as mentioned earlier. Intraoperative diagnosis is particularly important in patients with active endocarditis. Significant tricuspid or aortic regurgitation usually requires operative intervention; however, intraoperative echocardiography tends to underestimate the degree of tricuspid regurgitation because of optimization of the hemodynamics that usually results in a reduction of right-sided pressures and volume. Because the preoperative echocardiogram is generally performed under ambulatory conditions, it is a better guide to decision making with regard to tricuspid valve repair, as opposed to the intraoperative findings alone. Regional and global left ventricular function is best assessed using TEE from long- and short-axis transgastric views and various midesophageal long-axis views. The long- and short-axis views from any epicardial imaging window also show the left and right ventricle well. Right ventricular function is assessed by TEE in the midesophageal 45-degree view at the level of the short axis of the aortic valve, from the midesophageal transverse four-chamber view, or from a longitudinal transgastric view rotated clockwise to obtain a long-axis image of the right ventricle. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/165.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to |
others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Determining the Need for Mitral Valve Surgery in Patients Undergoing Cardiac Surgery for Other Reasons Intraoperative echocardiography increasingly is used to determine the need for a mitral valve operation in patients undergoing aortic valve surgery or revascularization procedures; this is especially true in the assessment of patients in whom the severity of the mitral regurgitation preoperatively is significantly different by cardiac catheterization and echocardiography, when the severity of mitral regurgitation over time is variable (such as in ischemic heart disease), and when the mitral regurgitation is of moderate severity. The following questions must be considered when determining the need for mitral valve surgery in addition to the primary surgery: 1. How severe is the mitral regurgitation? 2. Is there a primary abnormality of the mitral valve (such as a torn chord or prolapse)? 3. Will the mitral regurgitation change as a consequence of the primary operation? 4. Is the valve repairable or is prosthetic replacement necessary? 5. What is the additional risk imposed by the additional mitral valve procedure? The final decision on surgery is made by the surgeon; however, when the surgical objectives are changed in the operating room, telephone consultation with the referring cardiologist is advisable. In many patients, especially those in whom the regurgitation is secondary to ischemia or left ventricular dilation, 428 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 the severity of the regurgitation may be variable. Sometimes, the severity of regurgitation detected at the time of operation is different from that recorded preoperatively. Frequently the difference in severity is due to a true physiologic change. Compared with ambulatory conditions, the loading conditions during surgery often entail a lower intravascular volume and less peripheral vasoconstriction, both of which may reduce the severity of valvular regurgitation and reduce stenotic valve gradients. On other occasions this discrepancy reflects the superior ability of esophageal and epicardial echocardiography to visualize mitral regurgitation. When approaching patients whose regurgitation is 2+ or less, we often purposely increase the afterload with multiple boluses of 100 µg of phenylephrine to determine the severity of regurgitation at a mean arterial pressure that is transiently as high as 120 mm Hg. Patients with 3+ or more mitral regurgitation at rest, or during this afterload stress test, are generally considered candidates for a mitral valve operation. The threshold for surgery on the mitral valve also is affected by other factors, including whether there is a primary structural abnormality of the valve. If the valve appears to be repairable, the threshold for surgery is lower, given the relatively low morbidity and mortality associated with repair as compared with valve replacement, whereas the threshold for surgery is higher in patients with valves that are not reparable. In patients undergoing surgery for aortic stenosis, improvement in the severity of the mitral regurgitation can be expected postoperatively. Therefore, the threshold for concomitant mitral surgery is higher.[57] [58] A postpump assessment of the mitral regurgitation is made regardless of whether a surgical intervention on the mitral valve has been performed. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/166.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 4 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Postpump Intraoperative Echocardiography in Mitral Repair The most significant indication for intraoperative echocardiography in mitral valve repair (see Table 19-3) is to determine the competency of the repair immediately after cardiopulmonary bypass. If the repair is inadequate, further repair or replacement can be performed immediately during the same thoracotomy. Timing Return of the patient to normal loading conditions is necessary to make valid assessments of valvular performance. It is also best to make valvular assessments after ventricular function has reached its postoperative plateau. The most appropriate time to image after repair is when the patient is off cardiopulmonary bypass, the intravascular volume is replete, and the loading conditions are similar to those in the ambulatory state. Imaging can be initiated after the aortic cross clamp is off and when the left ventricle is at least partially filled, but abnormal findings at this time may result from abnormal left ventricle geometry. The surgeon should not act on these findings unless they are subsequently confirmed by further imaging after the cessation of cardiopulmonary bypass. Intraoperative Findings In most cases, with an experienced surgeon, mitral valve repair leads to a competent mitral valve with mild or no residual mitral regurgitation; however, there are potential complications of mitral valve repair that are readily recognized by postpump intraoperative echocardiography. Many of these complications may not be apparent clinically or may take longer to accurately diagnose without echocardiography. If left untreated, these complications may interfere with the long-term success of the procedure and require early reoperation. Complications seen after mitral valve repair by intraoperative echocardiography are shown in Table 19-5 . mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 4 Incomplete Mitral Repair Significant residual mitral regurgitation is the most common postpump problem detected by intraoperative echocardiography. The incidence of this complication varies with the cause of the valvular regurgitation, the complexity of the repair, the experience of the surgeon, and the threshold of the operative team to accept a suboptimal result. Frequently, if the echocardiographer can define the mechanism of the residual regurgitation, further repair of the valve leads to an improved result with reduction or elimination of mitral regurgitation. In some patients, TABLE 19-5 -- Management of Abnormal Findings on Doppler Echocardiography after Mitral Valve Repair Complication Management Residual mitral regurgitation Define mechanism. If ≤1 +, accept. If 2 +, give phenylephrine to recheck MR with increased afterload; if >2 +, further surgery is required. Systolic anterior motion with Assess LVOT gradient and MR. LVOT obstruction Increase ventricular volume, stop positive inotropes, and increase afterload. If these measures are not successful, further surgery is needed to revise repair. Dehisced ring or leaflet perforation Another pump run is needed to fix annuloplasty. Residual mitral stenosis Quantify severity. If mean gradient >5 mm Hg or area < 1.5 cm2 , consider further surgery. Significant tricuspid regurgitation If 3 + or more, consider further repair. Regional left ventricular Assess intracardiac air; if not resolved dysfunction after further time on pump, consider coronary bypass. Global (right or left) ventricular Assess volume status, afterload, and dysfunction response to medications. LVOT, left ventricular outflow tract; MR, mitral regurgitation. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 4 429 further repair is impossible or fails, and the patient requires another pump run to implant a prosthesis. Moderate (2+) or more mitral regurgitation, either at rest or following afterload challenge with phenylephrine as previously described, is generally considered excessive after mitral repair and is an indication for a further surgical procedure. If the regurgitation is mild (1+) or less, then the result is usually accepted, though individual surgeons vary in their willingness to accept even mild grades of regurgitation. The severity of mitral regurgitation detected by immediate postpump intraoperative echocardiography correlates well with angiographic or TTE and TEE estimates of severity obtained later.[59] [60] Rarely, changes in the early postoperative period such as chordal rupture, suture dehiscence, or early postoperative endocarditis may cause acute worsening of the mitral regurgitation. Thus, intraoperative echocardiography is a reliable measure of the severity of mitral regurgitation and the need for further intervention. Other considerations in deciding whether residual mitral regurgitation should be accepted or subjected to another surgical procedure include the mechanism of the mitral regurgitation, the overall condition of the patient, and left ventricular function. Postpump determination of the mechanism of the residual mitral regurgitation helps the surgeon to determine whether a further reparative procedure could lessen the regurgitation and yet conserve the valve. More mitral regurgitation than is usually desirable might be accepted when other surgical procedures such as aortic valve replacement or coronary artery bypass grafting also have been accomplished, particularly in elderly patients or those with significant left ventricular dysfunction. For example, in patients with extensive mitral annular calcification, mitral prosthetic insertion may be technically more difficult and more hazardous for the patient than accepting a 2+ or even 3+ mitral regurgitation.[61] In one study of 100 patients undergoing mitral valve repair, 8% needed a second pump run, and 3% had persistent mitral regurgitation that was greater than 2+. Further repair in all three patients led to an improvement in regurgitation. [35] In another study of 309 patients undergoing mitral valve repair, 26 (8%) had immediate failure and required further cardiopulmonary bypass. Ten of those patients (3.2%) had excessive residual regurgitation. Two of the 10 patients subsequently had mitral prosthetic implantation, and eight had further repair. The further repair mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 4 included chordal shortening in three patients, annuloplasty in four patients, and both procedures in one patient. Residual mitral regurgitation after the second repair was mild or absent in all patients. In this study, inadequate repair was associated with a degenerative cause of the mitral regurgitation and with the absence of an annuloplasty ring implantation at the time of initial repair.[62] In another study, residual mitral regurgitation caused by inadequate repair was seen in 4% of patients immediately postpump. In this study, need for reoperation because of inadequate repair or systolic anterior motion of the mitral valve was more common in patients with anterior mitral leaflet or bileaflet prolapse, as opposed to those with posterior prolapse.[63] Impact on Clinical Outcome The severity of residual mitral regurgitation after mitral valve repair is important for prognosis, as shown by several studies. In one of these studies, moderate or greater mitral regurgitation was associated with a higher incidence of congestive heart failure, repeat valve surgery, or postoperative death.[37] In a study of ischemic mitral regurgitation, residual regurgitation by postpump intraoperative echocardiography was a strong predictor of survival after mitral valve repair.[24] Residual mitral regurgitation in ischemic heart disease, however, correlates more with the degree of permanent contractile impairment rather than the technical success of the repair procedure. In another study, two patients with 3+ mitral regurgitation as determined by postpump intraoperative echocardiography who did not undergo a further pump run at the time of initial surgery required reoperation within 5 days because of hemodynamic instability and the inability to wean off mechanical ventilation.[35] Patients who undergo a second pump run for an initially inadequate repair have an in-hospital complication rate that is similar to that of patients who require a single pump run.[64] In one study, residual mitral regurgitation of 1+ or 2+ did not increase hospital complications when compared with trivial or no regurgitation postoperatively. There was a trend for patients with 1+ or 2+ mitral regurgitation, however, to need more reoperations in late follow-up than those with trivial or no mitral regurgitation.[65] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/167.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 4 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Other Complications of Mitral Valve Repair Systolic Anterior Motion of the Mitral Valve Significant left ventricular outflow obstruction caused by systolic anterior movement of the mitral valve (SAM) has long been recognized as a complication of mitral valve repair.[66] [67] This abnormality simulates that seen in hypertrophic cardiomyopathy, even though septal hypertrophy is absent. Similar to outflow obstruction in hypertrophic cardiomyopathy, SAM after mitral repair is dynamic and exacerbated by reducing the size of the ventricular chamber or augmenting the contractile state. SAM may cause pressure |
gradients of 100 mm Hg or more, severe hypotension, severe mitral regurgitation, and inability to wean the patient from cardiopulmonary bypass. Fortunately, this series of complications is readily recognized and quantified by an experienced echocardiographer on the postpump echocardiogram study (Fig. 19-13) . SAM has been reported in 2% to 9% of patients undergoing mitral valve repair.[35] [63] [68] Several mechanisms have been proposed to explain SAM following mitral valve repair. These mechanisms include anterior displacement of the posterior ventricular wall, anterior displacement of the posterior mitral leaflet, and narrowing of the angle between the mitral and aortic valves.[69] It is clear that SAM occurs primarily in patients 430 Figure 19-13 (color plate.) Series of images indicating the presence of systolic anterior motion at the end of the first pump run (A, arrow) leading to severe mitral regurgitation (B) and outflow obstruction (C). The maximal velocity measured in the outflow tract was 4.6 m per second, giving a pressure gradient of 85 mm Hg. with degenerative mitral valve disease, those with large mitral leaflets, and mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 4 in the presence of a hyperdynamic small ventricle.[63] SAM is usually seen only after annuloplasty ring insertion, but it has been reported after a suture annuloplasty.[63] It is seen more commonly with stiff than flexible annuloplasty rings.[63] [68] One quantitative study has shown that SAM is associated with anterior displacement of the mitral coaptation line. The anterior displacement is reduced or disappears after successful revision of the repair and elimination of SAM.[69] More recently, the ratio of the length of the anterior and posterior leaflet in the coapted state and the distance from the coaptation point to the septum were shown to be predictors of systolic anterior motion on preoperative TEE. The smaller the ratio between anterior and posterior leaflet and the narrower the distance between the coaptation point and the septum, the greater the likelihood of SAM.[70] When severe, SAM is easily recognized and may involve both leaflets. The left ventricular outflow gradient and the severity of mitral regurgitation are important indicators of the hemodynamic severity. The deep transgastric imaging window with the heart in an orientation similar to a transthoracic apical five-chamber image provides the best transesophageal window for assessing the left ventricular outflow tract gradient with continuous wave Doppler. When this examination cannot be reliably performed with the transesophageal approach, an epicardial study may be needed. The initial management of this condition should be to increase intracardiac volume by fluid repletion and to stop any positive inotropic agents that are being administered.[63] Systemic afterload can be supported by a pure alpha agonist (phenylephrine), avoiding any beta agonists. If these measures are inadequate to reduce the severity of SAM, another pump run to improve the SAM is indicated. Further procedures to improve SAM include (1) a sliding posterior leaflet advancement (sliding plasty), which reduces the anterior- posterior height of the posterior leaflet; (2) insertion of an annuloplasty of larger size; and (3) removal of the annuloplasty ring. Sliding annuloplasty is currently used as a component of the primary operative procedure on patients who are considered at risk for developing SAM and has significantly reduced the incidence of this complication in those patients in whom it has been used.[71] [72] If SAM persist despite these maneuvers, the final recourse is mitral prosthetic implantation. Patients in whom SAM is discovered by TTE days or longer after mitral valve repair, obviously a subset selected to have milder obstruction by successful weaning from bypass and extubation, may be treated medically with mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 4 negative inotropic agents. Some patients show a late reduction in the left ventricular outflow gradient, but this may remain inducible by amyl nitrite. [73] Suture Dehiscence 431 Occasionally, suture dehiscence leads to significant mitral regurgitation immediately after mitral valve repair. This complication occurred in 2% of operations in one series.[62] Dehiscence of a suture at the site of the leaflet resection in the posterior leaflet simulates a posterior leaflet perforation and is easily repaired on a second pump run. Another rare complication of mitral valve repair that can be detected by intraoperative echocardiography is partial dehiscence of the annuloplasty ring. The annuloplasty ring shows increased mobility and regurgitation originates outside the ring (Fig. 19- 14) . Left Ventricular Systolic Dysfunction Some reduction in left ventricular function often is detected after mitral valve repair.[74] [75] When dysfunction occurs, it is most often global and may reflect the unmasking of left ventricular dysfunction present preoperatively that had been concealed by the effects of increased ventricular preload and decreased afterload. In a minority of instances, a regional wall motion abnormality is detected, despite normal coronary vasculature preoperatively. This abnormality is usually caused by passage of air into a coronary vessel, and it can cause transient wall motion abnormalities and occasionally permanent infarction.[18] Because of its anterior position, air is more likely to travel to the right coronary artery in a supine patient, causing inferior wall motion abnormalities. Air within the left ventricular cavity is readily detected by echocardiography because it is echodense. The presence of large amounts of air on echocardiography is an indication for increased surgical venting of the left ventricle to prevent coronary embolization. In minimally invasive operations in which small hemisternotomy incisions are used, surgical venting may be difficult or impossible. In this situation, resumption of cardiopulmonary bypass may be necessary for a period of time in order to allow slow resolution of the air. Fortunately, most instances of air embolization of the coronary vessels resolve without significant long-term mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 4 ventricular dysfunction. A rare complication of mitral valve repair or of any mitral operation is the inadvertent entrapment of the circumflex artery in the annulus sutures, which causes a wall motion abnormality in the Figure 19-14 (color plate.) Ring dehiscence leading to severe mitral regurgitation. The dehisced portion of the ring is shown (arrow). basilar posterolateral wall that may also be detected echocardiographically. Tricuspid Regurgitation Generally, tricuspid regurgitation that is treated with a ring annuloplasty at the time of mitral surgery should be rechecked on the postpump intraoperative echocardiogram.[76] The success of the tricuspid surgery should be checked only after the intravascular volume status has been normalized. [77] Occasionally, tricuspid regurgitation that did not appear to be significant preoperatively may appear to be more severe on the postpump study and require a further pump run for tricuspid repair. Mitral Stenosis In performing a mitral valve repair in a nonrheumatic valve, the surgeon may remove a significant portion of the leaflet or perform an annuloplasty that reduces the size of the mitral annular orifice. Despite these anatomic derangements, it is unusual to have any significant stenosis in degenerative or ischemic mitral valve repair. The annulus area is 5 to 10 cm2 , varying with the size of the annuloplasty ring inserted. In contrast, residual stenosis of mild degree is common after rheumatic mitral valve repair because of the thickened leaflets and fusion of subvalvular chordae and commissures. The mitral valve gradient should be measured using continuous wave Doppler after every mitral valve repair. A mean gradient in excess of 5 mm Hg should arouse suspicion of some degree of stenosis of the valve. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/168.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Mitral Valve Repair Involving Commissurotomy Although balloon valvuloplasty is a common method of treating selected patients with mitral stenosis, mitral repair with open commissurotomy still has a place, especially in patients with moderate amounts of valve calcification or thickening, those with multivalvular disease, or those with combined stenosis and significant regurgitation. Before surgery, intraoperative echocardiography is used to determine the severity of stenosis as a reference to assess the success of surgery. The severity of mitral stenosis is determined by measuring the transmitral pressure gradient and the pressure half-time with continuous wave Doppler.[78] [79] An epicardial approach using a para-sternal short-axis equivalent view may be used to obtain views suitable for planimetry of the mitral orifice if needed, but most TEE short-axis views of the mitral valve from the transgastric short-axis view are not of sufficient quality. The mechanism of the stenosis, whether valvular or subvalvular, should also be determined. A splitability score generated in a manner similar to the transthoracic method used for percutaneous mitral valvuloplasty may help to determine the degree of valvular fibrosis and calcification and whether a valve-sparing procedure is feasible.[80] Because 432 the surgeon can débride the valve under direct vision, open commissurotomy is sometimes possible even with a moderately high splitability score of 9 to 11, when a balloon valvuloplasty is not as likely to be effective or durable (see Chapter 20) . The presence of mitral regurgitation is also determined, and its mechanism, usually restricted leaflet motion, is determined. It is important also to detect left atrial and appendage thrombus preoperatively so that the surgeon can remove it. Postpump mitral valve gradient and area and mitral regurgitation are assessed. The presence of residual mitral regurgitation of 2+ or greater, or a mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 mitral valve area of less than 1.5 cm2 is an indication for a further pump run, either to improve the repair or to implant a prosthesis. Frequently, when the patient has a large atrium or atrial fibrillation, the surgeon attempts to ligate the left atrial appendage in an effort to reduce the embolic risk. One study with TEE Doppler has demonstrated that these ligation attempts may be incomplete in up to one third of patients and in these instances blood still may enter and leave the appendage.[81] Patients with incomplete ligation remain susceptible to left atrial appendage thrombus formation and even thromboembolism. It has not been demonstrated that TEE evaluation of the competency of the ligation at the time of surgery improves the outcome. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/169.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Future Directions The acquisition and storage of digital images is available on many of the current echocardiographic machines and opens up new vistas for intraoperative echocardiography. This storage method preserves image quality better than does videotape. Retrieval of digital images also is more facile, but it depends on how and where the data is stored. Comparing previously performed studies directly with the current study provides a more reliable detection of change. Digital storage and retrieval of previously performed studies may reduce the need for prepump intraoperative studies, or at least shorten their duration. Appropriate training of additional personnel is changing intraoperative echocardiography for the better. Cardiac anesthesiologists are quickly learning the requisite skills, which could reduce the need for dedicated cardiology support to the cardiac operating rooms except to consult when specific problems arise. Online consultation is increasingly feasible with the availability of digital archival and retrieval of images on a common server. Additionally, training of cardiac surgeons in epivascular imaging of the aorta has the potential to reduce the involvement of other echocardiographers directly in image acquisition. New technology is constantly becoming available both in terms of the echocardiographic machines themselves and in terms of the available transducers. Image quality has improved remarkably, from faster computers and parallel processing circuitry. New technology including Doppler myocardial imaging, harmonic imaging, and contrast analysis software provides improved physiologic analysis. On the other end of the spectrum, smaller hand-held machines having many of the capabilities of bigger machines |
will soon become available in cardiac operating rooms, although they likely will need to be supplemented by more sophisticated technology for cases with significant diagnostic needs. As yet, these smaller machines have not had transesophageal capability, nor has their use in the operating mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 room been reported. Newer transducers that are currently being evaluated include transnasal probes.[82] These smaller transducers, inserted through the nasopharynx, lessen the risk to teeth and the interference with the endotracheal tube. Currently, these probes are not available with multiplane capabilities. They are therefore at a disadvantage compared with standard multiplane TEE probes. Three-dimensional echocardiography has tremendous potential in any analysis of complex cardiac morphology, including the assessment of lesions in which repair or reconstruction is being considered[83] (see Chapter 10) . The complex three-dimensional geometry of some valvular and congenital lesions is easier to display and understand using three-dimensional echocardiography.[84] , [85] Three- dimensional reconstruction may allow more appropriate selection of patients, help determine the most appropriate surgical procedure, and potentially allow the surgeon to map out the reconstruction ahead of time in three-dimensional computer space. Recently, the feasibility of intraoperative three-dimensional TEE has been shown, with acquisition time less than 3 minutes and reconstruction possible in greater than 90% of patients. Three-dimensional data yielded incremental information to TEE in up to 25% of patients but only led to a change in the operative plan in one of 60 patients studied.[86] Three-dimensional imaging for reconstruction of some structures has already been accomplished, including the regurgitant orifice area in patients with severe mitral valve prolapse.[87] Although real- time three-dimensional echocardiographic acquisition hardware is now a reality, transesophageal applications are not currently available and the exigencies imposed by the data acquisition render the image quality inferior to current two-dimensional echocardiographic images. Real-time acquisition of three-dimensional data has the potential to further expand echocardiographic abilities intraoperatively by allowing rapid changes in volume and structure to be quantified online and in allowing multiple slices of structure to be generated at a later time from one stored data set. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/170.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company 435 Chapter 20 - Echocardiography in the Patient Undergoing Catheter Balloon Mitral Commissurotomy Patient Selection, Hemodynamic Results, Complications, and Long-term Outcome Cheryl L. Reid MD Historical Background and Technique of Mitral Balloon Commissurotomy Mitral stenosis in the adult occurs most commonly as the late result of rheumatic fever. Rarely, mitral stenosis may be caused by congenital or mitral annular calcification, particularly in the elderly patient. The natural history of rheumatic mitral stenosis is progressive symptomatic deterioration owing to reduction in the mitral valve orifice area. In the 10 to 20 years following an initial bout of rheumatic fever, the effective mitral valve area decreases because of fusion of the commissures, thickening and calcification of the mitral leaflets, and fibrosis and retraction of the chordae tendineae. The normal mitral valve area of 4.0 to 5.0 cm2 gradually decreases to 2.0 cm2 or less, at which time symptoms begin to develop usually with moderate to severe exercise. When the mitral valve area is reduced to 1.5 cm2 or less, symptoms may become severe and complications may develop. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 Mechanical intervention for the treatment of mitral stenosis, either open or closed mitral commissurotomy, has evolved in the past 40 years. Surgery, which has been shown to be highly effective, is usually performed for the relief of symptoms. Surgical replacement of the mitral valve may be necessary in patients with rigid, calcified mitral valves or severe mitral regurgitation in whom results with commissurotomy are suboptimal. Early experience with surgical commissurotomy showed that M-mode echocardiography could be helpful in selecting patients who would have a successful surgical mitral commissurotomy. It is important to identify patients who will have a successful commissurotomy because of the well- recognized complications of valve prostheses, including thromboembolism, endocarditis, and higher operative mortality. The percutaneous approach to dilate a stenotic mitral valve was first reported by Inoue et al[1] in 1984, with subsequent evolution of catheter design and technique since the initial description. Simply stated, the technique consists of the percutaneous insertion of a dilating balloon into the right atrium. Using a trans-septal approach, the balloon catheters are then positioned across the stenotic mitral orifice and inflated at high pressures (1 to 2 atm). The desired result from inflation of the balloons is splitting 436 Figure 20-1 Technique of double-balloon valvuloplasty of the mitral valve. Top left, Two trans-septal sheaths from the right femoral vein are advanced to the left atrium (LA). Top center, Two end-hole balloon wedge catheters are positioned in the apex of the left ventricle (LV). Top right, Two curved exchange guidewires are inserted through the balloon catheters, which are then withdrawn. Bottom left, Two dilation balloon catheters are placed across the mitral valve orifice and into the LV apex. Bottom center, Two dilating balloon catheters are then fully inflated. Bottom right, Valve dilation balloons are removed. AO, aorta; IVC, inferior vena cava; RA, right atrium. (From McKay CR, Kawanishi DT, Rahimtoola SH: JAMA 1987;257:1753–1761, with permission. Copyright © 1987 American Medical Association.) of the fused mitral commissures with resultant increases in the mitral valve orifice area. The procedure can be performed using either the double- balloon or Inoue technique (Fig. 20-1) . In the double-balloon technique, two balloons are positioned side by side across the mitral valve orifice and then simultaneously inflated to achieve the desired result. The Inoue technique uses a unique self-seating single balloon that sequentially inflates mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 from the distal to proximal end of the balloon. In recent years, the technical complexity and potential for serious complications (specifically, cardiac rupture inherent with the double-balloon technique) have largely lead to the abandonment of the double-balloon technique in favor of the Inoue technique. Early results of the procedure showed that the increase in mitral valve area is comparable to that obtained with surgical mitral commissurotomy.[2] [3] [4] Mitral balloon commissurotomy is now considered the procedure of choice for the treatment of symptomatic mitral stenosis in selected patients. Two- dimensional Doppler echocardiography has played a major role in the evolution of mitral balloon commissurotomy, guiding our understanding of the mechanism by which the mitral valve area is increased. It is essential for the evaluation and selection of patients before the procedure and for the assessment of complications following the procedure. Hemodynamic measurement of the severity of the mitral stenosis and associated valve disease before the procedure, immediate hemodynamic changes during the procedure, and long-term follow-up can be reliably estimated with Doppler echocardiography (Table 20-1) . MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/172.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 8 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Evaluation of the Patient Before Mitral Balloon Commissurotomy Mechanisms of Increase in Mitral Valve Area Studies performed by two-dimensional echocardiography have shown that the primary mechanism for the increase in mitral valve area following mitral balloon commissurotomy is splitting of the fused commissures (Fig. 20-2) .[5] Tears of either the anterior or posterior mitral valve leaflet rarely occur and usually result in moderate to severe mitral regurgitation. In contrast to open, surgical commissurotomy in which the fused and retracted chordae can be manually separated, it is unclear that mitral balloon commissurotomy has a significant effect in dilating the subvalvular apparatus. Fortunately, the subvalvular region is rarely the primary orifice in patients with mitral stenosis. 437 TABLE 20-1 -- Role of Two-Dimensional Doppler Echocardiography in the Evaluation of Patients Undergoing Mitral Balloon Commissurotomy Initial studies Severity of valve disease Mitral valve gradient Mitral valve area Mitral regurgitation Initial valve morphology Left atrial thrombus During mitral balloon commissurotomy mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 8 Balloon position or trans-septal catheterization Changes in valve area or gradient Changes in mitral regurgitation Complications (rupture, atrial septal defect, etc.) Immediate results Changes in valve function Complications Long-term results Restenosis Mitral regurgitation Atrial septal defects Pulmonary artery pressure Ventricular size and function Other valve disease Mitral Valve Morphology The pathologic processes of rheumatic heart disease include (1) fusion of the commissures, (2) thickening and calcification of the valve leaflets, and (3) fusion and shortening of the chordae tendineae. These processes result in varying degrees of involvement of the mitral apparatus. Given that the mechanism of the increase in mitral valve area by surgical or percutaneous techniques is splitting of the commissures, it is expected that the morphology of the mitral valve apparatus will influence the results of the procedure. Experience with both surgical mitral commissurotomy and mitral balloon commissurotomy has confirmed this expectation. The characteristic feature of rheumatic mitral stenosis on two-dimensional echocardiography is doming of the body of the mitral valve leaflets during diastole caused by the fused commissures. As blood flows from the left Figure 20-2 Two-dimensional echocardiogram in the parasternal short- axis view at the level of the mitral valve during early diastole. A, Before double-balloon catheter balloon valvuloplasty the transverse diameter was 20 mm. Calcification of the posterior commissure was present. B, After catheter balloon valvuloplasty the transverse diameter increased to 27 mm. The increase in mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 8 transverse diameter suggests that the split occurred at the commissures. Figure 20-3 Left, Transthoracic two-dimensional echocardiogram from a patient with mitral stenosis. The mitral valve is mobile with doming of the anterior leaflet. Minimal valve thickening and no subvalvular disease is noted. Right, Transesophageal echocardiogram in the midesophagus four- chamber transverse view from the same patient. The mitral valve morphology in this patient is ideal for mitral balloon commissurotomy and excellent results would be expected. LA, left atrium. atrium to the left ventricle through the narrowed mitral orifice, the body of the leaflets balloon apically. The mobility of the leaflets (amplitude of doming) reflects the degree of calcification of the leaflets and commissural fusion. Both qualitative and semiquantitative criteria have been proposed for evaluation of leaflet morphology. [6] [7] In patients in whom the transthoracic echocardiogram is inadequate, transesophageal echocardiography can provide a similar analysis of the mitral valve morphology, although nonstandard image planes may complicate interpretation ( Fig. 20-3 and Fig. 20-4 ). [8] [9] In addition, subvalvular thickening and calcification may be underestimated on transesophageal imaging because of masking of the subvalvular region from thickening and calcification in the mitral valve leaflets. To some extent, these limitations can be avoided by use of biplane or multiplane transesophageal echocardiography with imaging of the subvalvular region in the transgastric longitudinal imaging plane. Total echocardiographic scoring systems based on leaflet morphology have been proposed as a guide to the selection of patients for mitral balloon commissurotomy. Although studies using these methods have been shown Figure 20-4 Left, Transthoracic two-dimensional echocardiogram from a patient with mitral stenosis undergoing evaluation for mitral balloon commissurotomy. The mitral valve is heavily calcified with decreased excursion of the mitral leaflets during diastole. Right, Transesophageal echocardiogram in the midesophagus transverse view, which again shows a heavily calcified immobile mitral valve. The assessment of the morphologic features of the mitral valve are similar between the transthoracic and transesophageal echocardiographic examinations. The increase in mitral valve area from mitral balloon commissurotomy in this patient would be expected to be minimal. LA, left atrium. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 8 438 Figure 20-5 The anatomic features of the mitral valve in relationship to the resultant mean mitral valve area immediately after |
catheter balloon valvuloplasty are shown for the presence or absence of calcification, subvalvular disease, and pliable or rigid mitral valves. The mean mitral valve area was greater in the groups with pliable mitral valves without calcification or subvalvular disease. to correlate with the immediate results, the wide scatter of the data makes their value questionable in an individual patient for predicting the hemodynamic results of the procedure ( Fig. 20-5 and Fig. 20-6 ). These criteria should be used, therefore, only as a guide to the severity of the individual morphologic variables of the mitral valve. Table 20-2 is a summary from the literature of the morphologic features of the mitral valve and the criteria used in assessment before mitral balloon commissurotomy. The single best echocardiographic morphologic variable that predicts the results of mitral balloon commissurotomy is leaflet mobility, which reflects the extent of commissural fusion and calcification of the mitral leaflets.[10] In the studies of the National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry and Reid et al,[6] [10] leaflet mobility was the only independent echocardiographic variable to predict the results of mitral balloon commissurotomy (Table 20-3) . The presence of calcification and the involvement of one or both commissures assessed in the two- dimensional echocardiography parasternal short-axis view may also be helpful in predicting the success of commissural Figure 20-6 Total morphology score by echocardiography versus mitral valve area (MVA) measured by cardiac catheterization after mitral balloon commissurotomy (MBC). There is significant (P < .001) but weak negative correlation (r = -0.24). splitting by the balloon dilation (see Fig. 20-2) .[11] In asymmetric involvement of the commissures, in which one commissure is heavily fibrosed or calcified, splitting occurs in the opposite commissure. If both commissures are equally fused without marked calcification, both commissures are expected to split. In one study, if at least one commissure split, 89% of patients had a good hemodynamic result.[11] The presence of severe subvalvular fibrosis and calcification may also result in suboptimal results from mitral balloon commissurotomy because it is unclear that balloon dilation is able to split chordal fusion. Isolated subvalvular disease, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 8 however, rarely occurs and is usually associated with extensive fibrosis and calcification of the commissures and valve leaflets. The best hemodynamic result based on echocardiographic evaluation is expected in a patient with a highly mobile mitral valve without evidence of calcification or severe subvalvular disease (see Fig. 20-3) . In this group of patients, a mean resultant mitral valve area greater than 2.0 cm2 is predicted.[6] Mitral valve morphology, however, should not be used alone in the selection of patients to undergo mitral balloon commissurotomy. In occasional patients, satisfactory hemodynamic and clinical improvement can occur with more severe mitral valve disease. Other variables that have been shown to influence the results of the procedure and should be considered in the selection of patients include evidence of long-standing disease such as a low cardiac output, baseline mitral valve area, and left atrial size and technical factors such as the balloon diameter used in the dilation. Assessment of Left Atrial Size and Left Atrial Thrombi As a result of chronic pressure overload, the response of the left atrium is progressive enlargement. With long-standing mitral stenosis, an extremely large or "giant" left atrium (>6.5 cm anteroposterior diameter) may result. The 439 TABLE 20-2 -- Two-Dimensional Echocardiographic Assessment of Mitral Valve Morphology Predicted Results Variable OPTIMAL SUBOPTIMAL Leaflet Highly mobile with restriction Minimal forward motion of motion of only leaflet tips and H/L leaflets in diastole or H/L ratio ≥ 0.45 ratio ≤ 0.25 Leaflet Leaflets < 4–5 mm or Leaflets > 8.0 mm thick or a thickening MV/PWAo ratio of 1.5–2.0 MV/PWAo ratio ≥ 5.0 Subvalvular Thin, faintly visible chordae Thickening and shortening disease tendineae with only minimal of chordae to papillary thickening below valve muscle; areas with echo mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 8 density greater than endocardium Commissural Homogeneous density of both Both commissures heavily calcium commissures calcified H, height of doming of mitral valve; L, length of dome of mitral valve; MV, mitral valve; PWAo, posterior wall of aorta. Data from Reid CL, Chandraratna PAN, Kawanishi DT, et al: Circulation 1989;80:515–524; and Abascal VM, Wilkins GT, Choong CY, et al: J Am Coll Cardiol 1988;2:257–263. enlarged left atrium can compress the inferior vena cava, resulting in increased Doppler flow velocities and an increased incidence of hepatomegaly.[12] Other well-recognized complications associated with an enlarged left atrium include the development of atrial fibrillation and blood stasis within the enlarged left atrium with thrombus formation. Left atrial thrombi occur in approximately 25% of patients with mitral stenosis and are seen even in patients in normal sinus rhythm. [13] In the majority of cases, the thrombi are confined to the body of the left atrial appendage, but they may also protrude into the body of the left atrium or attach to the left atrial wall or interatrial septum (Fig. 20-7) . In patients undergoing mitral balloon commissurotomy, the size of the left atrium has been noted to have a significant influence on outcome.[14] In patients with large left atria (>6 cm), technical difficulties may be encountered in performing the trans-septal puncture and crossing the mitral valve orifice. Enlarged left atria also are more frequently associated with a suboptimal increase in the resultant mitral valve area, perhaps because of technical difficulties or as an index of more severe and chronic disease. Conversely, smaller left atria are more frequently associated with the development of an atrial septal defect after mitral balloon commissurotomy. In such patients, shorter balloon sizes should be used or care taken during the procedure to prevent slippage of the balloon catheter against the interatrial septum. Systemic embolization has been reported in 0 to 4% TABLE 20-3 -- Predictors of Mitral Valve Area Variable R2 P value NHLBI-BVR[10] 0.31 <.001 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 8 Pre-MBC MVA <.001 Cardiac output .004 Leaflet mobility .01 Left atrial size .01 Balloon diameter .02 REID et al[6] 0.65 .0001 Leaflet motion .0001 EBDA .03 Cardiac output .002 EBDA, effective balloon dilating area; MBC, mitral balloon commissurotomy; MVA, mitral valve area; NHLBI-BVR, National Heart Lung, and Blood Institute Balloon Valvuloplasty Registry. of patients undergoing mitral balloon commissurotomy.[15] Because the dilating balloon catheters must traverse the left atrium to be positioned across the stenotic mitral orifice, the risk of embolization is increased if a left atrial thrombus is present. Transesophageal echocardiography has been shown to be more sensitive than transthoracic echocardiography in the identification of left atrial thrombi, especially for imaging of the left atrial appendage where most thrombi occur. Furthermore, by transthoracic echocardiography the left atrium lies in the far field of the ultrasound beam, thus the image quality is suboptimal. In contrast, the left atrium is the structure closest to the ultrasound beam by transesophageal echocardiography and thrombi therefore can be accurately located and characterized by size and shape. Identification of left atrial thrombi is especially important in patients who are undergoing mitral balloon commissurotomy because of the risk of systemic embolization.[16] Although some of these episodes are undoubtedly from left atrial thrombi, other sources also must be considered, such as atherosclerotic debris and catheter thrombi.[17] The role of transesophageal echocardiography in patients before mitral balloon commissurotomy is controversial. Although mitral valve morphology and hemodynamic Figure 20-7 Transesophageal echocardiograms from two patients undergoing evaluation for thrombi before mitral balloon mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 8 commissurotomy. Recordings were made at the midesophagus in a four-chamber view. Left, The interatrial septum through which the dilating balloon catheter is inserted is thin and without evidence of clot. Right, The interatrial septum is markedly thickened with evidence of a layer clot along the left atrial side of the septum (arrows). LA, left atrium; RA, right atrium. 440 assessment of the severity of the mitral valve disease can be reliably predicted in most patients by transthoracic echocardiography, only transesophageal echocardiography can accurately exclude the presence of a left atrial thrombus. Obviously, if a left atrial thrombus is detected by transthoracic echocardiography, then a transesophageal echocardiogram is not usually necessary. Although the presence of a left atrial thrombus is not an absolute contraindication for mitral balloon commissurotomy, it should only be considered in patients that are at high risk for surgical commissurotomy. In such patients, monitoring by transesophageal echocardiography during the mitral balloon commissurotomy can be used to help guide the placement of the balloon catheters to avoid the thrombus. [18] A layered thrombus along the interatrial septum is a particularly high risk because of the trans-septal puncture. If no contraindication to anticoagulant therapy is present, it is prudent to treat the patient with anticoagulants for 1 to 3 months before the mitral balloon commissurotomy because some thrombi may resolve with anticoagulant therapy. Transesophageal echocardiography should then be performed in close temporal relationship to the mitral balloon commissurotomy. If a left atrial thrombus is present, anticoagulant therapy may be continued if the patient is clinically stable to attempt to resolve the thrombus or the patient should be referred for surgical mitral commissurotomy. Although anecdotal cases of patients having successful mitral balloon commissurotomy with thrombi confined to the atrial appendage have been noted, the procedure should be considered in patients only after thorough consideration of the risks and potential benefits. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/173.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 10 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Hemodynamic Assessment of the Patient Undergoing Mitral Balloon Commissurotomy Hemodynamic assessment of the severity of mitral valve disease in the patient undergoing mitral balloon commissurotomy can be measured reliably by Doppler and two-dimensional echocardiography. The severity of the stenosis can be quantitated by measurement of the mitral valve area and gradient and the presence, and the severity of mitral regurgitation can be assessed by two-dimensional echocardiography in combination with spectral and color Doppler data. TABLE 20-4 -- Comparison of Mitral Valve Areas by Doppler Echocardiography with Gorlin-Formula Mitral Valve Areas Before and After Mitral Balloon Commissurotomy MVA, Mean ± SD (cm2 ) r Value Author Method BEFORE AFTER BEFORE AFTER Reid et al[6] T½ 1.0 ± 0.2 1.9 ± 0.4 0.73 0.42 2D echo 1.0 ± 0.2 2.2 ± 0.4 0.71 0.34 Abascal et al T½ 0.9 ± 0.2 1.5 ± 0.4 0.75 0.46 [7] 2D echo 0.9 ± 0.3 1.8 ± 0.4 0.81 0.75 Nakatani et al Continuity 0.9 ± 0.3 1.6 ± 0.4 0.77 0.86 [27] equation Chen et al[30] T½ 0.8 ± 0.2 2.4 ± 0.6 0.81 0.84 MVA, mitral valve area; SD, standard deviation; T½, pressure half-time; 2D echo, two-dimensional echocardiography. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 10 Mitral Stenosis Severity Pressure Gradients The mean diastolic mitral valve gradient is measured from Doppler flow velocity tracings based on the modified Bernoulli equation. In patients undergoing mitral balloon commissurotomy, Doppler gradients are accurate as shown by simultaneous measurement of mitral valve gradient before and after mitral balloon commissurotomy in comparison to cardiac catheter- derived gradients (r = 0.70 and 0.89, respectively). [19] Pressure gradients across stenotic valves depend on the volume flow rate and orifice size. Thus, the pressure gradient varies depending on the hemodynamic state of the patient. If the volume flow rate increases, such as with exercise, the gradient increases. Conversely, if the patient is dehydrated, the gradient may be low. Because of this flow rate dependency, calculation of mitral valve area is essential. Mitral Valve Area Two-Dimensional Echocardiographic Planimetry of Mitral Valve Orifice. Two-dimensional echocardiography or Doppler echocardiography is used for determination of the mitral valve area in patients with mitral stenosis. By two-dimensional echocardiography, the mitral valve orifice can be directly planimetered when visualized in the parasternal short-axis view. * Careful scanning by two-dimensional echocardiography of the mitral valve apparatus must be performed to identify the smallest or most restrictive orifice. The gain settings of the machine must be adjusted |
to prevent "blooming" because of the presence of calcification. The accuracy of this method in patients before mitral balloon commissurotomy has been confirmed in several studies with r values of two-dimensional echocardiography compared to cardiac catheterization ranging from 0.71 to 0.81 (Table 20-4) . The mitral valve area estimated by two-dimensional echocardiographic planimetry of the mitral valve orifice before mitral balloon commissurotomy, in reported series, ranges from 0.9 to 1.0 cm2 , with a resultant increase immediately following the procedure to 1.8 to 2.2 cm2 .[6] [7] After mitral *See Otto CM (ed): Textbook of Clinical Echocardiography, 2nd ed. Philadelphia, WB Saunders, 2000, pp 229–264. 441 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 10 balloon commissurotomy, the correlation ranges from an r value of 0.51 to 0.75.[19] [20] [21] [22] Similar to patients after surgical commissurotomy, in patients following mitral balloon commissurotomy the orifice becomes more irregular and technically difficult to planimeter, especially if calcium is present. Because of the accuracy of this technique, two-dimensional echocardiography measurement of the mitral valve area should be performed in all patients undergoing mitral balloon commissurotomy in whom it is technically feasible. Doppler Pressure Half-Time Mitral Valve Area. Doppler spectral tracings are used to estimate mitral valve area based on the pressure half-time method described by Hatle et al.[23] The pressure half- time (T ) is defined as the rate at which the initial mitral valve gradient 1/2 declines to one half of the initial value, with mitral valve area (MVA) calculated as: MVA = 220/T1/2 (Fig. 20-8) . Although several clinical studies have validated the accuracy of this method, there are limitations to the technique, some of which are unique to patients undergoing mitral commissurotomy. Factors that influence the accuracy of the Doppler pressure half-time method are both technical and hemodynamic. The accuracy of Doppler flow velocity tracings for hemodynamic measurements depends on the Doppler beam being parallel to the direction of blood flow. In patients with mitral stenosis, Doppler flow velocity recordings typically are made in the apical four-chamber view with the Doppler beam directed through the center of the mitral stenotic jet. Adequate tracings can be recorded in most patients with the aid of Doppler color flow to identify the stenotic jet even in patients for whom two-dimensional echocardiography is inadequate. In the rare patient in whom transthoracic flow velocity tracings cannot be obtained, transesophageal echocardiography can be performed to obtain the flow velocity tracings from a high esophageal position in a four-chamber view. Another technical limitation to the Doppler pressure half-time method is difficulty in identifying the diastolic deceleration slope. In some patients, the diastolic flow is Figure 20-8 Doppler transmitral flow velocity from a patient with mitral stenosis. The pressure half-time (T1/2 ) is the time required for the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 10 initial gradient to decrease to one half. This point is identified on the diastolic slope of the transmitral flow tracing. Figure 20-9 Transmitral Doppler flow velocity tracing from a patient with nonlinear flow (arrow). In this circumstance the mid-diastolic flow, which is more linear, should be extrapolated back to obtain the maximal initial velocity (dashed line). nonlinear (Fig. 20-9) . If linear flow cannot be obtained by careful angulation and placement of the Doppler beam, the mid-diastolic flow, which is more linear, should be used and the slope extrapolated back to obtain the initial maximum velocity.[24] In patients with rapid heart rates who are in sinus rhythm the A wave may be superimposed on the diastolic slope, making identification impossible. Similarly, rapid atrial fibrillation and atrial flutter may preclude identification of the early diastolic slope. Hemodynamic considerations in the application of the Doppler pressure half-time method include the effects of coexisting valve disease. When aortic regurgitation is present, the increased diastolic filling may result in a more rapid rise of the left ventricular end-diastolic pressure. As a result, the pressure half-time may be shorter than expected for the valve area; therefore, the severity of the mitral stenosis may be underestimated.[25] The severity of the aortic regurgitation can be assessed by color Doppler flow and, if mild or moderate, the pressure half-time method may be applied. If the aortic regurgitation is severe or acute (which is unusual in mitral stenosis patients), the limitation of the pressure half-time method should be recognized and an alternative method applied for estimation of the mitral valve area. One of the major limitations of the Doppler pressure half-time method is calculation of the mitral valve area when hemodynamics are changing rapidly. With the advent of mitral balloon commissurotomy, it was recognized early that calculation of the mitral valve area immediately following mitral balloon commissurotomy might be inaccurate.[5] The Doppler pressure half-time method assumes that the left atrial and left ventricular compliances are stable (Fig. 20-10) .[26] This assumption is not valid following relief of the mitral stenosis by balloon dilation because there are rapid changes in the left atrial pressure and left ventricular filling with consequent changing compliances of both the left atrium and left ventricle. The mitral valve mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 10 442 Figure 20-10 Left atrial (LA) and left ventricular (LV) compliance curves showing the relative changes in LV and LA pressures and volumes before and after percutaneous mitral valvuloplasty (PMV). The LA pressure- volume relationship (top) shifts to the left after PMV because of reduced LA size and pressure, whereas the LV pressure-volume relationship (bottom) shifts to the right because of increased diastolic ventricular filling. Despite these significant shifts in individual chamber compliance, the net compliance remains almost constant before and after valvuloplasty. (From Thomas JD, Wilkins GT, Choong CY, et al: Circulation 1988;78:980–993.) area by the pressure half-time method also varies directly with the square root of the initial pressure gradient across the mitral valve, further complicating post-mitral balloon commissurotomy data as pressures rapidly fall. It should be noted, however, that the widely accepted catheter-derived mitral valve area based on the Gorlin formula also may be inaccurate following mitral balloon commissurotomy because of significant mitral regurgitation and the presence of an atrial septal defect leading to inaccurate measurement of transmitral volume flow.[27] In patients before mitral balloon commissurotomy, the noninvasive estimation of mitral valve area correlates well with invasive estimates (see Table 20-4) , with a standard error of the estimate ranging from 0.15 to 0.11 cm2 (r = 0.71-0.81) for Doppler pressure half-time method, 0.22 cm2 (r = 0.77) for the continuity equation method, and 0.17 cm2 (r = 0.71-0.81) for the two- dimensional echocardiographic planimetry method.[19] [20] [21] [22] [23] [27] Immediately following mitral balloon commissurotomy, however, the Doppler pressure half-time method correlates less well with invasive data or with two-dimensional echocardiographic planimetry of valve area (see Table 20-4) . This inaccuracy is multifactorial and includes the rapid hemodynamic changes and the development of an atrial septal defect in many patients post mitral balloon commissurotomy.[28] In this setting, the pressure half-time method may overestimate the mitral valve area and depends on the magnitude of the shunt. In one study, occlusion of the atrial septal defect in patients after mitral balloon commissurotomy decreased the difference in the mitral valve area calculated by hemodynamic measurements and by the Doppler pressure half-time method.[29] This difference was due largely to a decrease in the mitral valve area calculated by the Gorlin formula when the atrial septal defect was occluded. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 10 The accuracy of the Doppler pressure half-time method has been shown to improve with time from the procedure. At 24 to 48 hours, hemodynamic equilibrium may be reached and the Doppler pressure half-time accuracy improves.[27] Furthermore, the mitral valve area calculated by the continuity equation decreases slightly at 24 hours probably because of a loss of "stretch" of the mitral valve. Because of these many considerations, caution should be taken in estimating the noninvasive mitral valve area immediately following mitral balloon commissurotomy. Doppler Continuity Equation Mitral Valve Area. The calculation of mitral valve area by the continuity equation is based on the law of conservation of mass. The mitral valve area is calculated as MVA = (AVA [or PVA] × TVI [or TVI ])/TVI where MVA is mitral a p m valve area, AVA (PVA) is aortic (pulmonary) valve area measured from two-dimensional echocardiography, TVIa (TVIp ) is time velocity integral of the aortic (pulmonary) flow, and TVI is time velocity integral of m transmitral flow. One advantage of the continuity equation is that it is theoretically independent of transvalvular gradient and compliance. The continuity equation method, however, is much more difficult to perform. In addition, application of the continuity equation requires that the flow across the stenotic valve and another valve must be equal, based on the conservation of mass. In patients with associated mitral regurgitation, particularly if greater than mild, the stroke volume across the valves is different. Similarly, if greater than mild aortic regurgitation is present, pulmonary flow should be used. If the continuity equation is used to calculate the mitral valve area in the presence of mitral stenosis and an atrial septal defect, the transaortic Doppler flow should be used to avoid the effect of shunt flow volume. Other limitations of the technique include difficulty in measuring accurate pulmonary and aortic diameters. Regardless of the technical difficulty, studies have shown the method to be accurate in the calculation of mitral valve area with a correlation of r = 0.81 before mitral balloon commissurotomy and r = 0.84 after mitral balloon commissurotomy.[30] Stress Doppler Echocardiography The clinical decision on interventional therapy for the relief of mitral stenosis must take into consideration the patient's symptoms in addition to the severity of the stenosis based on area and gradient. In some patients, symptoms of mitral stenosis caused by the elevated left atrial pressure and mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 10 pulmonary congestion may be present 443 only during exercise. The transmitral gradient is dependent on flow volume and, thus, the severity of the mitral stenosis is underestimated in patients with low cardiac output at rest. Exercise hemodynamics have been used in patients with mitral stenosis to determine whether the mitral stenosis limits the transmitral flow and contributes to the patient's symptoms.[31] [32] Stress testing in patients with mitral stenosis is performed during supine bicycle or pharmacologic stress, which allows recording of the Doppler flow velocity. The calculation of mitral valve area by Doppler methods is controversial and the reliability of the pressure half-time in this setting is questionable.[32] [33] Calculation of the mitral valve area by the continuity equation in this setting is technically difficult. The severity of the mitral stenosis still can be reliably assessed by measurement of the transmitral gradient and pulmonary artery systolic pressure and assessment of the patient's symptoms. Studies have shown that mitral flow dynamics are improved in patients who have undergone mitral balloon commissurotomy with a decrease in the transmitral gradient and heart rate at maximal stress. [34] [35] Associated Lesions Mitral Regurgitation Mitral regurgitation, in varying degrees of severity, is commonly associated with mitral stenosis. The severity of associated mitral regurgitation can be assessed using standard Doppler echocardiography techniques (see Chapter 17) . Because most patients undergoing mitral balloon commissurotomy have transesophageal echocardiography, the variability in assessing the severity of mitral regurgitation by transesophageal and transthoracic echocardiography should be recognized. Because of the closer proximity of the transesophageal probe to the flow, shallower depth setting, decreased attenuation of the Doppler signals, and higher transducer frequency, the flow disturbance by the mitral regurgitation appears larger by transesophageal echocardiography.[36] [37] [38] Thus, there is a tendency to overestimate the severity of the mitral regurgitation when assessed by transesophageal echocardiography. Caution must be taken in estimating the severity of the mitral regurgitation in association with mitral stenosis. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 10 Patients with severe mitral regurgitation associated with mitral stenosis are not considered candidates for either balloon or surgical commissurotomy. In patients with moderate mitral regurgitation (grade 2+), commissurotomy should only be undertaken based on the patient's symptoms and the degree of mitral stenosis. Mild mitral regurgitation is not considered a contraindication to mitral balloon commissurotomy. In patients with associated mild or moderate mitral regurgitation, however, left atrial size is greater, which may cause more technical difficulties during the procedure. Pulmonary Hypertension |
In patients with severe, long-standing mitral stenosis, the elevated left atrial pressure results in pulmonary hypertension and elevated pulmonary vascular resistance. Initially, the increase in pulmonary artery pressure is "passive" because of the increased resistance to the pulmonary venous drainage within the left atrium. With chronic elevation of the left atrial pressure, the pulmonary hypertension becomes "reactive" with an increase in the pulmonary vascular resistance.[39] Secondary effects of pulmonary hypertension include the development of right ventricular hypertrophy, right ventricular enlargement and dysfunction, and tricuspid regurgitation because of annular dilation. Estimation of the degree of pulmonary hypertension can be made based on the velocity of the tricuspid regurgitant jet.[40] The simplified Bernoulli equation applied to the peak tricuspid regurgitant jet velocity can be used to calculate the right ventricular peak systolic pressure when added to the estimate of right atrial pressure. In patients without right ventricular outflow tract obstruction, the right ventricular systolic pressure reflects pulmonary artery systolic pressure. Pulmonary vascular resistance, however, cannot be determined directly with Doppler echocardiography techniques. The severity of the pulmonary hypertension and pulmonary vascular resistance shows a significant relationship to the mitral valve area (Fig. 20-11) . Because of the wide variation in pulmonary pressures observed with a any given degree of mitral obstruction, however, specific predictors of pulmonary hypertension cannot be identified based solely on the severity of the mitral stenosis.[39] In patients in whom the pulmonary hypertension is out of proportion to the severity of the mitral stenosis, other possibilities, such as coexisting pulmonary disease, should be considered. In patients undergoing mitral balloon commissurotomy, there is a significant decrease in the pulmonary artery pressure as estimated by Doppler echocardiography immediately following mitral balloon mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 10 commissurotomy despite the presence of severe pre-existing pulmonary hypertension.[40] Following mitral balloon commissurotomy, there is an immediate decrease of approximately 10 mm Hg in pulmonary artery pressure. The decrease in pulmonary hypertension following mitral balloon commissurotomy, however, cannot be predicted based on baseline characteristics. [39] Despite the initial improvement in pulmonary artery pressures, Doppler estimate of right-sided pressures should be followed closely for evidence of persistently elevated or increasing pressures.[41] Associated Other Valve Disease Rheumatic heart disease affects not only the mitral valve but also the aortic valve and to a lesser incidence the tricuspid valve. The severity of these lesions can be assessed using standard Doppler echocardiography techniques. Patients that have significant stenosis of the aortic or tricuspid valve can be considered for concurrent dilation with the mitral valve. The symptomatic improvement in patients with aortic stenosis, however, may be limited because of the less than favorable results with balloon aortic valvuloplasty. Associated aortic regurgitation of mild or moderate severity does not significantly affect the hemodynamic and 444 Figure 20-11 Mitral valve area at catheterization on x-axis versus pulmonary vascular resistance on y-axis with inverse curve fit. (From Otto CM, Davis KB, Reid CL, et al: Am J Cardiol 1993;71:876. Reprinted with permission from Excerpta Medica Inc.) symptomatic improvement obtained with mitral balloon commissurotomy. [42] The severity of the tricuspid regurgitation can be semiquantitated, similar to mitral regurgitation, based on the size of the regurgitant jet. Increasing severity of tricuspid regurgitation is directly related to the severity of the mitral stenosis. Patients with severe tricuspid regurgitation have a less favorable long-term result from mitral balloon commissurotomy than patients with mild or moderate regurgitation. [43] Ventricular Function The presence of mitral stenosis results in a chronic restriction in left ventricular diastolic filling. Left ventricular volumes are reduced in patients mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 10 with isolated mitral stenosis compared with normal patients.[44] Left ventricular systolic function is normal. Increased left ventricular diastolic volumes suggests the presence of concomitant mitral or aortic regurgitation. Following successful mitral balloon commissurotomy, left ventricular end-diastolic volume and mass increase without significant change in end-systolic volume or ejection fraction. [45] Right ventricular end-diastolic volumes are increased in patients with severe mitral stenosis. Right ventricular volumes and function in patients with mitral stenosis are affected by the increased afterload because of pulmonary hypertension and the presence and severity of associated tricuspid regurgitation. Successful mitral balloon commissurotomy significantly improves but does not normalize right ventricular function.[46] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/174.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 8 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Role of Doppler Echocardiography in Predicting Results and Complications of Mitral Balloon Commissurotomy Patient Selection Doppler echocardiography plays a major role in the selection and evaluation of patients to undergo mitral balloon commissurotomy (see Table 20-1) . In patients with symptomatic mitral stenosis (mitral valve area < 1.5 cm2 ), the ideal candidate for mitral balloon commissurotomy based on the Doppler echocardiographic examination is one in whom the mitral valve is highly mobile without significant calcification of the leaflets or subvalvular apparatus. The presence of mitral regurgitation of greater than 2+ severity and a large left atrial thrombus within the left atrium or attached to the interatrial septum is considered a contraindication to mitral balloon commissurotomy. Immediate and long-term results are less successful in patients with evidence of long-standing disease such as large left atrium (>6 cm) or low cardiac output, although results vary in individual patients. The presence of significant other valvular disease such as critical aortic stenosis or severe aortic or tricuspid regurgitation and coronary artery disease may warrant consideration for surgical referral. The decision to perform mitral balloon commissurotomy in patients considered to be high risk for surgery because of other medical diseases, suboptimal mitral valve morphology, or a left atrial thrombus must be based on consideration of the risk-to-benefit ratio and the patient's desire. During Mitral Balloon Commissurotomy Doppler echocardiography plays a major role not only in the selection and evaluation of patients before mitral balloon commissurotomy but also is a useful adjunct during the procedure (see Table 20-1) . Doppler echocardiography equipment should therefore be available during the procedure to assess the immediate results and potential complications. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 8 Imaging by two-dimensional echocardiography of the interatrial septum can be performed to confirm and aid in the proper location of the trans- septal catheter in difficult circumstances. Variability in the location of the interatrial septum may occur because of aortic root dilation, right atrial dilation, or cardiac deformity owing to scoliosis, 445 and in these settings, fluoroscopy may be misleading. Echocardiography can be useful in this setting by visualization of the interatrial septum and confirming by contrast saline injection the location of the needle within the left atrium once the trans-septal puncture is performed.[15] The identification of the needle tip may be difficult if it is out of the imaging plane, but it can be assessed indirectly by the "tenting" of the interatrial septum. Following the trans-septal puncture, two-dimensional echocardiography can aid in positioning the catheters across the stenotic mitral orifice. This positioning is important if the double-balloon technique is used. The Inoue balloon technique involves a unique self-seating design, which makes positioning of the balloon catheter easier. Echocardiography is helpful to prevent inadvertent inflation within the left atrium, which may result in an atrial septal defect if it butts against the interatrial septum. In patients with left atrial thrombi considered high risk for surgical commissurotomy, transesophageal echocardiography may be beneficial in preventing inadvertent migration of the catheter into the left atrial appendage. Two-dimensional echocardiography can also be used during the procedure to assess the affects of sequential balloon dilation. The transmitral gradient and changes in mitral regurgitation can be rapidly assessed to determine the need for further inflations. If the mitral regurgitation increases by one or more grades the procedure should be terminated. The success of mitral balloon commissurotomy has been shown to be related to the mitral anulus–to–balloon diameter ratio.[47] The mitral anulus by two-dimensional echocardiography can be measured to aid in selecting the appropriate balloon sizes. The increase in mitral valve is directly related to the mitral anulus–to–balloon diameter ratio. If the balloon diameter is too large, however, excessive tearing of the commissures or mitral leaflets may occur resulting in significant mitral regurgitation. In patients undergoing double- balloon dilation, a ratio of the sum of diameters of the two dilating balloons to mitral anulus of ≥1.1 is associated with a significant increase in mitral regurgitation without further increase in mitral valve area. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 8 Complications of Mitral Balloon Commissurotomy Complications that may occur with mitral balloon commissurotomy are those known to be associated with invasive procedures, including death, myocardial infarction, stroke, bleeding, and heart failure. In the National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry, the incidence of serious complications was 12% and inhospital deaths 1%.[48] The reported complications of mitral balloon commissurotomy that can be detected by Doppler echocardiography are shown in Table 20-5 . Doppler echocardiography provides a rapid method for the early detection of complications and a noninvasive technique for serial evaluation. Atrial Septal Defects The creation of an atrial septal defect in patients undergoing mitral balloon commissurotomy results from the TABLE 20-5 -- Complications of Mitral Balloon Commissurotomy Detected by 2D Doppler Echocardiography Event Incidence (%) Thrombus (systemic embolization) 2 Cardiac perforation (tamponade) 4 Left-to-right shunt (atrial level) 10 Valve related Acute mitral regurgitation (requiring early surgery) 3 Increase in MR 12 Inadequate result (MVA < 1.5 cm2 ; ≥ 2 + increase 36 MR) Restenosis ? MR, mitral regurgitation; MVA, mitral valve area. Data from National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry Participants: Circulation 1992;85:448–461, 2014– 2024. trans-septal approach. The reported incidence of atrial septal defects depends on the method of detection. By oximetry immediately following mitral balloon commissurotomy, the reported incidence ranges from 7% to 33% depending on the type of balloons used and diagnostic criteria.[3] [49] [50] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 8 [51] Transesophageal echocardiography is the most sensitive method for detection of left-to-right shunting after mitral balloon commissurotomy and defects have been reported in 87% of patients examined within 24 hours of the procedure.[52] Transthoracic echocardiography detects left-to-right shunting in about half of the patients immediately following mitral balloon commissurotomy.[53] The detection of left-to-right shunting after mitral balloon commissurotomy requires a thorough evaluation of the interatrial septum in any patient who has undergone mitral balloon commissurotomy. The optimal view of detecting defects of the interatrial septum is obtained from the subcostal approach (Fig. 20-12) . In this position, the cardiac flow is parallel to the ultrasound beam, which is optimal for detection by color Doppler. The characteristic Doppler flow pattern is a continuous or late systolic- holodiastolic left-to-right flow caused by the high pressure gradient between the right and left atrium in patients with mitral stenosis. The size of the defects range from 0.3 to 1.5 cm in diameter. By color Doppler, a jet width less than 0.5 cm is not likely to be detected by oximetry. Atrial septal defects greater than 1.0 cm are associated with significant right heart oxygen stop-ups. Shunt flow volumes calculated by Doppler echocardiographic methods range from 0.08 to 4.87 L per minute. The highest incidence of atrial septal defects is reported immediately after mitral balloon commissurotomy. Defects that are less than 0.7 cm in diameter usually close within 6 months.[54] Factors that have been associated with the development of atrial septal defects after mitral balloon commissurotomy include smaller increases in mitral valve area, the presence of mitral valve calcification, and smaller left atria. Atrial septal defects have also been reported to be initially detected during follow-up. Persistence of an atrial septal defect during follow-up is associated with larger sizes, a decrease in mitral valve area, and an increase in the mitral valve gradient. Clinically, significant problems are not associated with small atrial 446 Figure 20-12 (color plate.) Two-dimensional echocardiogram in the subcostal view from a patient after mitral balloon commissurotomy. Color Doppler flow mapping shows flow from the left to right atrium through |
a large atrial septal defect. The defect created by the dilating balloons measured 0.9 cm in diameter. RA, right atrium; LA, left atrium. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 8 septal defects. The effect on the right heart hemodynamics of large atrial septal defects with or without restenosis of the mitral valve remains to be determined. Mitral Regurgitation Mitral regurgitation is a frequent complication of mitral balloon commissurotomy (Fig. 20-13) . The presence and severity of the mitral regurgitation should be carefully Figure 20-13 (color plate.) Transthoracic and transesophageal echocardiograms from a patient who had undergone mitral balloon commissurotomy (MBC). A, Transthoracic apical four-chamber view before MBC, which by color Doppler flow mapping shows a small blue jet in the left atrium during systole (arrow) consistent with mild mitral regurgitation. B, Same echocardiographic view obtained during the procedure following the first balloon inflation. The Doppler flow mapping shows turbulent flow into the left atrium. The mitral regurgitant jet is directed along the lateral wall and wraps around, almost completely filling the left atrium. C, Transesophageal echocardiogram from the midesophagus longitudinal view, which shows both the anterior and posterior leaflets of the mitral valve are flail with ruptured chordal attachments. LA, left atrium; LV, left ventricle. evaluated by Doppler echocardiography using standard techniques before mitral balloon commissurotomy so that any change in severity can be recognized and evaluated immediately. Creation of new or an increase in pre-existing mitral regurgitation has been reported in 19% to 85% of patients undergoing mitral balloon commissurotomy.[5] [55] [56] [57] [58] [59] In most patients, however, the increase in mitral regurgitation is mild. An increase of greater than 2 grades in mitral regurgitation occurs in only 3% to 10% of patients. [48] [55] [56] [57] [58] [59] In the National Heart, Lung, and Blood Institute Balloon Valvuloplasty Registry early surgery for mitral valve replacement owing to severe mitral regurgitation occurred in 2% of patients.[55] This rate is comparable to results of surgical mitral commissurotomy. Although some patients who develop severe mitral regurgitation require urgent surgery for mitral valve replacement, others may tolerate the mitral regurgitation acutely. The mechanisms in the development of mild increases in mitral regurgitation differs significantly compared with the mechanisms of severe mitral regurgitation.[58] [59] [60] [61] [62] Echocardiographic studies of patients who develop mild increases in mitral regurgitation have shown that the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 8 regurgitant jet originates from the split commissures. Severe mitral regurgitation following mitral balloon commissurotomy, however, results from tearing of the valve leaflets or rupture of the chordal attachments. In one study of patients having balloon commissurotomy with the Inoue technique, the incidence of severe mitral regurgitation was 7.5%.[59] The most common cause was rupture of the chordae tendinae to the anterior or posterior leaflet in 43% of cases. A heavily calcified posterior leaflet resulted in tearing of the leaflet in 30%. Other variables that have been associated with the development of severe mitral regurgitation include severe calcification of both commissures and extensive subvalvular disease. [60] Splitting of the commissures, which most commonly is associated with mild increases in mitral regurgitation, can, if "excessive," result in severe regurgitation owing to incomplete coaptation of the valve leaflets during systole. 447 Unfortunately, the development of severe mitral regurgitation in patients undergoing mitral balloon commissurotomy cannot be reliably predicted from baseline characteristics, valve morphology, or technical factors during the mitral balloon commissurotomy procedure. The incidence of severe mitral regurgitation is not significantly different between patients undergoing double-balloon or Inoue techniques.[48] [56] [57] [58] [59] [60] [61] [62] [63] Similarly, stepwise inflation with the Inoue balloon technique has not reduced the frequency of severe mitral regurgitation. Indeed, inadvertent inflation of the Inoue balloon within the subvalvular apparatus, which may occur because of the unique design of the balloon catheter, can result in rupture of the chordal attachments or tear of the leaflets. Care must be taken in the positioning of the catheter before inflation. In one study, calcification of the posterior leaflet of the mitral valve resulted in a tear of the leaflet in the region of the calcification.[62] After each sequential balloon inflation, Doppler echocardiography should be performed to evaluate changes in mitral regurgitation. Two-dimensional echocardiography in the parasternal short-axis view permits evaluation of commissural splitting to assess the need for subsequent balloon inflations. Cardiac Perforation Perforation of a cardiac chamber can occur during mitral balloon commissurotomy and is a major cause of death in these patients (see Table 20-5) . Atrial perforation can occur during the trans-septal catheterization mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 8 and left ventricular perforation during the balloon inflations. The incidence of cardiac perforation is directly related, in part, to the dilation technique. In the Balloon Valvuloplasty Registry of patients undergoing mitral balloon commissurotomy with either a single- or double-balloon technique, the incidence of perforation was 4%. Perforation was the most common cause of death during the procedure, usually left ventricular perforation, and the most frequent indication for emergency cardiac surgery.[48] Cardiac perforation with the Inoue technique is much less common (<2%).[56] [61] [62] Left ventricular perforation occurs in the relatively thin apex owing to the positioning of the catheters and guidewires used in the technique. Manipulation of the catheters can then result in puncture of the apex. Perforation of the left ventricle usually results TABLE 20-6 -- Follow-up by Doppler Echocardiography of Patients Undergoing Mitral Balloon Commissurotomy Mean F/U MVA (cm2 ) No. of Author Method Patients Mo RANGE BEFORE AFTER F/U Vahanian et al[63] 2D 235 18 1–48 1.1 2.0 1.9 Desideri et al[65] T½ 57 19 9–33 1.0 2.2 1.9 Georgeson et al T½ 33 17 1–38 1.1 2.0 1.7 [41] 2D 1.1 1.9 1.7 Park et al[67] T½ 59(I) * 13 — 0.9 1.8 1.6 2D 61(D) † 0.9 1.9 1.7 Hernandez et al T½ 561 39 — 1.0 1.8 1.7 [70] F/U, follow-up; MVA, mitral valve area; T½, pressure half-time; 2D, two-dimensional valve area. *Inoue balloon technique. †Double-balloon technique. in abrupt hemodynamic collapse. Prompt recognition of this complication is essential. The role of echocardiography in the early diagnosis of this devastating complication is the most commanding reason for availability of echocardiographic equipment during the procedure. Echocardiography can mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 8 identify the presence of cardiac tamponade caused by the perforation and guide the pericardiocentesis required to stabilize the patient. Although the incidence of left ventricular perforation has been reduced with the Inoue technique, the risk of perforation of the atria is common to both procedures. This risk is due to the need for trans-septal catheterization to position the balloons across the mitral orifice. Perforation of the atria, however, usually has less devastating consequences and can frequently be treated with pericardiocentesis or careful observation. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/175.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Long-term Outcome The reported follow-up of patients who have undergone mitral balloon commissurotomy for mitral stenosis have ranged from 6 to 69 months.[40] [41] [57] , [64] [65] [66] [67] [68] [69] [70] [71] Early improvement in functional status occurs in approximately 90% of patients with the majority being in New York Heart Association functional class I or II. Sustained clinical improvement in functional status has been shown to be predicted by baseline characteristics.[64] [65] [67] [68] [69] [70] [71] [72] Patients with noncalcified valves by echocardiography and an excellent result from the mitral balloon commissurotomy (mitral valve area > 2.0 cm2 , < 2 + mitral regurgitation) have an event-free survival rate of 79% at 5 years.[67] Noninvasive testing with Doppler echocardiography eliminates the need for repeat cardiac catheterization in the hemodynamic evaluation of these patients during long-term follow-up. In the limited reported studies, the mitral valve area by Doppler echocardiography has shown a small decrease in valve area but remains significantly greater than that measured before the procedure (Table 20-6) . Restenosis (loss of 50% of the initial increase and a valve area of < 1.5 cm2 ) occurs in 6% to 21% at a mean follow-up of 19 to 22 months depending on the type of valve anatomy.[64] [66] Clinical and echocardiographic variables that have been shown to predict a poor long-term result are shown in Table 20-7 . The strongest predictor of the long-term 448 TABLE 20-7 -- Baseline Variables Associated with Poor Long-term Results Following Mitral Balloon Commissurotomy Clinical mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 Advanced Age 64, 67, 69 Higher NYHA 43, 67, 69 Previous commissurotomy 43, 63 Hemodynamics Lower initial valve area 63 Presence of MR 43, 64, 68 Poor valve morphology or 43, 64, 65, 66, 67, 69, 70, 71 calcification 43 Severe tricuspid regurgitation 67 Higher pulmonary artery pressure 67, 69 Immediate Hemodynamic Results Poor initial result (MVA ≤ 1.5 cm2 ) 43, 63, 65, 67, 70 Severe MR (> 2T) 63, 70, 71 Procedural EBDA 67, 68 EBDA, effective balloon dilating area; MR, mitral regurgitation; NYHA, New York Heart Association functional class. results, as with the immediate results of mitral balloon commissurotomy, is the degree of valve deformity. Patients with severe calcification of the mitral valve have both a poorer immediate result and long-term outcome than patients with more favorable valve anatomy. Other predictors of an adverse outcome include a lower initial valve area, the presence of mitral regurgitation or severe tricuspid regurgitation, and a higher pulmonary artery pressure. Increases in mitral regurgitation, which are common following mitral balloon commissurotomy, are generally well tolerated during follow-up. Although patients who develop severe mitral regurgitation usually require valve replacement during short-term follow-up, the changes in the mild to moderate mitral regurgitation are variable. The degree of mitral regurgitation by color Doppler echocardiography in reported series remains unchanged in 46% to 60%, decreases in 30%, and increases in 20% to 10% of patients.[64] [66] Multivariate analyses, however, have shown that the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 presence of mitral regurgitation both before and after mitral balloon commissurotomy is associated with a lower event-free survival.[65] [68] Thus, patients with either pre-existing or new mitral regurgitation should be followed closely after mitral balloon commissurotomy with clinical and echocardiographic evaluation for the development of symptoms or changes in valve function. The long-term effects of atrial septal defects is yet undetermined. Small defects close in about two thirds of patients during follow-up, and small defects that persist are generally well tolerated. Factors that are associated with the persistence of an atrial septal defect are a pulmonary-to-systemic shunt ratio of greater than 1.5, elevated right and left atrial pressures, smaller mitral valve area following mitral balloon commissurotomy, and evidence of restenosis.[66] These findings are not unexpected because elevation of left atrial pressures either caused by a poor initial result or restenosis would favor shunting through the atrial septal defect and perhaps prevent healing of the atrial septum. The long-term effects of the right ventricular volume overload is unknown. If the patient requires mitral valve surgery during follow-up, the atrial septum should be carefully examined and any defect surgically closed. Difficult management problems, however, occur in patients who have a successful mitral valve dilation but in whom a significant atrial septal defect results. Unfortunately, the hemodynamic burden of mitral stenosis in these patients is exchanged for an iatrogenic Lutembacher's syndrome. Importantly, these patients should be closely evaluated by Doppler echocardiography during follow-up to evaluate the atrial septal defect and evidence of developing right ventricular volume overload or restenosis. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/176.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: |
The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Technical Limitations and Alternate Approaches The technique of mitral balloon commissurotomy has proved that sustained clinical and hemodynamic improvement occurs in most patients treated for symptomatic mitral stenosis. The immediate results are equal to those obtained with surgical commissurotomy. The technique is not, however, without its limitations. Suboptimal results and complications occur in a number of patients regardless of whether the double-balloon or Inoue technique is used. Doppler echocardiography has been invaluable in the evaluation of patients and the technique as mitral balloon commissurotomy has evolved. Patients with mitral stenosis who require intervention can be identified and the results predicted by careful Doppler echocardiographic evaluation. Before intervention, patients with mitral stenosis can be evaluated reliably by the pressure gradient, valve area, severity of valvular regurgitation, and indirect evidence such as chamber size and intracardiac pressures. Thus, the majority of patients with isolated mitral stenosis do not require more invasive testing with cardiac catheterization. In older patients, in whom the presence of coronary artery disease is a consideration, coronary angiography should be performed. Furthermore, cardiac catheterization, either as the initial evaluation or in patients in whom restenosis is suspected, should be reserved for those patients in whom there is a discrepancy between the physical or clinical signs and the Doppler echocardiographic examination. The choice of mitral balloon commissurotomy or surgical commissurotomy in patients identified who require intervention depends on a number of factors. Presently, mitral balloon commissurotomy should be considered the procedure of choice in patients with isolated mitral stenosis with favorable mitral valve anatomy because it is cost-effective and safe. In other patients, mitral balloon commissurotomy may be required if the patient refuses surgery or the medical condition makes surgery high risk. In mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 patients with less favorable valve anatomy, the decision for mitral balloon commissurotomy or surgical commissurotomy must be made based on the consideration of risks and benefit of each procedure. Mitral balloon commissurotomy, however, should only be considered a palliative procedure, which may delay the time in which surgical 449 intervention may be required for mitral valve replacement. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/177.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Future Directions Although the immediate and current follow-up of patients undergoing mitral balloon commissurotomy is favorable and comparable to surgical commissurotomy, several issues remain. Potential long-term questions remain unresolved. For example, does the presence of persistent small atrial defects significantly alter the clinical course of patients? In order to answer this question and others, continued follow-up of patients who have undergone mitral balloon commissurotomy is required. Further refinements in the technique and in the development of balloon catheters also may be expected; however, whether these changes will result in significant improvement in the expected outcome depends on careful patient selection. The development of intracardiac echocardiography also may be of benefit in the guidance of the procedure.[73] Regardless of these considerations, mitral balloon commissurotomy has become a proven technique and will continue to play a major role in the treatment of patients with symptomatic mitral stenosis. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/178.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company 451 Chapter 21 - Clinical Decision Making in Endocarditis Nelson B. Schiller MD Infection of the endocardium walls or lining layer of the heart—whether on valve leaflets or chordae, congenital defects, chamber walls, paraprosthetic tissue, or the attachment of implanted shunts or conduits—is known as infective endocarditis. The major milestones in our understanding of infective endocarditis include availability of diagnostic blood culture techniques in the first decades of the 20th century; reversal of its invariably fatal course with antibiotics; palliation of potentially fatal valvular complications with surgery; and, most recently, immediate and accurate diagnosis of its anatomic and hemodynamic manifestations with echocardiography. Although no technique in isolation can always establish this diagnosis, echocardiography has a very high sensitivity for detection of valvular vegetations and complications of infective endocarditis. Thus, echocardiography is the only imaging modality that has a significant role in the clinical diagnosis and treatment of infective endocarditis. The American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the clinical application of echocardiography (Table 21-1) indicate that echocardiography is an essential technique in the diagnosis and treatment of endocarditis and is mandatory in nearly all patients with this disease. [1] This chapter discusses the use of echocardiography in infective endocarditis mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 with emphasis on both clinical applications and utility in research studies. The weaknesses and pitfalls of the technique are discussed, particularly how these factors might cause the performance of echocardiography in practice to fall short of published data. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/180.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 6 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Basic Principles Underlying a discussion of the use of echocardiography in patients with suspected infective endocarditis must be an attempt to come to terms with a clinical definition of the diagnostic criteria of the syndrome. First, should the diagnostic criteria include echocardiography? The studies that initially evaluated the role of echocardiography in the diagnosis of infective endocarditis could not, of course, use an echocardiographic definition of this disease. Instead, TABLE 21-1 -- ACC/AHA Guidelines for Use of Echocardiography in Patients with Infective Endocarditis CLASS I (Evidence or general agreement that echocardiography is definitely indicated) Detection and characterization of valvular lesions, their hemodynamic severity, and/or ventricular compensation * Detection of vegetations and characterizations of lesions in patients with congenital heart disease suspected of having infective endocarditis Detection of associated abnormalities (e.g., abscesses, shunts) * Re-evaluation studies in complex endocarditis (e.g., virulent organism, severe hemodynamic lesion, aortic valve involvement, persistent fever or bacteremia, clinical change, or symptomatic deterioration) Evaluation of patients with high clinical suspicion of culture-negative endocarditis * CLASS IIA (Conflicting data, but the weight of evidence/opinion is in favor of the usefulness of echocardiography) Evaluation of bacteremia without a known source * Risk stratification in established endocarditis * CLASS IIB (Conflicting data, but efficacy is less well established) Routine re-evaluation in uncomplicated endocarditis during antibiotic mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 6 therapy CLASS III (Not indicated) Evaluation of fever and nonpathologic murmur without evidence of bacteremia Modified from Cheitlin MD, Alpert JS, Armstrong WF, et al: J Am Coll Cardiol 1997;29:862–879. *Transesophageal echocardiography (TEE) may provide incremental value in addition to information obtained by transthoracic echocardiography. The role of TEE in first- line examination awaits further study. 452 TABLE 21-2 -- Clinical Definition of Infective Endocarditis Definite Direct evidence based on histology from surgery or autopsy or bacteriology by Gram stain or culture of valvular vegetation or arterial embolus Probable A. Persistently positive blood cultures plus one of the following: 1. New regurgitant murmur or 2. Predisposing heart disease and vascular/immunologic phenomena (e.g., splinter hemorrhages, Osler's nodes, glomerulonephritis) B. Negative or intermittently positive blood cultures (<2 of 2 or 3 of 3 or 70% positive if more than four obtained) plus all three of the following: 1. Fever 2. Predisposing heart disease and 3. Vascular/immunologic phenomena Possible A. Persistently positive blood cultures plus one of the following: 1. Predisposing heart disease or mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 6 2. Vascular phenomena B. Negative or intermittently positive blood cultures with all three of the following: 1. Fever 2. Predisposing heart disease and 3. Vascular/immunologic phenomena C. For Streptococcus viridans cases only: At least two positive cultures without an extracardiac source and fever Rejected A. Infective endocarditis unlikely and alternative diagnosis apparent B. Infective endocarditis possibility warrants antibiotic therapy C. Culture-negative infective endocarditis diagnosed but excluded by autopsy Modified from Von Reyn CF, Levy BS, Arbeit RD, et al: Ann Intern Med 1981;94(part 1):505–518. most studies adopted or modified the criteria of Von Reyn et al[2] (Table 21- 2) . These somewhat complex criteria have been useful in developing the literature that has established echocardiography as a required part of the clinical work-up, but they now have been replaced by criteria incorporating echocardiographic findings. New criteria ( Table 21-3 and Table 21-4 ) that incorporate echocardiographic findings in the diagnostic criteria for endocarditis have been developed by the Duke Endocarditis Service and have been prospectively tested at several centers.[3] [4] [5] [6] [7] [8] [9] [10] [11] In the initial Duke study, each of 405 retrospectively reviewed suspected cases was classified as definite/probable, possible, or rejected using both the old (nonechocardiographic) and new (echocardiographic) criteria. Only 51% of the pathologically definite cases were detected using the older Von Reyn criteria compared with 80% using the newer Duke criteria. Confirming these findings, in a small prospective study of 63 patients admitted to a nonreferral hospital with a diagnosis of suspected endocarditis,[4] [5] the detection rate for pathologically confirmed cases increased from 50% to 100% when echocardiographic data were used for diagnosis. In this study, all patients had both transthoracic mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 6 echocardiography (TTE) and transesophageal echocardiography (TEE). In the 17 cases with echocardiographic evidence of a vegetation, TABLE 21-3 -- Definitions of Terminology in Duke Criteria for Endocarditis Major Criteria I. Positive blood culture for infective endocarditis Typical microorganism for infective endocarditis from two separate blood cultures (Streptococcus viridans, Streptococcus bovis, HACEK group, community-acquired Staphylococcus aureus or enterococci) in the absence of a primary focus or Persistently positive blood cultures of an infective endocarditis consistent organism recovered from a. Cultures drawn at least 12 hours apart or b. The majority of four cultures spanning more than an hour II. Evidence of endocardial involvement Echocardiogram positive for infective endocarditis by 1. Oscillating mass on valve or apparatus or in jet pathway or on implanted material in absence of alternative explanation or 2. Abscess or 3. New prosthetic dehiscence or III. New valve regurgitation (increase or change in pre-existing murmur not sufficient) Minor Criteria I. Predisposition: predisposing heart condition or intravenous drug history II. Fever ≥ 38°C III. Vascular phenomena: major arterial emboli, septic pulmonary embolism/infarction, mycotic aneurysm (with and without hemorrhage), conjunctival hemorrhage, and Janeway lesions IV. Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth spots, and rheumatoid factor V. Microbiologic evidence: positive blood culture but not meeting major criteria (excludes coagulase-negative staphylococci and organisms not causing infective endocarditis) or serologic evidence of infective mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 6 endocarditis organism VI. Echocardiogram consistent with but not meeting major criteria for endocarditis Modified from Durack DT, Lukes AS, Bright DK: Am J Med 1994;96:200–209. the process was detected only by TEE in 7 cases (41%) (Table 21-5) . In the past 5 years, the Duke criteria have received extensive confirmation. [6] [7] [8] [9] [10] [11] Some studies have suggested ways of improving the criteria while confirming that they TABLE 21-4 -- Duke Criteria for Endocarditis Using Definitions in Table 21-3 I. Definite infective endocarditis Pathologic criteria Microorganisms: demonstrated by culture or histology in a vegetation (in situ or embolized) or in an intracardiac abscess Pathologic lesions: vegetation or intracardiac abscess confirmed active by histology Clinical |
criteria using definitions in Table 21-3 2 major criteria or 1 major and three minor or 5 minor II. Possible infective endocarditis Findings consistent with but falling short of I Definite but not III Rejected III. Rejected Firm alternative diagnosis for manifestations Resolution of manifestations with 4 days or less of antibiotics No surgical or pathologic evidence with 4 days or less of antibiotics Modified from Durack DT, Lukes AS, Bright DK: Am J Med 1994;96:200–209. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 6 453 TABLE 21-5 -- Clinical versus Echocardiographic-Based Criteria: Results of Two Trials Retrospective Duke Trial * Clinical criteria identified 51% of pathologically definite infective endocarditis Echocardiographic/clinical criteria identified 80% Prospective Harbor/UCLA Trial † Clinical criteria identified 50% Echocardiographic/clinical criteria identified 100% (41% by TEE only) *Data from Durack DT, Lukes AS, Bright DK: Am J Med 1994;96:200–209. †Data from Bayer AS, Ward JI, Gintzon LE, Shapiro SM: Am J Med 1994;96:211– 219; Bayer AS: Clin Infect Dis 1996;23:303–304. are the preferred systematic diagnostic approach. One suggestion is to eliminate minor criterion status for a nondiagnostic echocardiogram[12] based on the widespread use of TEE. Another suggestion is to consider a positive Staphylococcus aureus blood culture or Q fever seropositivity as major criteria. However, regardless of possible modifications of the Duke criteria, these studies provide compelling evidence for the inclusion of echocardiography as an integral element in the diagnosis of infective endocarditis. The remainder of this chapter concentrates on the details of the echocardiographic approach to the patient with infective endocarditis by discussing the strengths and weaknesses of each component of the echocardiographic examination as it relates to the detection and analysis of vegetations and complications and the estimation of prognosis. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/181.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 13 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Vegetations The first goal of the echocardiographic examination is identification, characterization, and localization of valvular vegetations. For many reasons, the process is one of integrating circumstantial findings and epiphenomena, and, through indirect (albeit compelling) evidence, reaching a reasonable conclusion that a given echocardiographic set of observations has identified the pathologic hallmark of endocarditis, the vegetation. Once a vegetation has been identified, criteria can be applied to judge clinical prognosis. This diagnostic process first depends on a solid knowledge of the normal appearance of cardiac structures seen in a variety of technically mediated circumstances. These circumstances include the choice of transducer frequency, variations among commercial ultrasound instruments, the unique technical characteristics of each patient, the settings of the instrument, variations in technique among technicians, and the duration and intensity of the examination as influenced by the level of pretest and intratest index of suspicion regarding the likelihood of disease (Table 21-6) . Qualitative and Technical Factors Transducer Frequency Lower frequency transducers (i.e., nominal center line frequency of approximately 2.5 MHz) are the type most commonly employed in adult patients because they combine superior penetration with optimal color flow and spectral Doppler sensitivity. Although the images obtained at lower frequencies are easier to acquire, they are lower in resolution than those obtained at higher frequencies, particularly in the middle and far fields of the image where beam spread causes image degradation. From the precordial window, the mitral valve lies in the middle field, and from the apical window, it lies in the far field. At these distances, a normal valve examined with low frequency insonation tends to take on an irregular or mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 13 lumpy appearance. If present, small vegetations tend to be obscured and normal irregularities magnified. For these reasons, sequential use of both a lower frequency and higher frequency transducer is recommended for routine examinations in order to develop familiarity with the normal appearance of cardiac structures generated under both circumstances and to promote recognition of genuine pathologic changes. Harmonic imaging has become widely available and will soon become the standard modality for most examinations. In this technique, insonation is accomplished by transmission at a standard frequency, but with detection of the reflected signal at its harmonic frequency (one-half the transmitted value). For example, if 3.5 MHz is used for transmission, the received signal is analyzed at 1.75 MHz. The technique provides greater sensitivity for the low-level signals arising from the endocardium, allowing better evaluation of regional ventricular wall motion. Tradeoffs for this beneficial increase in contrast resolution include accentuation of normal leaflet irregularities and homogenation of valve texture; both tend to reduce specificity for identifying a mass as vegetation. The chordal attachment points are particularly likely to take the appearance of small lumps. At the time of this writing, the technique is not available with TEE because it has not been possible to adapt it to the higher frequencies at which TEE examinations are conducted. It is, therefore, not uncommon to perform a TEE examination at 7 MHz in a patient with a "lumpy" mitral valve on transthoracic harmonic imaging but find that the valve is absolutely normal in appearance on TEE. Commercial Instruments and Instrument Setting Variation Dynamic range options, pre- and postprocessing algorithms among instruments, and changes in these settings within instruments alter the appearance of valves. Depth settings, probe frequency, deployment of electronic focusing, and sector width have differing influences on the frame rate at which the image is displayed. At greater TABLE 21-6 -- Technical Factors Affecting Detection of Valvular Vegetations Transducer frequency (particularly low-frequency imaging) Instrument characteristics and settings (especially harmonic imaging) Patient characteristics Pretest expectations and probability mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 13 454 depth settings (e.g., 20 cm), slower frame rates, especially in the far field, may obscure the characteristic rapid vibrations of many vegetations. Some devices offer "B color" tagging of tissue images. This method expands the dynamic range of the display and may influence the appearance of valve pathology. The highly reflective nature of calcific degeneration may be easier to differentiate from the tissue or thrombus-like appearance of vegetations when using this type of image postprocessing. Patient Physical Characteristics Obesity, hyperinflated lungs, narrow interspaces, valvular and annular calcification, and valve prostheses impede the transmission of ultrasound between the transducer and the heart. A tall patient may have greater distance from the apical impulse location to the mitral valve. All of these factors can obscure a vegetation that might have been seen under other circumstances. TEE is less sensitive to these constraints and nearly always provides an excellent examination. The difference between TTE and TEE must be considered when analyzing the endocarditis literature or when choosing the ideal imaging modality for a given patient. Pretest Expectations The physician or sonographer begins each examination with some notion about what is being sought in each patient. If there is strong suspicion of endocarditis, it is only natural to scrutinize the valves with augmented intensity using a complete array of probes and processing algorithms. Under such circumstances, maximal "performance" of the technique may be approached. However, as sensitivity rises, specificity must fall pari passu. Under the magnification of increased surveillance, small, normally unseen irregularities, anatomic variants, and artifacts may be mistaken for vegetations. When only transthoracic imaging was available, considerable time and care was taken to visualize the valve structures in patients with suspected endocarditis with reported sensitivities for detection of valvular vegetations much higher than in subsequent studies comparing TEE with TTE. The lower sensitivities in these studies may possibly be due to a shifting of attention to the TEE arm of the study. Nonetheless, these lower sensitivities are probably more representative of what may be expected in daily clinical practice. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 13 M-mode Echocardiography M-mode echocardiography was the first ultrasound imaging modality widely applied in endocarditis. With M-mode imaging, the smallest size of vegetation that can be detected is estimated to be about 5 mm.[13] Although the role of M-mode imaging is less important when two-dimensional imaging is used, the M-mode approach remains useful in specific situations. M-mode echocardiography offers high sampling rates and fine resolution when compared with two-dimensional imaging (>1000 Hz vs. two-dimensional echocardiography at 30 to 60 Hz). M-mode imaging not only allows recognition of vegetations that prolapse (by location) but also can detect their characteristic tissue level images and typical vibrations. These vibrations occur as the prolapsing mass, composed of platelets, thrombus, bacteria, inflammatory cells, and disrupted valve tissue, is caught in the regurgitant jet. Although it is normal for the aortic valve to vibrate slightly during systole, diastolic vibrations almost certainly indicate that the mass is a vegetation, a torn leaflet, or both (Fig. 21-1A) (Figure Not Available) . Similarly, systolic vibrations of the mitral leaflet are highly suggestive of a vegetation, ruptured valve, or both (see Fig. 21-1B) (Figure Not Available) . In seeking to confirm a mass as a vegetation, it is useful to employ these specific but insensitive signs,[14] but when doing so, to remember that in modern ultrasound equipment their sensitivity has been diluted by lowered resolution and the limited frame rate of the video display in comparison with a single crystal probe combined with a strip chart recorder. Two-Dimensional Echocardiographic Imaging of Vegetations In a meta-analysis of 16 early studies (641 patients) O'Brien and Geiser[15] reported a mean sensitivity of 79% for two-dimensional echocardiography in the detection of vegetations in infective endocarditis. M-mode imaging sensitivity from the same series was only 52%. In one of the first reports of two-dimensional echocardiography in definite (autopsy/surgery) cases of infective endocarditis, Gilbert et al[14] noted good agreement between the location and identity of large vegetations and pathologic findings but encountered difficulties when comparing exact ultrasound measurements to pathologic reality. More importantly, this study found that "several" small vegetations of less than 3 mm in maximum dimension were undetectable by two-dimensional echocardiography. This lower size limit on vegetation detection continues to be a current problem in the use of TTE. In the decade since the Gilbert et al study, the sensitivity mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 13 of TTE has dropped despite major improvements in ultrasound equipment (Table 21-7) . For example, on review of 7 studies performed between 1989 and 1994[16] [17] [18] [19] [20] [21] [22] [31] the mean sensitivity for TTE was 62%, whereas for TEE it was 92%. As stated, the reason for the decrease in TTE sensitivity is probably a combination of more rigorous and less biased case selection in the contemporary studies and less intense scrutiny of the patient with TTE than with TEE. TABLE 21-7 -- Two-Dimensional Echocardiography versus M-mode Echocardiography versus TEE: Sensitivity for Detecting Vegetations Meta-Analysis of 16 Early Studies M-mode, 52% Two-dimensional echocardiography, 79% Meta-Analysis of 7 More Recent Studies Two-dimensional echocardiography, 62% Transesophageal echocardiography, 92% 455 Figure 21-1 (Figure Not Available) A, M-mode image of a disrupted aortic valve showing coarse systolic vibrations (arrowheads) specific for vegetation, disruption, or both. Very fine systolic vibrations are normally seen and can be barely discerned. B, M-mode image of an infected mitral valve showing increased thickness and systolic vibrations specific for vegetation, disruption, or both. The accuracy of the measurement of structures in echocardiographic images is limited by resolution. Because TTE underestimates the size and complexity of large vegetations and fails altogether to detect small vegetations (<3 mm in diameter), it is reasonable to conclude that if knowledge of the size and behavior of vegetations is predictive of prognosis and useful in guiding therapy, TTE underachieves as a prognostic and therapeutic guide. Furthermore, in a review of the literature of infective endocarditis, none of the studies stated the carrier frequency of the transthoracic transducer. From this omission, it may be inferred that there is considerable variation in performance of TTE within and among studies, weakening the use of size criteria in clinical practice. In a comprehensive published study of the prognostic value of the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 13 morphologic details of TTE images of vegetations, Sanfilippo |
et al[23] retrospectively studied 204 patients who met clinical criteria of infective endocarditis. Documented clinical events were correlated with echocardiographic vegetation characteristics. The events or complications were as follows: 1. Failure of febrile illness to respond to an appropriate course of antibiotics so that a change in treatment was required 2. Congestive heart failure on or after admission 3. Pulmonary, systemic, or peripheral embolization 4. Surgery 5. Death Valvular vegetations were defined as "a discrete mass of echogenic material adherent at some point to a leaflet surface and distinct in character from the remainder of the leaflet." Separate classifications were made for nonspecific thickening ("diffuse irregularities"), aortic valve disease, mitral valve disease, mitral prolapse, prosthetic valve, and no evidence of vegetations. If a mass was identified as a vegetation (Table 21-8) , it was analyzed according to four properties: Size: Two largest orthogonal diameters perpendicular and orthogonal to the leaflet (Fig. 21-2) (Figure Not Available) Mobility: Grade 1, fixed; grade 2, fixed base, free edge; grade 3, pedunculation; grade 4, prolapsing (Fig. 21-3) (Figure Not Available) Density: Grade 1, calcified; grade 2, partially calcified; grade 3, more dense than myocardium but not calcified; grade 4, equivalent to myocardium Extent: Grade 1, single; grade 2, multiple on a single leaflet; grade 3, multiple leaflets; grade 4, extending to extra valvular structures The overall incidence of complications was 55%, with equivalent rates for native and prosthetic valves and for clinical endocarditis in nonspecifically thickened valves. Unexpectedly TABLE 21-8 -- Five Characteristics Allowing a Valve Mass to Be Designated a Vegetation Texture Gray scale and reflectance of myocardium mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 13 Location Upstream side of valve in path of jet Characteristic motion Chaotic and orbiting Shape Lobulated and amorphous Accompanying Abscess and pseudoaneurysm abnormalities Fistulas Prosthetic dehiscence Paravalvular leak: significant pre-existing or new regurgitation 456 Figure 21-2 (Figure Not Available) Vegetation size is measured in two axes or diameters. D1 is the maximum size of the vegetation perpendicular to the leaflet; D2 is the maximum extent of the vegetation parallel to the leaflet surface. The larger of the two dimensions was used for analysis. Ao, aorta; LA, left atrium; LV, left ventricle. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191– 1199. Reprinted with permission from the American College of Cardiology.) high rates of complications were found for tricuspid endocarditis (77%) and studies with no abnormality (27%). There tended to be more complications with higher grades of mobility and lesion extent. Vegetation consistency did not predict complications except that those with calcified vegetations had no clinical complications (Fig. 21-4) (Figure Not Available) . Size was perhaps the most powerful predictor of complications. The probability of sustaining a complication was 10% in 6-mm vegetations, 50% in 11-mm vegetations, and almost 100% at 16-mm vegetations in maximum dimension (Fig. 21-5) (Figure Not Available) . Sanfilippo et al also proposed a "score" for risk, calculated as the sum of the scores for size, mobility, and extent (each grades 1 to 4). The highest possible score Figure 21-3 (Figure Not Available) A vegetation mobility grading scheme is illustrated (see text). (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.) Figure 21-4 (Figure Not Available) Complication rates by the extent of a graded vegetation abnormality: mobility, extent, and consistency. The numerator above each mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 13 subgroup refers to the number of patients with a given complication, and the denominator refers to the total number in that subgroup. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.) for any valve is 12. As Figure 21-6 (Figure Not Available) (mitral) and Figure 21-7 (Figure Not Available) (aortic) show, a high score is always present in patients with complications (i.e., high sensitivity), but only half or less of those with high scores actually develop complications (i.e., low specificity). There is a trend for aortic valve endocarditis to have a higher complication rate, but the statistical significance is not clear from this study. These figures are reproduced here because they may prove useful in clinical decision making; however, their "exportability" to TEE findings is uncertain. Because a given vegetation on TEE is likely to appear larger, a higher score may be required for a given level of risk when using the newer modality. Seeking to improve on this study, De Castro et al[24] examined 57 patients with large (>10 mm) vegetations and no previous embolic events at the time of the study using both TTE and multiplane TEE. In the course of the Figure 21-5 (Figure Not Available) Complications relative to vegetation size. Note that this graph is not limited to any one complication such as peripheral embolization but plots all complications relative to size. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.) 457 Figure 21-6 (Figure Not Available) Mitral valve vegetations are scored by adding the grades of size, mobility, and extent. Bottom, The sensitivity, specificity, and predictive accuracy are given for several scores. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.) study, 44% sustained clinically apparent embolic events. Although this study confirmed that large vegetations define a high-risk population, within this group, no single characteristic of vegetation location, mobility, or appearance predicted embolization. Millaire et al[25] used advanced imaging techniques (e.g., magnetic resonance imaging, computed tomography, and other modalities) in 102 patients meeting the Duke criteria for infective endocarditis. Combining the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 13 results of imaging with a 21-month follow-up, the investigators found that 51% had imaging evidence of embolization and that many were clinically inapparent. There was a trend toward higher mortality in those with emboli (20% versus 12%), but the trend did not reach statistical significance. From these data it was concluded that demonstrable embolization is far more common than previously thought; therefore, a study seeking to predict events by vegetation characteristics needs to use advanced imaging as a reference standard. There is no evidence that such a study has been performed, and the question of the capability of echocardiography to predict outcome remains unsettled. Transesophageal Echocardiography When two-dimensional imaging supplanted M-mode echocardiography as the imaging mode of choice, some published cases still suggested suboptimal sensitivity even with two-dimensional echocardiography.[26] These suspicions were shown to be well founded when TEE was applied to the study of patients with suspected endocarditis.[27] It was not until almost a decade later, however, when a number of studies addressed the marked differences in sensitivity between TTE and TEE[19] ( Fig. 21-8 , Fig. 21-9 , Fig. 21-10 ). The role of TEE in endocarditis is a direct result of its high sensitivity in detecting the defining manifestation of Figure 21-7 (Figure Not Available) Aortic valve vegetations are scored by adding the grades of size, mobility, and extent. Bottom, The sensitivity, specificity, and predictive accuracy are given for several scores. (From Sanfilippo AJ, Picard MH, Newell JB, et al: J Am Coll Cardiol 1991;18:1191–1199. Reprinted with permission from the American College of Cardiology.) 458 Figure 21-8 Discrepancy between TTE and TEE. Left, Apical four- chamber view showing only subtle changes in the posterior leaflet of the mitral valve (arrow). Right, TEE shows a flail, thickened valve with evidence of a vegetation at the tip of the posterior leaflet (pML). The anterior leaflet (aML) has normal thickness and is normally positioned. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. Figure 21-9 Four small vegetations (small arrows) arrayed along the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 13 anterior mitral leaflet. By transthoracic echocardiography, only one of these (large arrow) was suspected. 459 Figure 21-10 A, Four-chamber TEE view taken in the transverse plane. Small solitary vegetation (Veg, arrow) is seen at the coaptation of the anterior and posterior mitral leaflets (aML, pML) but was not apparent on transthoracic echocardiography. Note the gray texture of the mass, which closely resembles myocardium. This appearance is typical of a vegetation. Ao, aorta. B, Larger vegetation detected by TTE but found to be 3 mm larger by TEE. C, Transverse plane view of the base of the heart from TEE. The left atrial (la) appendage (laa) is occupied by an irregular mass whose shape, location, and motion are typical of thrombus (thr). Note that the gray texture of the mass is indistinguishable from that of vegetation. Thus, vegetations and thrombi are identified by circumstantial rather than direct evidence. 460 TABLE 21-9 -- Reported Sensitivity and Specificity of TEE for Native Valve Endocarditis TTE (%) TEE (%) Sample Size (n) SENSITIVITY/SPECIFICITY SENSITIVITY/SPECIFICITY Shively et al 66 44/98 94/100 (1991)[19] Pedersen et 24 50/— 100/— al (1991)[31] Birmingham 61 et al (1992) [28] Aortic 25/— 88/— Mitral 50/— 100/— Sochowski 105 —/— 91/— and Chan mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 13 (1993)[21] Shapiro et al 64 60/91 87/91 (1994)[30] TOTAL 256 46/95 93/96 TTE, transthoracic echocardiography; TEE, transesophageal echocardiography. the disease, valve vegetations. The comparison of the sensitivity of TTE to that of TEE is an important issue because if the two methods are similar in this regard, the less invasive and less expensive modality will be used. Five studies that address the differences in sensitivity between TTE and TEE in detecting vegetations[19] [28] [29] [30] are presented in Table 21-9 . Generally, patients reported in these studies are considered to have vegetations when a valve abnormality (mass) has the characteristics that allow it to be identified as a vegetation with a "high degree of certainty."[23] These characteristics include the texture of the mass, its location, characteristic motion, shape, and accompanying abnormalities. In general, experienced readers recognize a vegetation as having a gray scale and a low level of reflectance similar to myocardium (Fig. 21-11) . Vegetations are usually positioned on the upstream side of the valve (e.g., on the atrial side of the mitral valve and on the ventricular side of the aortic valve) and concentrated at the point where a regurgitant or stenotic jet impinges on the valve or wall. The mass is usually lobulated, amorphous, and mobile. The mobility Figure 21-11 TEE image of a bulky vegetation involving the atrial surface of the mitral valve and the annulus. Note the amorphous shape and gray texture, which resembles myocardium. This patient also had moderate to severe mitral regurgitation. LA, left atrium. may be chaotic, appear to orbit around the valve, or have fine vibrations imparted by the jet of abnormal flow. Abnormalities that accompany vegetations include periannular abscesses (solid or cystic), fistula formation, and severe regurgitation (Fig. 21-12) . In prosthetic endocarditis, paravalvular leaks, valve dehiscence, and occasional obstruction are seen (Fig. 21-13) . Vegetations also characteristically prolapse into the upstream chamber: mitral vegetations into the atrium in systole, aortic vegetations into the left ventricular outflow mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 12 di 13 tract during diastole. As stated, they tend to flank the regurgitant jet or form on a jet target. Characteristics that identify an abnormal mass as being unlikely to be a vegetation include high reflectivity, bistable appearance (white not gray), fibrillar appearance with narrow base of attachment (Fig. 21-14) , and lack of associated regurgitation (Table 21-10) . These characteristics are used by experienced readers regardless of whether a transthoracic or transesophageal window is used. Their appearance on TEE, however, is considerably more vivid, and the resolution for very small vegetations is higher. The superior sensitivity of TEE is clearly and consistently documented by the studies listed in Table 21-9 , in which the differences between modalities were strongly significant statistically. From these findings and from the study of Lowry et al[32] it can be concluded that a transesophageal echocardiogram with a negative result makes the probability of endocarditis very low; it does not, however, eliminate the possibility, and the physician must always temper interpretations with clinical judgment. For example, it may be appropriate to repeat an initial TEE examination with a negative result after 1 to 2 weeks if the clinical suspicion and disease course continue |
to suggest endocarditis. As the sensitivity of a test increases, specificity is likely to decrease. False- positive findings in TEE arise because small, previously invisible irregularities and degenerative processes are clearly seen in magnified format. A two-center study, in which this researcher participated as an "expert" blinded reader, compared TTE with TEE in infective endocarditis. Although no false positives occurred, some minor irregularities were encountered.[19] For example, tiny mobile strands on either valve are frequently encountered. These strands probably represent a normal degenerative process and are known as Lambl's excrescences. Strands, possibly from the same source, can arise on the sewing ring of prosthetic valves. Occasionally, a suture end can be visualized and might be mistaken for a pathologic finding. Redundant chordae or false tendons in the left ventricle as well as Chiari's remnant on the TABLE 21-10 -- Characteristics of a Mass Not Likely to Be a Vegetation Texture Reflectance of calcium/pericardium (appears white) Location Outflow tract attachment, downstream surface of valve Shape Stringy or hairlike strands with narrow mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 13 di 13 attachment Lack of accompanying No regurgitation abnormalities 461 Figure 21-12 Endocarditis of the mitral and aortic valves leading to abscess (Ab)/pseudoaneurysm, aortic and mitral vegetations (veg), severe aortic insufficiency (AI), and fistula formation (not shown) between the aorta (Ao) and left atrium (LA). A, Contiguous vegetations on both aortic and mitral leaflets. B, Thick-walled, expansile abscess of the aortic root. C (color plate.), Broad jet of aortic insufficiency filling the outflow tract. D (see color plate), Width and timing of jet seen in C documented by color M-mode echocardiography. Wide jets that occupy more than 65% of the left ventricular outflow tract are indicative of severe regurgitation. LVOT, left ventricular outflow tract; RA, right atrium. 462 Figure 21-13 (color plate.) Prosthetic dehiscence due to endocarditis. Note that the ring of this mechanical prosthesis is displaced from its expected plane and separated from the posterior aortic (Ao) root (top). Bottom, Color flow documents that the site of aortic insufficiency (AI) is paraprosthetic. right side may pose as vegetative masses. All of the masses mentioned in this paragraph have a tendency to be highly reflective in appearance with the approximate echodensity of pericardium or aortic root. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/182.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Prosthetic Valve Endocarditis Prosthetic valve endocarditis is a special case (Table 21-11) . The materials used to construct these devices usually do not allow passage of ultrasound and, as a result, these valves shadow or obscure structures lying between the valve and the transducer. For example, it is usually impossible to image the atrial side of the mitral prosthesis or the arterial side of the aortic prosthesis from an apical TABLE 21-11 -- Prosthetic Valve Endocarditis: A Special Case Both transesophageal echocardiography and transthoracic echocardiography must be used to circumvent shadowing— Ventricular side of mitral valve: Transthoracic echocardiography Atrial side of mitral valve: Transesophageal echocardiography Two or three prostheses: Shadow one another TABLE 21-12 -- Prosthetic Valve Endocarditis: Comparison of TEE to TTE Sensitivity TEE TTE Sample Size Sensitivity Sensitivity (n) (%) (%) Daniel et al (1993)[33] 33 82 36 Zabalgoitia et al (1993)[35] Bioprostheses 44 86 44 Abscess 4 100 25 TTE approach. TEE solves this problem in mitral prostheses and improves it in aortic prostheses. When both mitral and aortic devices are present, however, shadowing from the mitral device tends to obscure the region of mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 the aortic prosthesis. Multiplanar TEE probes allow improved imaging in this situation, but some areas may remain obscured; therefore, a combination of TTE and TEE imaging may be needed for complete visualization of the valvular structures. Tricuspid and pulmonic devices pose similar problems, but they are effectively evaluated by TEE. Daniel et al[33] reported on 33 cases of prosthetic endocarditis studied with both TEE and TTE and found sensitivities of 82% and 36%, respectively. Alton et al[34] reported similar findings but with smaller numbers. In a study of TEE in 44 patients with bioprosthetic valves who were going to surgery, Zabalgoitia et al[35] found that TTE had a sensitivity of 44%, whereas TEE had a sensitivity of 86% (Table 21-12) . In abscess identification, TEE was 100% sensitive, whereas TTE was only 25% sensitive (Fig. 21-15) . Figure 21-14 Ruptured chordae tendineae (rct) of the posterior mitral leaflet. This prolapsing mass is thin and brighter in appearance than a vegetation (similar to the aortic root and anterior leaflet). Although this condition was associated with severe mitral regurgitation, there were no other clinical features of endocarditis. 463 Figure 21-15 Large posterior abscess in a bioprosthesis. A, TEE image of a thick-walled abscess with an abscess cavity or pseudoaneurysm posterior to the aortic root and protruding into the left atrium. The arrow points to the collapsed cavity during diastole. Note that the cavity is contiguous with the posterior stent of the aortic prosthesis. B, Systolic expansion of the cavity (arrow). Note the anterior shadowing of structures that lie beyond the prosthesis. C, Transthoracic echocardiography in the same patient showing little more than the sewing ring (sr) of the prosthesis and a vague outline of the aortic ring (short arrow). The large gulf in resolution between these two modalities is illustrated here. a, anterior; p, posterior. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/183.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Prediction of Clinical Outcome Once a native valve vegetation is identified, the attending physician is obligated to estimate the risk that the process poses to the patient's recovery or survival and to decide on an appropriate therapeutic plan. Unexpectedly, the bacteriology of the responsible organism was not found to be of prognostic importance in the Sanfilippo et al[23] or Mugge et al[16] studies. Prognostic estimations and decisions, however, can be made by a careful analysis of the clinical and TEE presentation. There are interesting and provocative studies that the clinician can use in making these decisions.[16] [36] [37] [38] Using TTE to predict embolic events, researchers at Duke[38] looked at the site, size, mobility, shape, and attachment of vegetations. They found high interobserver agreement on the presence and location of vegetations but less agreement on the size, mobility, and shape. A vegetation size of greater than 10 mm was associated with an embolic rate of greater than 50%, whereas a vegetation size of less than 10 mm was associated with an embolic rate of 42%. In contrast to the study by Sanfilippo et al,[23] these researchers found that characteristics of vegetations from TTE were not helpful in predicting complications. In applying TEE to the same question, Mugge et al[16] concurred with the lack of correlation between site, mobility, shape, and attachment of the vegetation and prediction of embolic events. Mugge et al, however, probably owing to the increased sensitivity of TEE imaging, found a stronger association between vegetation size and embolic events than did researchers of the Duke study, particularly if the vegetation was present on the mitral valve. A vegetation size of greater than 10 mm was associated with an embolic rate of 46%, whereas vegetation size less than 10 mm was associated with only a 20% risk (P < .001). These observations are not comparable to the TTE study of Sanfilippo et al,[23] in which all complications were related to vegetation characteristics: the use of mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 vegetation characteristics to predict specific complications such as systemic embolism was not examined. Also, if all studies had employed TEE and surveillance imaging for subclinical embolic events, perhaps a better correlation between size and outcome would have been demonstrated. In one of the most interesting and useful studies, Rohmann et al[36] performed serial TEE in 83 patients and found that if a vegetation size increased or remained static during 4 to 8 weeks of therapy, prognosis was much worse than if vegetation size decreased with therapy. These differences were striking and included incidence of valve replacement (45% versus 2%), embolic events (45% versus 17%), abscess formation (13% versus 2%), and mortality (10% versus 0%) (all P < .05). These data suggest that it may be logical to temporize by performing serial studies in patients who have not experienced complications and who present with large vegetations that tempt early surgical intervention. They also dispel somewhat the concern that a shrinking vegetation is tantamount to embolization of a fragmenting mass. When indicated, it is appropriate to repeat the TEE after 7 days of antibiotic therapy and compare the size of the vegetations. Although this time scale is considerably shorter than the 4 464 TABLE 21-13 -- TEE Vegetations and Outcome Size Mugge et al (1989) >10 mm: 46% emboli <10 mm: (P < .001) [16] 20% Heinle et al (1994) >10 mm: >50% <10 mm: (P = ns) [38] emboli 40% Temporal Behavior Rohmann et al (1991)[36] Serial TEE at 4–8 wk: Static or enlarged Smaller vegetation vegetation Valve replacement 45% 2% Embolic events 45% 17% Abscess formation 13% 2% mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 Death 10% 0% (P < .05 for all) to 6 weeks in the Rohmann et al study, dramatic decreases in vegetation size may be seen after only 1 week of treatment. A prospective study is needed to determine the shortest time interval required between the first observation at the beginning of treatment and the second observation to reliably establish a patient as a responder or nonresponder to antibiotic therapy (Table 21-13) . It is also important to consider the implications of a TEE examination that fails to show vegetations in a patient with suspected infective endocarditis (Table 21-14) ; Shively et al[19] found a negative predictive value of 98% for a TEE study with a negative result in patients with suspected endocarditis. Sochowski and Chan,[21] however, using monoplane TEE, found 65 of 105 patients with suspected infective endocarditis with a negative finding on initial examination. Of these, 56 patients never developed definite endocarditis, but in five patients, infective endocarditis was eventually documented. In three of these five, repeat TEE demonstrated new vegetations. The most common type of patient with infective endocarditis in whom initial TEE fails to detect a vegetation is one with an aortic prosthesis. Although a false-negative TEE examination occurs in only 5% or less of patients with infective endocarditis, all negative studies impose an obligation on the physician to follow patients until a sustained afebrile status is confirmed. Under some circumstances it may be permissible to withhold antibiotics while monitoring for signs of infective endocarditis. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/184.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 4 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Intracardiac Complications of Endocarditis In the process of bacterial infiltration and proliferation in valve tissue, the integrity of the leaflet may be destroyed. This TABLE 21-14 -- Implications of an Initial TEE with a Negative Result Shively et al (1991)[19] 98% negative predictive value Sochowski and Chan 65 of 105 suspected cases had a negative result on (1993)[21] |
initial examination 56 never developed infective endocarditis 5 eventually developed disease (3 showed vegetations on repeat examination) Aortic prosthetic endocarditis was most likely to be negative destruction leads to regurgitation of varying severity. Etiology makes little difference in the echocardiographic features of severe mitral regurgitation. There is a distinct feature of valves in infective endocarditis, however, that merits consideration; that is, it is very difficult to differentiate a disrupted, prolapsing, and flail segment of leaflet from a mobile prolapsing vegetation. Both have the same motion during the cardiac cycle and the same visual tissue characteristics, and both may be simultaneously present in the same location. Measuring a flail leaflet that has been mistaken for a vegetation may lead to miscalculation of risk level, or worse, an incorrect diagnosis of endocarditis. TEE substantially improves the likelihood of distinguishing leaflet from vegetation; this ability probably contributes to its advantages as a prognostic and diagnostic tool. Beyond this feature, the principles that govern the Doppler and two-dimensional evaluation of the severity of valvular regurgitation remain the same and are discussed thoroughly elsewhere in this book. When the endocardial infectious process spreads beyond the valve leaflets mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 4 or endocardium it invades the continuous basal myocardium and tissue of the fibrous cardiac skeleton. Early in this process, the contagion produces cellulitis. If tissue necrosis and white cell activity continue, the central portion of this process undergoes pyogenesis and forms an abscess cavity ( Table 21-15 ; see also Fig. 21-12 , Fig. 21-15 , and Fig. 21-16 ). Because the abscess wall is under considerable pressure, the weakened necrotic tissue may disrupt, resulting in communication with a ventricle, atrium, or great vessel (Fig. 21-16) . In the setting of this fistulous communication the abscess cavity can also be viewed as a pseudoaneurysm,[39] particularly if it involves the aortic wall directly. Examples of fistulous communications include aorta to left atrium (associated with a new continuous murmur) and left ventricle to right atrium. If the abscess extends into the septum, the conduction system may be interrupted or slowed and a right bundle branch block with first-degree A-V block may ensue. [40] In a landmark study of the effectiveness of TEE in detecting abscesses in endocarditis, Daniel et al[20] studied 118 cases and found evidence of abscess formation in 37%. The mortality rate among those with abscess was 23% versus 14% for those without. The sensitivity and specificity of TTE imaging was 28% and 99%, respectively, whereas TEE imaging had a sensitivity and specificity of 87% and 95%, respectively, for detection of paravalvular 465 TABLE 21-15 -- TEE Myocardial Abscess Leung et al (1994) Daniel et al (1991)[20] [41] Sample Size n = 118 n = 34 (all aortic) Abscess Formation 44 (37%) 11 (32%) Detection by TTE Sensitivity 28% 36% Specificity 99% 100% Detection by TEE Sensitivity 87% 100% Specificity 95% 100% mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 4 Mortality With abscess 23% * 5/11 (45%) Without abscess 14% * p = NS Staphylococcus aureus With abscess 52% † Without abscess 16% † p <.001 Site of Infection Native aortic root 14/44 (32%) Para-aortic prosthesis 12/44 (27%) *P = ns. †P < .001. abscess. Karalis et al[40] found a similar disparity in sensitivity between TTE and TEE. From these data it is also evident that abscess-related lesions are relatively common in endocarditis (especially when the infecting organism is S. aureus) and patients with a demonstrable abscess on echocardiography represent a subgroup that is at high risk for death. In one study the mortality rate was as high as 45% when an abscess was detected.[41] Because of proximity to the transducer, TTE is most effective in detecting an anterior abscess at the aortic septal junction and least effective in detecting those that lie more posteriorly. Its overall adequacy is insufficient for detection of abscesses because its Figure 21-16 (color plate.) Aortic root abscess in communication with the aortic root. In this case of aortic endocarditis, there is a large vegetation on a partly destroyed aortic valve (AV) and a root abscess (Ab). Note that color flow imaging demonstrates both severe aortic regurgitation (right, large arrow) and flow into the abscess cavity (arrowheads). LA, left atrium; RVOT, right ventricular outflow tract; SVC, superior vena cava. sensitivity is far too low and the extent of the lesion is unlikely to be fully mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Right-Sided Infective Endocarditis Vegetations of the tricuspid valve are commonly encountered in populations of intravenous drug users. Most reported series use TTE to study this group of patients. Hecht and Berger[42] collected 132 instances of right-sided infective endocarditis in 121 intravenous drug users. S. aureus was the organism in 82% (108 of 132). The tricuspid valve was the site in 127 patients, the pulmonic valve in 4 patients, and both valves in 1 patient. In 80% the vegetation was 1 cm or greater in diameter. There was a strongly significant association between vegetation size greater than 2 cm and mortality rate (33% in those with a vegetation > 2 cm vs. 1.3% in those with a vegetation < 2 cm; P > .001). San Roman et al[43] studied 48 intravenous drug users suspected of having infective endocarditis with both TEE and TTE. Both techniques were equally sensitive and specific, each identifying the same 22 vegetations. In no instance did TEE find a vegetation that was overlooked by TTE. In 63%, however, the vegetation was better characterized by TEE. From this study San Roman concluded that TEE did not confer sufficient advantage to justify its routine use in intravenous drug users with suspected right-sided endocarditis. This study met with criticism because it was mostly conducted with monoplane equipment. In my own experience, the use of multiplane TEE in these cases has increased the yield of pulmonic vegetations[44] ( Fig. 21-17 and Fig. 21- 18 ). Another concern is the possibility of left-sided involvement in patients with right-sided vegetations. If the duration of medical therapy would be affected by the presence of left-sided vegetations, TEE may be needed. It remains to be seen whether further experience will justify an expanded role for TEE in right-sided endocarditis. For the moment, the issue remains unsettled. 466 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 Figure 21-17 (color plate.) Four-chamber view from TEE in a patient with a tricuspid valve vegetation. The color flow image of tricuspid regurgitation (arrow) obscures the vegetation. Note that the interatrial septum is bulging abnormally from right to left, confirming the severity of the regurgitant lesion. Figure 21-18 Transverse (left) and longitudinal (right) plane images of a pulmonic valve vegetation (Veg). The use of multiplane TEE was probably responsible for the identification of this vegetation, because it was very difficult to appreciate in the transverse plane. LVOT, left ventricular outflow tract; RVOT, right ventricular outflow tract. 467 TABLE 21-16 -- Key Points in Echocardiographic Evaluations of Patients with Endocarditis 1. Echocardiography has a central role in diagnosis and management of infective endocarditis 2. All patients with infective endocarditis should undergo serial TTE 3. Most if not all patients with infective endocarditis should undergo TEE at least once 4. Technical factors are paramount 5. Experienced operators and readers are essential 6. High-frequency probes and biplanar/multiplane TEE are required MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/186.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Summary In summary (Table 21-16) , echocardiography has an unassailable place in the diagnostic evaluation and management of infective endocarditis. TTE and TEE are complementary from the point of view of comprehensively evaluating hemodynamics and anatomy. TEE is superior to surface imaging by dint of its greater sensitivity in detecting native valve vegetations, prosthetic valve vegetations, paravalvular abscesses, and other pyogenic complications. A negative finding on a TEE study makes endocarditis unlikely, and a large vegetation that fails to shrink during therapy connotes a poor prognosis. Based on these considerations and clinical experience, it is an established medical fact that all patients with infective endocarditis should undergo TTE, and it is the firm opinion of most experts that these patients should also have at least one TEE examination. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/187.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 18 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company 469 Chapter 22 - Aortic Stenosis Echocardiographic Evaluation of Disease Severity, Disease Progression, and the Role of Echocardiography in Clinical Decision Making David M. Shavelle MD Catherine M. Otto MD Evaluation of Stenosis Severity The echocardiographic evaluation of the patient with valvular aortic stenosis focuses on quantitation of stenosis severity and assessment of the left ventricular response to chronic pressure overload. However, complete evaluation also includes quantitation of coexisting aortic and mitral regurgitation, estimation of pulmonary artery pressures, assessment of left ventricular diastolic function, measurement of the degree and extent of aortic root dilation, and evaluation of any other coexisting cardiac abnormalities. Evaluation for concurrent coronary artery disease may require additional diagnostic procedures. The basic clinical echocardiogram includes measurement of maximum aortic jet velocity and calculation of continuity equation aortic valve area, as detailed in the Textbook of Clinical Echocardiography. [1] Although echocardiographic measures of stenosis severity have been well validated, it still is the responsibility of each echocardiographer to be aware of the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 18 theoretical basis of these techniques and potential pitfalls in their clinical application. In some clinical situations, other measures of stenosis severity may be helpful in patient management. In addition, a more detailed assessment of stenosis severity may be important for understanding the natural history of this disease and for assessment of interventions to slow or reverse disease progression. Pressure Gradient versus Jet Velocity The velocity of blood flow through the narrowed aortic orifice is related to the pressure difference across the valve as described by the Bernoulli equation. For valvular aortic stenosis, the simplified Bernoulli equation, ∆P = 4v2 , which ignores the effects of acceleration and viscous losses, has proven to be remarkably accurate as compared with simultaneous invasive pressure gradient measurements. The relationship between Doppler velocity and manometric pressure measurements has been evaluated in in vitro models of a stenotic valve, in animal models of valvular and nonvalvular stenosis, and in patients with clinical disease.[2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] In these studies, simultaneous measurements show a close correlation between Doppler and 470 invasive maximum instantaneous and mean pressure gradients over a wide range of stenosis severity. In addition, the Doppler technique accurately measures changes in pressure gradient with changes in flow rate.[11] [13] [15] Of course, nonsimultaneous recordings of Doppler and manometric data correlate less well, since interval physiologic changes in transaortic volume flow rate and heart rate may result in interval changes in the transaortic gradient. Some clinicians may be confused by the use of Doppler velocity and maximum gradient measurements if the differences between maximum instantaneous, peak-to-peak, and mean systolic gradients are not appreciated. The Doppler maximum velocity corresponds to the maximum instantaneous pressure gradient |
across the valve (Fig. 22-1) . The "peak-to- peak" gradient measured manometrically—the difference between peak left ventricular and peak aortic pressures—does not correspond to a specific Doppler measurement, since these two pressure peaks are not simultaneous and thus this "pressure difference" does not actually occur at any time point in the cardiac cycle. In a physiologic sense, the "peak-to-peak" gradient does not truly exist. Clarity in the echocardiographic report prevents any mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 18 potential confusion on the part of the referring physician in regard to differentiating between the maximum Doppler gradient and the "peak-to- peak" catheter gradient. Measurement of Doppler mean gradients is more comparable to the mean gradient measured in the catheterization laboratory because both represent the average pressure difference across the valve during the systolic ejection period. Of note, maximum and mean transaortic pressure gradients (∆P) are linearly related when measured either by Doppler or manometric techniques. The regression Figure 22-1 Relationship of pressures to Doppler velocities in normal and aortic stenosis. Note that the maximum pressure gradient (double- headed arrow) corresponds to the maximum Doppler velocity in both situations, but the timing of the left ventricular (LV) to aortic (Ao) pressure gradient is quite different when valve obstruction is present. equations described for this relationship[16] [17] [18] include the following: Mean ∆P = (max ∆P/1.45) − 2.2 mm Hg and Mean ∆P = 2.4(V )2 max where Vmax is maximum aortic jet velocity. These two equations, derived from separate patient populations, give similar results. It is important to recognize that these equations apply only to native aortic valve stenosis because the close correlation between maximum and mean gradient is dependent on a similar shape of the velocity curve (or pressure difference) with respect to time among the patient population. Given this linear relationship between maximum and mean pressure gradients, it becomes clear that there is little additional information content provided by gradient calculations versus simply reporting the Doppler aortic jet velocity alone. Since maximum and mean gradients are linearly related, and since maximum gradient is related to maximum velocity as stated in the simplified Bernoulli relationship, a given maximum velocity consistently corresponds to a given maximum and mean gradient. For example, a maximum jet velocity of 4 m per second corresponds to a mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 18 maximum gradient of 64 mm Hg and a mean gradient of 38 mm Hg. Similarly, a maximum jet velocity of 5 m per second corresponds to a maximum gradient of 100 mm Hg and a mean gradient of 60 mm Hg. These close relationships between maximum jet velocity, maximum gradient, and mean gradient explain why maximum jet velocity data alone are so useful in clinical decision making in adults with valvular aortic stenosis. The technical aspects of recording aortic jet velocities in patients with valvular aortic stenosis cannot be overemphasized (Fig. 22-2) . The utility of Doppler data in patient management clearly is dependent on accurate data recording. Since the direction of the aortic jet is unpredictable and often eccentric, careful examination from multiple acoustic windows is needed for detection of the highest velocity signal. Use of a small, dedicated continuous wave Doppler transducer, careful patient positioning with an apical "cut-out" in the examination bed, and operator experience all are critical factors in obtaining accurate data. ( See Chapter 9 of the Textbook of Clinical Echocardiography for further details on data acquisition.) Even with an experienced operator and attention to technical details, there is some degree of measurement variability, as for any clinical measurement. In the absence of interval physiologic changes, the coefficient of variability for recording and measuring aortic jet velocity is 3%,[19] so that a change in jet velocity greater than 0.2 m per second and a change in mean gradient greater than 4 mm Hg are outside the range of measurement variability. Another physiologic issue that needs to be considered in the Doppler assessment of pressure gradients in patients with aortic stenosis is the phenomenon of distal pressure recovery.[20] [21] [22] [23] [24] [25] The fluid dynamics of valvular aortic stenosis [26] are characterized by a laminar high- velocity jet in the 471 Figure 22-2 One of the technical pitfalls in recording aortic jet velocities is correct recognition of the velocity signal. In this patient, three high-velocity systolic signals were obtained from an apical transducer position. The aortic stenosis jet (A) is distinguished by a shorter ejection time than either mitral (B) or tricuspid (C) regurgitation. Other factors helpful in identifying the signal include mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 18 the accompanying diastolic flow signal and the shape of the velocity curve. When identification is problematic, use of two-dimensional and color-flow guided continuous wave Doppler echocardiography may be helpful. 472 narrowed orifice with the narrowest segment of the flow stream (the vena contracta) occurring downstream from the anatomic valve orifice. As the jet expands and decelerates beyond the vena contracta, the associated turbulence results in an increase in aortic pressure ("pressure recovery") such that when aortic pressure in measured in the distal ascending aorta, the left ventricular to aortic pressure difference is less than if aortic pressure is measured in the vena contracta. No doubt pressure recovery accounts for some of the discrepancies between Doppler and invasive data reported in the literature. Clinically, however, the observed magnitude of pressure recovery is only 5 to 10 mm Hg, an effect that is unlikely to affect clinical decision making. The magnitude of pressure recovery is greater with a larger valve area and with a smaller aortic root. Thus, patients with severe aortic stenosis and poststenotic aortic root dilation may show less pressure recovery than patients with mild to moderate stenosis and a small or normal aortic root dimension. In any case, the phenomenon of pressure recovery supports the use of Doppler data in evaluation of aortic stenosis patients. Since the maximum aortic jet velocity reflects the pressure difference between the left ventricle and the vena contracta, pressure recovery is a "problem" only in comparing the Doppler data with manometric data measured downstream from the vena contracta. In effect, the Doppler velocity measures the physiologic variable of most importance; it is the manometric data that must be interpreted with caution. The major potential limitation of Doppler velocity data in evaluation of patients with valvular aortic stenosis is that velocities (and pressure gradients) are volume flow rate dependent. When coexisting aortic regurgitation results in a high transaortic volume flow rate, aortic jet velocity may be high even if the degree of valve narrowing is only moderate. Conversely, when transaortic volume flow rate is reduced because of left ventricular systolic dysfunction or coexisting mitral regurgitation, jet velocity may be only moderately elevated despite severe valve narrowing. In an individual patient with aortic stenosis, aortic jet velocity varies with volume flow rate. For example, jet velocity increases with exercise as transaortic volume flow rate increases. Thus, comparisons of stenosis severity at different time points in an individual patient may be mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 18 confounded by interval changes in transaortic volume flow rate. In each of these clinical situations, calculation of valve area, which takes the transaortic volume flow rate into account, is needed. Continuity versus Gorlin Formula Valve Areas: Assumptions and Accuracy Aortic valve areas have traditionally been calculated from invasive hemodynamic data using the formula of Gorlin and Gorlin.[27] Gorlin valve area calculations have provided accurate and important data for clinical decision making since the initial publication of the formula in 1951. More recently, however, Doppler echocardiography has allowed noninvasive calculation of valve area using the continuity equation.[19] [28] [29] [30] [31] [32] Since Gorlin valve areas have been used as the standard of reference for validation of continuity equation valve areas, it is important to review the derivation of these equations to understand the differences between these two approaches (Fig. 22-3) . Aortic valve area (AVA) is calculated using the formula of Gorlin and Gorlin as AVA = (cardiac output) / (C × SEP × ∆Pmean ) where mean ∆P is measured manometrically, SEP is systolic ejection period, and C is a constant. As for any clinical measurement, careful data acquisition is important. Accurate pressure gradient measurements depend on careful attention to frequency response, damping, and catheter positioning. The use of a double-lumen catheter or, alternatively, two separate catheters (with measurements obtained in the left ventricle and in the aorta), as opposed to measurement of the femoral artery pressure as a surrogate of the aortic pressure, provides more accurate results. Cardiac output should reflect transaortic volume flow rate. Although a Fick or thermodilution output can be used for isolated aortic stenosis, when aortic regurgitation is present, an angiographic cardiac output measurement is more appropriate. When both mitral and aortic regurgitation are present, accurate invasive determination of the transaortic volume flow rate in the clinical setting is not possible. The constant in the Gorlin formula, which has been empirically derived, attempts to account for several factors. The Gorlin constant incorporates (1) the coefficient of contraction, which reflects the difference between the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 18 anatomic valve area and the area of the vena contracta, (2) the coefficient of velocity, which relates to the conversion of potential to kinetic energy, (3) measurement of pressure in mm Hg, and (4) an empirical "correction" factor. Both in vitro and in vivo studies suggest that the Gorlin constant may vary with changes in volume flow rate, orifice shape, and stenosis severity.[33] [34] [35] [36] [37] Despite potential limitations of Gorlin valve areas, alternative reference standards for quantitation of aortic stenosis severity remain problematic. Unlike rheumatic mitral stenosis, in which commissural fusion results in a fixed anatomic orifice that can be measured directly at surgery, calcific aortic valve stenosis is characterized by stiff leaflets that open to a variable degree depending on the force applied by the surgeon's finger. This limits attempts at direct measurement of aortic valve area. Doppler continuity equation valve area calculations provide the advantages of noninvasive data collection and absence of an empirical constant.[3] [13] [28] , [29] [31] [38] , [39] Continuity equation aortic valve area (AVA) can be calculated using either velocity time integrals or maximum velocities (V) as follows: AVA = (VLVOT × CSALVOT ) / VAS-JET where left ventricular outflow tract (LVOT) diameter is measured from a two-dimensional parasternal long-axis view, parallel and adjacent to the aortic valve plane, for calculation of a circular cross-sectional area (CSA); LVOT flow velocity is measured from an apical approach using pulsed Doppler ultrasonography; and the aortic stenosis jet (AS-JET) velocity is measured with continuous wave 473 Figure 22-3 Comparison of valve areas by the continuity equation (A) and the Gorlin formula (B). Doppler echocardiography from the echocardiographic window that yields the highest velocity signal (Fig. 22-4) . Continuity equation valve area calculations assume accurate recording of the maximum aortic jet velocity, as discussed earlier for pressure gradients. However, the largest source of variability in continuity equation valve area calculations is in the measurement of the outflow tract diameter. The mean coefficient of interobserver and intraobserver measurement variability is 5% to 8%, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 18 resulting in a measurement variability for valve area of 0.15 cm2 for a valve area of 1.0 cm2 . In an individual patient, outflow tract diameter remains relatively constant over time, such that a change in valve area greater than 0.1 cm2 most likely represents an actual interval change. Continuity equation valve area calculations depend on accurate measurement of transaortic volume flow rate. In theory, volume flow rate could be measured at any one of several intracardiac sites (pulmonary artery, mitral annulus, left ventricular outflow tract). However, when there is coexisting aortic regurgitation (which is present to some degree in more than 80% of adults with valvular aortic stenosis), volume flow measured across other valves does not equal the volume flow rate across the aortic valve.[19] From a technical standpoint, flow measurements just proximal to the stenotic aortic valve are feasible in nearly all adult patients, whereas volume flow rate calculations at other intracardiac sites often are limited by image quality. Thus, in practice, the left ventricular outflow tract is used for measurement of transaortic volume flow rate in |
nearly all cases. Volume flow measurement proximal to the stenotic aortic valve assumes that (1) the cross-sectional area of flow is circular in systole and flow fills the anatomic cross-sectional area, (2) the pattern of blood flow is laminar with uniform parallel stream lines of flow, (3) cross-sectional area and flow velocity are measured at the same site, and (4) the spatial flow velocity profile is relatively "flat" during ventricular ejection; that is, flow velocities are the same in the center and at the edges of the flow stream. The assumptions of a circular cross-sectional area with flow filling the anatomic area have been corroborated by careful short-axis two-dimensional and color flow imaging in animal models and in patients with valvular obstruction.[5] Laminar flow is confirmed by recording a narrow band of velocities throughout ejection on the pulsed Doppler spectral tracing. The circular cross-sectional area of the outflow tract is calculated from a two-dimensional parasternal long-axis measurement of mid-systolic diameter, immediately adjacent and parallel to the aortic valve plane. Since the outflow tract is perpendicular to the ultrasound beam from this view, axial resolution provides a more accurate diameter measurement than the use of apical views. Flow velocity is measured from an apical approach, because Doppler measurements are most accurate when the ultrasound beam is parallel to the direction of blood flow. To ensure that the diameter and flow measurements are recorded from the same anatomic site, it is important that both measurements be made as close to the aortic valve as mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 18 possible. On the two-dimensional image, the valve leaflet insertions provide an accurate and reproducible landmark, and on the Doppler recordings, the aortic valve closing click ensures that the sample volume is adjacent to the aortic valve. Although a region of flow acceleration occurs on the left ventricular side of the stenotic aortic valve, this area is spatially small and is easily avoided by recognition of spectral broadening on the Doppler velocity recording. In theory, the spatial flow profile in the outflow tract should be relatively flat because of the tapering of the 474 Figure 22-4 Continuity equation valve area is calculated based on a parasternal left ventricular outflow tract diameter (2.6 cm) for calculation of a circular cross-sectional area (A), placement of a sample volume immediately proximal to the aortic valve in an anteriorly angulated apical four-chamber view (B) with pulsed Doppler recording of laminar flow proximal to the aortic valve with a maximum velocity of 0.9 m per second (C). The highest velocity aortic signal (4.9 m per second) was obtained from an apical approach using continuous wave Doppler (D) in this patient. In this example, the continuity equation valve area is 1.0 cm2 . Ao, aorta; LA, left atrium; LV, left ventricle; SV, sample volume. outflow tract and acceleration of blood during systole, both of which result in blunt flow profiles at the entrance to large vessels (Fig. 22-5) . Direct examination of the spatial flow profile in the left ventricular outflow tract proximal to the stenotic aortic valve initially was performed with conventional pulsed Doppler by carefully recording flow at sequential sites across the two-dimensional image in both apical long-axis and anteriorly angulated four-chamber views of the outflow tract.[19] [40] A more recent study, using color flow imaging to map the spatial flow profile, showed variable skewing in the spatial flow profile, most often with highest velocities along the septum, in 10 patients with aortic stenosis both before and after aortic valve replacement[41] (Fig. 22-6) . In another study, patients with predominant aortic stenosis were found to have relatively flat flow profiles, whereas normal subjects and patients with aortic regurgitation had skewed velocity profiles, with the highest velocities occurring anteroseptally[42] (Fig. 22-7) . In practical terms, even when the flow profile is somewhat skewed, if the recorded flow velocity is a reasonable approximation of the spatial and temporal flow velocity in the outflow mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 18 tract, then a reasonably accurate volume flow rate will be calculated. It is likely that in most patients, when the Doppler sample volume is positioned near the center of the outflow tract in two orthogonal views, the recorded flow velocity approximates the spatial mean velocity across the outflow tract. Rather than examining the assumptions underlying the Doppler approach to volume flow rate calculations, a more pragmatic approach to validation of the accuracy of transaortic volume flow measurements is to compare 475 Figure 22-5 (color plate.) An apical long-axis view (in the same patient as shown in Fig. 22-4) shows relatively laminar flow in the left ventricular (LV) outflow tract proximal to the stenotic valve (arrow) with a flow disturbance in the ascending aorta (Ao) corresponding to the high-velocity jet and post-jet flow disturbance. Doppler data with an established standard of reference. This has been difficult in clinical studies because most patients with aortic stenosis have coexisting aortic and mitral regurgitation. Although the degree of regurgitation may not be hemodynamically "significant," when regurgitation is present, neither the forward (Fick or thermodilution) nor the total (angiographic) cardiac output will accurately represent the volume flow rate across the aortic valve. In the research setting, transaortic volume flow rate can be measured directly, with an electromagnetic or transit time flow meter (Fig. 22-8 (Figure Not Available) and Fig. 22-9 (Figure Not Available) ). In both acute and chronic models of valvular aortic stenosis, Doppler transaortic volume flow rates have been shown to be accurate (Table 22-15, 15 ) with a standard error of TABLE 22-1 -- In Vivo Studies of Simultaneous Invasive and Doppler Vo Measurements from Left Ventricular Outflow Tract at Aortic Annulus in Su Aortic Stenosis and Subjects Without Aortic Stenosis Cardiac Output Strok Patients, Standard of RANGE SEE, RA Study Model N Reference r L/MIN L/MIN r m Burwash Chronic 75 Transit time- 0.86 0.9– 0.50 0.86 9 et al[15] valvular flow 6.2 AS mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 18 (closed- and open- chest dogs) altered volume flow rate Otto et al Acute 52 Electromagnetic 0.90 0.9– 0.25 0.88 5 [38] valvular flow 3.2 AS (open- chest dogs) altered volume flow rate Stewart Normal 33 Roller pump 0.98 0.5– 0.30 NA N et al ‡ (open- 5.0 chest dogs) altered volume flow rate Lewis et Patients 35 Thermodilution 0.91 2.1– 0.63 0.95 24 al † (no AS) 9.5 Labowitz Patients 31 Thermodilution 0.90 1.6– 0.95 NA N et al * (no AS) 8.4 AS, aortic stenosis; NA, not available; SEE, standard error of the estimate. ‡Stewart et al: J Am Coll Cardiol 1985;6:653. †Lewis et al: Circulation 1984;70:425. *Labowitz et al: Am Heart J 1985;109:327. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 12 di 18 Figure 22-6 Three-dimensional plot of velocity distribution in left ventricular outflow tract close to the level of aortic annulus. Velocity is plotted against position in the left ventricular outflow tract diameter and against time. There are 20- msec intervals along the time axis and approximately 2 mm between each observation along the diameter axis. (From Wiseth R, Samseth S, Rossvoll O, et al: J Am Soc Echocardiogr 1993;6:279–285.) the estimate of 2 to 4 mL for stroke volume and 0.25 to 0.5 L per minute for cardiac output over a wide range of flow rates (Fig. 22-9 (Figure Not Available) and Fig. 22-10 ). In comparing Gorlin and continuity equation valve areas, it is important to bear in mind that although they both describe stenosis severity, they measure different parameters. The Gorlin formula examines the hydraulic load and calculates an anatomic orifice area, whereas the continuity equation describes the physiologic flow area of the vena contracta.[43] [44] Thus, it is neither expected nor essential that these two measurements be identical to each other. In terms of clinical decision making, the precision, reproducibility, and ability to predict patient outcome of these measures are more important than agreement or disagreement between the two approaches. As Gorlin and Gorlin note, "We need not be frustrated when valve areas derived by two different methods are not the same. Rather, we should, like the princes of Serendip, seize upon the difference for what it reveals about the anatomy of the valve orifice as opposed to the physiology of the total obstructing valve tract under active pressure and flow conditions."[45] 476 Figure 22-7 (color plate.) The two photos show the color Doppler registrations from a patient with aortic regurgitation: A, three-chamber view; B, five-chamber view. In the left ventricular outflow tract, a line, drawn along the transverse axis from the posterior to the anterior wall in the three- chamber view and from the septal to the lateral wall in the five-chamber view, shows the location (x) from where velocity information (v) is obtained. The lower panels show, from top to bottom, the uncorrected and the angle-corrected velocity profile along the two transverse axes as they appear on the computer screen. Below them, the time- (and angle-) corrected spatial velocity profiles from the beginning of the color Doppler sweep are shown. A, anterior wall; AO, aorta; L, lateral wall; LA, left atrium; LV, left ventricle; P, posterior wall; RA, right atrium; RV, right ventricle; S, septal wall. (From Sjöberg BJ, Ask P, Loyd D, Wranne B, et al: J Am Soc Echocardiogr mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 13 di 18 1994;7:276–285.) Other Measures of Stenosis Severity Continuity equation valve areas provide an accurate, reproducible, and useful measure of stenosis severity in patients with valvular aortic stenosis when data are recorded carefully with attention to technical details of data acquisition. However, other measures of stenosis severity may be needed in individual patients if the results of clinical and diagnostic evaluation are discrepant. In these situations, it may be helpful to utilize Gorlin formula valve areas derived from invasive data, other noninvasive measures of stenosis severity, or continuity equation valve areas calculated under conditions of altered transaortic volume flow rate. Even within the physiologic range, the degree of aortic valve opening appears to depend on the interaction between the force applied to the valve leaflets (as reflected in the transaortic volume flow rate) and the stiffness and rigidity of the valve leaflets. Changes in valve area of 20% to 30% can be observed for a 50% change in volume flow rate.[46] [47] [48] [49] [50] [51] [52] This potential flow dependence is of most concern in patients with coexisting left ventricular systolic dysfunction in whom separating the effect of reduced left ventricular force from the effect of leaflet stiffness on the degree of valve opening remains difficult. This clinical dilemma has led to a search for a flow-independent measure of stenosis severity. Several alternative measures of stenosis severity have been proposed, including two-dimensional valve area on transesophageal imaging,[52] [53] left ventricular stroke work loss,[48] [54] valve resistance,[50] [55] [56] [57] changes in aortic valve area during the cardiac cycle,[58] three-dimensional valve area, [59] and scoring of valve calcium.[60] [61] On transthoracic imaging, planimetry of the aortic orifice is limited by image quality. In addition, the anatomy of the stellate stenotic orifice is complex in three dimensions (Fig. 22-11) , so that it is not always possible to obtain a planar image of the valve orifice. Similar considerations apply to the higher quality images obtained on 477 Figure 22-8 (Figure Not Available) Simultaneous volume flow and pressure data in a canine model of aortic stenosis. The electrocardiographic (ECG) recording is displayed on top, instantaneous volume flow rate in the middle, and left ventricular (LV) and aortic (Ao) pressures at the bottom. The recordings on the left demonstrate mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 14 di 18 the hemodynamics at one flow rate. The recordings on the right display the hemodynamics at a larger volume flow rate during dobutamine infusion. Pmax , maximum instantaneous pressure gradient; Pmean , mean pressure gradient; SV, stroke volume. (From Burwash IG, Thomas DD, Sadahiro M, et al: Circulation 1994;89:827–835.) Figure 22-9 (Figure Not Available) Typical Doppler echocardiographic recordings made in one subject at two different volume flow rates. The left ventricular outflow tract (LVOT) velocity profile and velocity time integrals (VTI) (A) and aortic stenosis (AS JET) velocity (Vmax ) and velocity time integral (VTI) (C) are displayed at one flow rate. Increases in LVOT velocity (B) and AS JET velocities (D) were observed in the |
same subject with a dobutamine-induced increase in volume flow rate. (From Burwash IG, Thomas DD, Sadahiro M, et al: Circulation 1994;89:827–835.) 478 Figure 22-10 Correlation of simultaneous Doppler echocardiography and ascending aortic transit time-stroke volume (SV) and cardiac output (CO) during 75 separate interventions. (From Burwash IG, Forbes AD, Sadahiro M, et al: Am J Physiol 1993;265:H1734–1743.) transesophageal imaging. In addition, significant calcification of the valve can limit accurate delineation of the aortic valve orifice.[62] Some investigators have reported favorable correlations between planimetered stenotic orifice areas obtained on multiplane transesophageal echocardiography and continuity equation valve areas and/or Gorlin valve areas, but this approach is likely to be needed Figure 22-11 Anatomic specimen showing calcific aortic stenosis with nodular deposits of calcium within the aortic cusps and no commissural fusion. in only a small subset of patients.[52] [53] [63] [64] Other investigators have found planimetry of the aortic orifice to be difficult and less accurate than continuity equation valve areas obtained from transthoracic imaging. [65] Multiplane transesophageal echocardiography does appear to provide more accurate determination of aortic valve morphology (bicuspid versus tricuspid valve) than biplane imaging.[66] More recently, Doppler transesophageal echocardiography has been applied using both biplane and mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 15 di 18 multiplane imaging from the transgastric view.[67] [68] Aortic valve area as derived from Doppler transesophageal echocardiography was similar to that measured by planimetry but could not be obtained in approximately 70% of patients because of failure to align the Doppler beam adequately.[67] The amount of work expended by the left ventricle in keeping the aortic valve open in systole compared with the amount of work resulting in effective forward blood flow has appeal as a potential measure of stenosis severity. This measure may reflect the intrinsic stiffness of the valve leaflets, and thus be less dependent on volume flow rate.[48] [54] [69] With a normal aortic valve, work calculated from left ventricular or aortic pressure tracings will be nearly identical. However, when aortic stenosis is present, the difference between work calculated from left ventricular pressures versus aortic pressures should be related to the amount of work "lost" in opening the stiff leaflets. To calculate work, a power curve is generated by multiplying instantaneous flow times pressure, with total potential stroke work calculated by integrating power over the systolic ejection period[69] using either left ventricular (for total work) or aortic (for effective work) pressures. The steady component of work is defined as mean systolic pressure times stroke volume; pulsatile work is defined as total minus steady work. Stroke work loss then represents the difference between left ventricular and effective work and can be calculated for total, steady, and pulsatile components[48] as follows: LV stroke work loss = LV work − effective work Since potential work obviously will increase with increases in flow rate, the potential work loss across the stenotic valve is indexed for volume flow rate and expressed as the percentage of left ventricular stroke work loss: Given that stroke work is calculated as the instantaneous product of pressure and flow, and stroke work loss is simply the ratio of left ventricular to aortic work, this proposed index of stenosis severity also is likely to vary with volume flow rate if the actual degree of valve opening varies. Note that when the ratio of left ventricular to aortic work is calculated, the terms for transaortic volume flow rate cancel each other, so that stroke work loss can be determined from Doppler pressure calculations alone. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 16 di 18 A new index of energy loss that takes body surface area into account and can be calculated from Doppler-derived data was recently evaluated in an experimental model.[70] The model used fixed stenoses and bioprosthetic valves 479 of two sizes that were evaluated at different flow rates. With use of this model, the effective orifice area was compared to the energy loss index. In a retrospective analysis of 138 patients with moderate or severe aortic stenosis, the index and valve area were compared in predicting clinical outcome, defined as death or need for valve replacement. This energy loss index was the better predictor of clinical outcome, with a positive predictive value of 67%. Valve resistance is calculated from invasive or Doppler data as follows[56] [57] Resistance = (∆Pmean \ Qmean ) × 1333 where ∆P is mean transaortic pressure gradient in mm Hg, Q is mean mean mean volume flow rate in milliliters per second, 1333 is a conversion factor, and resistance is in units of dynes per second per cm-5 . Several investigators have observed a curvilinear relationship between valve resistance and valve area (with both invasive and Doppler data[56] [57] ) (Fig. 22-12) . This observation is not surprising given the mathematical derivation of the valve area and resistance concepts. In fact, the concepts of valve area and valve resistance are to some extent mutually exclusive. Valve area calculations with the Gorlin formula assume a quadratic relationship between pressure gradient and flow rate. Conversely, the valve resistance concept assumes a linear relationship between these two variables. Most clinical and experimental data support the concept of a quadratic, rather than linear, relationship between pressure gradient and flow rate across a stenotic valve[71] (Fig. 22-13) (Figure Not Available) . More complete modeling of the interaction between the left ventricle, valve, and peripheral vasculature may enhance our understanding of the hemodynamics of valvular aortic stenosis.[72] Aortic valve resistance has largely been used as a research tool and has not gained widespread acceptance into clinical practice. The reasons for mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 17 di 18 Figure 22-12 Relationship between aortic valve resistance and aortic valve area for patients with severe aortic stenosis confirmed at surgery (group I; circles) and the 95% confidence limits of this relation (dashed curves). Values for patients with milder, noncritical stenosis (group II triangles) were plotted against this relation; in seven of eight group II patients, values were outside the confidence limits. (From Cannon JDJ, Zile MR, Crawford FAJ, Carabello BA: J Am Coll Cardiol 1992; 20:1517–1523.) Figure 22-13 (Figure Not Available) Plot of square-law dependence of pressure gradient on flow demonstrated for circular stenoses with orifices from 0.5 to 2.0 cm2 . (From Voelker W, Reul H, Heinhaus G, et al: Circulation 1995;91:1196–1204.) this are multifactorial and include familiarity of most cardiologists with gradients and valve areas and a lack of consensus among studies in terms of the added information valve resistance provides above more traditional measures of stenosis severity.[56] [73] [74] Aortic valve area changes during the cardiac cycle, and the valve has been shown to open and close more slowly in patients with aortic stenosis than in those with normal valves.[75] The rate of change in the aortic valve area during the cardiac cycle has therefore been proposed as an additional measure of aortic stenosis severity and in predicting disease progression. [58] When the rate of change in the aortic valve area throughout the ejection phase of the cardiac cycle was expressed as a ratio (AVA ratio), patients with a large AVA ratio were found have more rapid disease progression than those with a lower AVA ratio. This new measure may prove useful in patients with valve areas of borderline significance (i.e., 1.0 cm2 ) by identifying patients with a higher probability for rapid disease progression (Fig. 22-14) (Figure Not Available) . Three-dimensional echocardiography has largely been used as a research tool to evaluate left and right ventricular chamber size and structural dimensions of the mitral valve. However, this imaging modality was used to planimeter the inner surface of the aortic valve leaflets in 23 patients undergoing aortic valve replacement.[76] Measurements were feasible in all but one patient, and valve area was comparable to that derived by the Gorlin formula. Progressive calcification of the aortic valve occurs with all causes of aortic stenosis and eventually leads to impaired leaflet mobility and valve obstruction. The degree of aortic valve calcification can be evaluated on the short-axis view with transthoracic echocardiographic imaging. In a recent mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 18 di 18 study of 126 asymptomatic patients with severe aortic stenosis (aortic jet velocity of at least 4 m per second), the extent of aortic valve calcification was the only independent predictor of clinical outcome, defined as death or need for valve replacement (Fig. 22-15) .[61] In addition, the combination of severe valve calcification and a rapid increase in aortic jet velocity (at least 0.3 m per second per year) predicted an extremely poor prognosis with 79% of patients undergoing surgery or dying within 2 years. In this study, calcification was graded on a scale of 1 (no calcification) to 4 (extensive thickening and 480 Figure 22-14 (Figure Not Available) Relationship of the change in valve area during the systolic ejection to the rate of progression of aortic stenosis. The aortic valve area ratio (AVA ratio) was calculated as the aortic valve area during the midpoint of deceleration divided by the valve area during the mid-point of acceleration. A larger AVA ratio indicates stiffer aortic valve leaflets. Rapid progression was defined as a decrease in valve area of 0.20 cm2 per year or more. In patients with a baseline AVA of 1.2 cm2 or greater, the number of rapid and slow progressors for a ratio less than 1.25 and 1.25 or greater is shown (A). In patients with a baseline AVA of 1.2 cm2 or greater, the receiver operating curve for AVA ratio (B) indicates the sensitivity and specificity of various AVA ratios for predicting rapid progression of disease. AUC, area under the curve. (From Lester SJ, McElhinney DB, Miller JP, et al: Circulation 2000;101:1947–1952.) calcification of all cusps). Other studies have also found aortic valve calcification to predict more rapid disease progression.[60] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/189.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 6 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Physiologic Variability in Measures of Stenosis Severity Exercise Hemodynamics in Valvular Aortic Stenosis Although exercise testing should be performed with caution, if at all, in symptomatic patients with valvular aortic stenosis because of the high risk of complications,[55] studies in asymptomatic patients have provided insight into the relationship between hemodynamic severity and clinical symptoms (Table 22-2) . [46] [47] [48] [49] [51] , [77] [78] [79] [80] In patients with asymptomatic aortic stenosis, exercise is associated with an appropriate rise in heart rate and cardiac output. The increase in cardiac output with upright exercise is mediated almost entirely by heart rate, with little change in stroke volume. However, even though stroke volume does not change, mean and maximum transaortic volume flow rates are increased because of concurrent shortening of the systolic ejection period. Thus, exercise results in an increase in maximum aortic jet velocity, with a corresponding increase in the mean transaortic gradient as predicted by the Bernoulli equation. The continuity equation predicts a linear relationship between maximum volume flow rate (Q ) and maximum jet velocity (V ) for any given max max valve area.[78] This linear relationship has been verified using both invasive and noninvasive data in an animal model of valvular aortic 481 Figure 22-15 Kaplan-Meier analysis of event-free survival among 25 patients with no or mild aortic valve calcification, as compared with 101 patients with moderate or severe calcification. The vertical bars indicate standard errors. All the subjects in this study had an initial aortic jet velocity of at least 4.0 m per second (mean 5.0 ± 0.6 m per second). (From Rosenhek R, Binder T, Porenta G, et al: N Engl J Med, 2000;343:611–617.) stenosis.[81] In clinical studies, only two data points typically can be mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 6 acquired, but the slope of the change in V relative to Q in patients max max with no change in valve area with exercise parallels the slope predicted by this relationship. In patients with an increase in valve |
area with exercise, the observed slope is greater than predicted for a fixed valve area. Changes in Aortic Valve Area with Changes in Volume Flow Rate The effect of changes in volume flow rate on Gorlin and continuity equation valve areas also has been examined in in vitro models, in animal models, [82] and in patients with valvular aortic stenosis (Fig. 22-16) . These studies consistently show an increase in valve area with an increase in transaortic volume flow rate for most stenotic aortic valves.[46] [47] [48] [49] [50] [51] [83] [84] [85] Although these apparent increases, to some extent, could be due to errors in the valve area formulas, both in vitro pulsatile flow model data [71] and video imaging of flow-dependent changes in valve opening support the concept that valve area itself, both anatomic and physiologic, varies with transaortic volume flow rate.[86] This conclusion is not all that surprising given the well-known observation that even normal aortic valve leaflets open less when volume flow rate is decreased, for example, in patients with a dilated cardiomyopathy. Change in Other Measures of Stenosis Severity with Change in Volume Flow Rate Although some investigators have suggested that valve resistance is independent of flow rate,[50] [87] other investigators have shown changes in valve resistance with changes in volume flow rate in in vitro models,[71] in animal models, and in patients with asymptomatic aortic stenosis.[15] [83] In part, the relative stability of valve resistance with changes in flow rate observed in some studies[56] [57] may relate to the range of stenosis severity evaluated (see Fig. 22-12) . Because of the curvilinear relationship between resistance and valve area, with "larger" valve areas (right side of 482 TABLE 22-2 -- Physiologic Changes with Exercise in Adults with Valvular Aortic Stenosis Bache Ettinger Otto et Martin Burwash et al[47] et al[79] al[78] et al[49] et al[51] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 6 Patients, N 20 10 28 85 110 Measurements Invasive Invasive Doppler Invasive Doppler echo echo Type of Exercise Supine Supine Treadmill Supine Treadmill bicycle bicycle bicycle Heart Rate, bpm Rest 79 ± 3 87 ± 5 71 ± 17 71 ± 2 63 ± 14 Exercise 112 ± 5 109 ± 5 147 ± 28 98 ± 2 104 ± 23 Systolic Blood Pressure, mm Hg Rest 120 ± 3 118 ± 8 139 ± 15 — 143 ± 22 Exercise 136 ± 3 133 ± 8 155 ± 24 — 163 ± 29 Stroke Volume, mL Rest — — 98 ± 29 — 103 ± 30 Exercise — — 89 ± 32 — 96 ± 30 Qmean , mL/sec Rest 245 ± 14 — 300 ± 85 275 ± 8 319 ± 80 Exercise 318 ± 21 — 366 ± 325 ± 10 400 ± 140 159 Cardiac Output, L/min Rest 5.4 ± 0.3 8.6 ± 1.1 6.5 ± 1.7 6.0 ± 0.2 6.3 ± 1.7 Exercise 8.5 ± 0.6 9.2 ± 0.9 10.7 ± 9.3 ± 0.2 9.9 ± 3.8 4.4 Mean Pressure Gradient, mm Hg Rest 59 ± 4 Exercise 74 ± 5 37 ± 9 39 ± 20 37 ± 2 30 ± 14 38 ± 11 52 ± 26 41 ± 2 41 ± 18 Vmax (m/sec) Rest — — 4.0 ± 0.9 Exercise — — 4.6 ± 1.1 — 3.6 ± 0.8 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 6 — 4.3 ± 0.8 Aortic Valve Area, cm2 Rest 0.8 ± 0.1 1.8 ± 0.3 1.2 ± 0.5 1.1 ± 0.1 1.4 ± 0.5 Exercise 0.9 ± 0.1 1.9 ± 0.3 1.3 ± 0.7 1.3 ± 0.1 1.6 ± 0.7 Valve Resistance, dyne/sec/cm-5 Rest — — — 191 ± 12 137 ± 81 Exercise — — — 182 ± 12 155 ± 97 Stroke Work Loss, % Rest — — — 26 ± 1 17 ± 7 Exercise — — — 25 ± 1 20 ± 9 Left Ventricular End- Diastolic Pressure; mm Hg Rest 12 ± 6 15 ± 3 — — — Exercise 20 ± 2 15 ± 4 — — — V , maximum aortic jet velocity. max curve) resistance changes very little even with substantial changes in valve area, whereas with smaller valve areas (left side of curve), large changes in resistance are expected with only small changes in valve area. Similarly, left ventricular stroke work loss has been found to vary with changes in volume flow rate.[51] [71] [88] Overall, both total and steady left ventricular stroke work losses correlate inversely with valve area. However, for a specific valve anatomy, work loss increases with an increase in stroke volume despite a concurrent increase in valve area. This suggests that for a given degree of leaflet stiffness, greater opening of the valve is achieved at the expense of greater work loss. Alternatively, since work includes both potential and kinetic energy, a decrease in the percentage of potential work converted to kinetic work would lead to this observation. In studies to date, only potential work has been measured because of the conceptual and technical difficulties in measurement of kinetic work. Changes in the effective frictional loss component with changes in volume flow rate also mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 6 may affect calculated measures of stenosis severity. Which Measure of Stenosis Severity Is Best? The anatomy of degenerative valvular aortic stenosis is characterized by thickened and stiff leaflets without commissural fusion (see Fig. 22-11) . Given this anatomic substrate, it is not surprising that the degree of valve opening varies with the amount of "force" applied to the valve, whether this force is represented by the surgeon's finger, a balloon valvuloplasty catheter, or the rate and volume of blood ejected by the left ventricle. Most investigators to date have found that each proposed measure of stenosis severity, when examined in detail, varies with changes in volume flow rate. These measures include peak left ventricular to aortic pressure gradient, mean transaortic pressure gradient, maximum Doppler aortic jet velocity, Gorlin valve area, continuity equation valve area, left ventricular stroke work loss, and valve resistance. Of note, despite this potential limitation, most clinical decisions can be made with a high degree of reliability using these, albeit imperfect, indices of disease severity. To 483 Figure 22-16 Relationship of rest and continuity equation aortic valve area (A), aortic valve resistance (B), and percentage of left ventricular stroke work loss (C) in 110 exercise studies. The slopes of the regression lines (solid line) are greater than the line of identity (dashed line), demonstrating an increase in all three indexes with exercise. AVA, aortic valve area; LVSW, left ventricular stroke work. (From Burwash IG, Pearlman AS, Kraft CD, et al: J Am Coll Cardiol 1994;24:1342–1350.) define the "best" measure of stenosis severity, the specific goals in quantitating the degree of stenosis must be clarified. These goals fall into two distinct categories: clinical patient management and research applications. In terms of clinical decision making, the ideal measure of stenosis severity should reflect disease severity and should have an acceptable intraobserver and interobserver reproducibility. In addition, it should be easily applicable, noninvasive, and inexpensive. Most importantly, it should be predictive of clinical outcome. Clearly, Doppler echocardiographic measures of jet velocity and valve area meet these criteria, as discussed subsequently. In the clinical setting, the impetus to derive a flow-independent measure of stenosis severity arises from the relatively unusual clinical situation in mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 6 which there is coexisting left ventricular systolic dysfunction and an anatomically abnormal aortic valve. Potential approaches to this clinical dilemma are discussed in the following sections. For specific research applications, the "best" measure of stenosis severity must possess additional characteristics. One research goal is to explain the paradox of the marked overlap in hemodynamic severity between symptomatic and asymptomatic patients with aortic stenosis. Some patients with hemodynamically severe disease remain asymptomatic, whereas other patients with only moderate valve obstruction develop definite symptoms. [89] [90] [91] Whether these apparent discrepancies between hemodynamic severity and clinical manifestations of disease are related to other factors (such as ventricular diastolic function[92] ) or whether they reflect the inadequacy of available measures of stenosis severity remains unclear. A second and more important research goal is to follow disease severity over time to define the natural history of this disease and to identify factors that predict progression in individual patients. This goal requires measures of stenosis severity that have a high degree of reproducibility over time and among institutions. This application will allow use of Doppler echocardiographic measures of aortic stenosis severity as end points in intervention trials to prevent or slow disease progression. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/190.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 4 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Left Ventricular Response to Valvular Aortic Stenosis Diastolic Function The initial physiologic response to chronic pressure overload of the left ventricle is impaired early diastolic relaxation as manifested by a prolonged time constant of relaxation (tau), a lengthened isovolumic relaxation time (IVRT), and a reduced early diastolic filling velocity, similar to the changes seen in patients with systemic hypertension ( see Chapter 6 and Chapter 32 ). [93] [94] [95] [96] [97] Changes in diastolic function typically precede evidence of systolic dysfunction and thus may be present early in the disease course. Although some investigators suggest that Doppler measures of early and late diastolic filling velocities (or rates) may not be sensitive for detection of early diastolic dysfunction,[94] others propose that diastolic parameters can distinguish symptomatic from asymptomatic patients.[92] Later in the disease course, decreased diastolic compliance plus a rightward shift on the passive diastolic pressure-volume relationship may result in a filling pattern characterized by a shortened IVRT, increased early diastolic filling velocity, rapid early deceleration slope, and reduced atrial contribution to diastolic filling, a pattern often referred to as pseudonormalization. [96] Wall Stress and Concentric Hypertrophy 484 As the severity of stenosis increases, concentric left ventricular hypertrophy develops in response to the chronic elevation in left ventricular systolic pressure. This increase in myocardial wall thickness allows maintenance of normal wall stress given that wall stress is directly related to chamber pressure and dimension, but inversely related to wall thickness. Left ventricular hypertrophy is assessed most reliably by calculation of left mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 4 ventricular mass from two-dimensional images, although simple chamber dimensions and diastolic wall thickness may be adequate for clinical evaluation in many patients. Meridional and circumferential wall stress can be calculated from two-dimensional echocardiographic data in conjunction with Doppler evaluation of the aortic valve gradient and a cuff blood pressure measurement, as described in Chapter 4 . In general, the time course for development of left ventricular hypertrophy parallels the course of stenosis severity in most patients. In some individuals, the degree of hypertrophy appears out of proportion to the severity of aortic stenosis. In these cases, other causes for hypertrophy, such as hypertension, coexisting hypertrophic cardiomyopathy, or an infiltrative myocardial process should be considered. It is particularly important to evaluate these possibilities carefully on two-dimensional imaging because the clinical presentation of hypertrophic cardiomyopathy may be similar to that of valvular aortic stenosis. Genetic factors also play a role in the degree of left ventricular hypertrophy. For example, a recent study found that certain polymorphisms of the angiotensin-converting enzyme gene were associated with increased left ventricular hypertrophy.[98] Gender Differences in the Left Ventricular Response to Aortic Stenosis Several investigators have found significant gender differences in the left ventricular response to the chronic pressure overload of aortic stenosis. [99] In symptomatic patients referred for aortic valvuloplasty, although women and men had similar valve areas, women had higher transaortic gradients, higher relative wall thicknesses, and a higher prevalence of left ventricular hypertrophy using gender-specific hypertrophy criteria. In addition, women had a lower functional status score for the same degree of aortic valve obstruction.[100] Another study observed higher peak |
left ventricular pressures, higher ejection fractions, smaller left ventricular end-diastolic dimensions, and a higher relative wall thickness in women, as compared with men, with aortic stenosis.[101] Although left ventricular mass did not differ in women versus men, left ventricular geometry differed as reflected in a lower circumferential wall stress for a given degree of hypertrophy. Similar findings were observed in a consecutive series of asymptomatic aortic stenosis patients.[102] Even though there were no gender differences in aortic stenosis severity, women reported more functional limitation and had smaller left ventricular end-diastolic and end-systolic volumes and mass index, but had a higher relative wall thickness and fractional shortening as compared with men. In addition, women had a shorter treadmill exercise mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 4 duration and a smaller increase in cardiac output with exercise, even though heart rate and blood pressure responses were similar in men and women.[102] The importance of gender differences in the left ventricular response to chronic pressure overload are illustrated by the observation that after aortic valve replacement in patients with depressed left ventricular systolic function (ejection fraction < 45%), women had a greater improvement in ejection fraction at a mean of 1.4 years after valve replacement, although survival was similar between men and women. The ejection fraction increased from 33% ± 8% to 48% ± 15% in women, compared with an increase from 32% ± 9% to 42% ± 15% in men (P < .02).[103] In summary, the degree of increase in left ventricular mass is variable, in both men and women. However, women tend to have small ventricles with thick walls, low wall stress, and normal or hyperdynamic systolic function (Fig. 22-17) . In contrast, men tend to have left ventricular dilation with normal wall thickness, increased wall stress, and depressed systolic function. Systolic Dysfunction Left ventricular systolic dysfunction due to valvular aortic stenosis usually occurs late in the disease course. Given the high ventricular afterload caused by the stenotic valve, left ventricular contractility typically remains normal, despite a low ejection fraction. Relief of the high afterload with valve replacement often leads to rapid normalization of systolic function. In adult patients, however, left ventricular systolic dysfunction may be due to causes other than aortic stenosis, such as coronary artery or myocardial disease. Patients with these conditions often fail to improve with valve replacement. In the patient with a moderate aortic valve gradient, distinguishing poor left ventricular systolic function caused by severe aortic stenosis from that caused by concurrent ischemic or myocardial disease with only moderate aortic valve disease remains a difficult dilemma. One approach to this problem is to use a flow-independent measure of stenosis severity or to look at the change in stenosis severity with a change in volume flow rate; an alternate approach is to utilize a load-independent measure of left ventricular contractility to evaluate myocardial function. Unfortunately, a load-independent measure of contractility has proven as elusive as a flow-independent measure of stenosis severity.[94] [101] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Evaluation of Coexisting Coronary Artery Disease In the patient undergoing valve replacement for symptomatic aortic stenosis, most cardiac surgeons recommend concurrent coronary artery bypass grafting if significant coronary artery disease is present. Although the need for coronary bypass grafting in the aortic stenosis patient remains somewhat controversial, reported operative mortality 485 Figure 22-17 In this elderly woman with calcific aortic stenosis and mitral annular calcification, severe concentric hypertrophy is present as shown in an end-diastolic image in an apical four-chamber view (A). Aortic jet velocity is 5.1 m per second corresponding to a maximum gradient of 104 and a mean gradient of 62 mm Hg (B). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. in patients with both aortic stenosis and coronary artery disease is only 1.1% to 4.8% when valve replacement plus coronary bypass grafting is performed, versus 4.0% to 13.2% when valve replacement alone is performed.[104] [105] In aortic stenosis patients with angina, the prevalence of significant coronary artery disease ranges from 40% to 80%, so that coronary angiography is needed for planning the operative procedure. Aortic stenosis patients without symptoms of angina also have a prevalence of significant coronary artery disease between 0% and 54% (average 16%). The appropriate diagnostic approach to these patients is less clear. Exercise treadmill testing in aortic stenosis patients is often nondiagnostic for the presence of coronary artery disease because most of these patients (even when asymptomatic) have significant ST segment depression with exercise, possibly related to left ventricular hypertrophy. [78] [106] In addition, it is important to recognize the potential risk of exercise testing in symptomatic aortic stenosis patients. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 The utility of echocardiographic stress imaging for the diagnosis of coronary artery disease in aortic stenosis patients has not been extensively evaluated. Studies on the exercise physiology of aortic stenosis or on the response to inotropic stimulation with dobutamine have focused on Doppler evaluation of aortic stenosis severity and cardiac output rather than on segmental wall motion abnormalities of the left ventricle.[87] A recent study of 50 patients with severe aortic stenosis evaluated the use of adenosine stress echocardiography for the detection of coronary artery disease.[107] The sensitivity and specificity of stress echocardiography were 85% and 97%, respectively. In addition, no major complications occurred during the procedure. Clearly, these observations need confirmation in other studies. In our experience, definite exercise-induced reversible segmental wall motion abnormalities have been seen in a few patients with aortic stenosis in whom subsequent coronary angiography confirmed significant coronary artery disease. More often, however, no definite wall motion abnormalities are seen, even though subsequent catheterization does show greater than 50% narrowing in the coronary arteries. Whether this lack of sensitivity relates to exercise limitation by aortic stenosis itself (the ischemic threshold is not reached), to diffuse subendothelial ischemia obscuring segmental abnormalities, or whether the degree of stenosis being treated with bypass grafting is insufficient to cause ischemia remains unclear. Further studies of stress echocardiography in aortic stenosis patients may clarify this issue. Exercise tomographic thallium imaging in aortic stenosis patients has a sensitivity of 90% and a specificity of 70% for the presence of significant (greater than 50% luminal diameter narrowing) coronary artery disease.[108] Similarly, adenosine thallium stress testing in aortic stenosis patients has a sensitivity of 92% and a specificity of only 71%.[109] When combined with a pretest likelihood of disease (based on gender, age, and cardiac risk factors), the post-test likelihood of coronary artery disease can be helpful in deciding whether coronary angiography is necessary and may result in a reduction in overall costs of patient evaluation.[110] However, many clinicians choose to perform coronary angiography because of the low risk associated with this procedure and the potential impact of the diagnosis on the operative procedure and survival in a specific individual. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/192.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 10 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Disease Progression Natural History of Aortic Valve Stenosis The natural history of valvular aortic stenosis is characterized by a long time period during which the patient is asymptomatic but there is gradually increasing obstruction 486 to left ventricular outflow (Table 22-3) .[111] [112] The duration of this asymptomatic period is variable. With a congenital unicuspid valve, symptoms typically are recognized in childhood or adolescence. Occasionally, however, young adults may present with symptomatic congenital aortic stenosis, either due to restenosis after a surgical valvotomy as a child or in the absence of previous surgical procedures. In patients with a congenital bicuspid aortic valve, the onset of symptoms typically is at 50 to 60 years of age.[113] [114] In the elderly patient with degenerative valve disease, symptom onset typically is at 70 to 80 years of age, but the interval between observing aortic valve "sclerosis" by echocardiography and clinical evidence of severe stenosis may be only 5 to 10 years. Rheumatic valvular aortic stenosis has a variable course with significant aortic valve obstruction (in conjunction with mitral valve involvement) occurring over a wide age range. Because disease progression results in reduced leaflet opening, the antegrade velocity across the valve increases in direct relation to the degree of valve obstruction. Transaortic pressure gradients increase as predicted by the Bernoulli equation; although it is noteworthy that little increase in the pressure gradient is seen until the valve area is reduced to one half the normal area, whereas an increase in velocity will be noted with only minimal TABLE 22-3 -- Natural History of Valvular Aortic Stenosis mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 10 Aortic Mea Entry Symptom Patients, Age, Stenosis Follo Study Criteria Status N yrs Severity up Frank et ∆P ≥ 80% 15 32– AVI 0.4 al[111] peak 50 > 2 y mm Hg or symptomatic 59 ± 0.1 AVI < 0.7 cm2 /m2 cm2 /m2 Chizner et Cardiac cath, 76% 42 22– AVA 0.7 5.4 y al[133] no AVR symptomatic 77 ± 0.3 (0.2–1.1) cm2 O'Keefe Severe aortic Symptomatic 50 77 Vmax 4.5 1.7 y et al[134] stenosis, no m/sec, AVR, age ≥ 60 AVA 0.6 (0.3–8) cm2 (60– 89) Turina et Cardiac cath, Symptomatic 125 43 Mean ∆P 6.6 y al[91] no AVR 69 mm Hg AVA 0.56 cm2 (16– 73) Asymptomatic 65 Mean ∆P 57 mm Hg AVA 0.76 cm2 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 10 Horstkotte Catheterization Asymptomatic 142 Mild AS et al[89] for other (AVA > reasons 1.5 cm2 ) Catheterization Asymptomatic 236 Moderate for other AS reasons (AVA 0.8–1.5 cm2 ) Refused Symptomatic 35 Severe surgery AS (AVA < 0.8 cm2 ) Kelly et al V [131] max ≥ 3.6 Asymptomatic 51 63 ± ∆P 68 ± 15 ± m/sec 19 19 mos Symptomatic 39 72 ± ∆P 68 ± 11 19 Pellikka Doppler V mptomatic 143 72 Vmax 4.4 20 m et al[132] max Asy ≥ 4 m/sec (4–6.4) m/sec (40– 94) Kennedy Moderate 18% 66 67 ± AVA 35 m et al[135] aortic stenosis asymptomatic 10 0.92 ± at cath, no 0.13 AVR (0.7–1.2) Otto et al Abnormal Asymptomatic 123 63 ± V 16 max < 2.5 y [128] valve with 3.0 m/sec Vmax > 2.6 m/sec V 3–4 max m/sec Vmax > mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 10 4.0 m/sec Rosenhek Abnormal Asymptomatic 128 60 ± V 5.0 27 ± et al[61] valve with 18 max ± 0.6 mos Vmax > 4.0 m/sec m/sec AS, aortic stenosis; AVA, aortic valve area; AVI, aortic valve index, AVR valve replacement; cath, catheterization; ∆P, pressure gradient; V , maxim max jet velocity. * Event-free survival. obstruction. Continuity equation valve areas will reflect accurately the degree of impairment of valve opening. In the past, "severe" or "critical" aortic stenosis has been defined in terms of a specific valve area or valve area index. More recent studies[89] [91] [115] have shown marked overlap in hemodynamic severity between symptomatic and asymptomatic patients, indicating that the "critical" degree of valve narrowing varies from patient to patient (Fig. 22-18) . This observation has been confirmed in prospective studies showing that symptom onset occurs with a jet velocity as low as 3.0 m per second or may be delayed until the jet velocity is over 5.0 m second. Similarly, some patients remain asymptomatic with a valve area less than 0.7 cm2 , whereas others have definite symptoms with a valve area greater than 1.0 cm2 . Hemodynamic Progression Until recently, data on the hemodynamic progression of valvular |
aortic stenosis was limited to studies of patients in whom two cardiac catheterizations had been performed (Table 22-4) . [116] [117] [118] [119] [120] [121] The impact of selection bias on these data is difficult to assess, since only patients who did not die or undergo valve replacement after the first catheterization, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 10 487 Figure 22-18 Hemodynamically severe aortic stenosis: mean aortic pressure gradient, valve orifice area, cardiac index, and left ventricular end-diastolic pressure in severely symptomatic (open circles) and asymptomatic or mildly symptomatic (closed circles) patients. Mean value (horizontal line) and statistical difference between both groups are indicated. NS, not significant. (From Turina J, Hess O, Sepulcri F, Krayenbuehl HP: Eur Heart J 1987;8:471–473.) yet required a second catheterization for clinical indications, are included in these series. In general, these studies showed an average rate of increase in mean pressure gradient between 0 and 12 mm Hg per year and a decrease in valve area between 0.02 and 0.3 cm2 per year. Marked individual variability in the rate of progression was noted, however, and no clear factors were identified that predicted the rate of progression. The availability of an accurate, noninvasive method to evaluate hemodynamic severity has allowed larger and more detailed studies on the rate of hemodynamic progression.[58] [60] , [61] [90] , [115] [122] [123] [124] [125] [126] [127] In these studies, the average rate of increase in aortic jet maximum velocity ranges from 0.2 to 0.4 m per second per year, with an increase in mean gradient of 6 to 7 mm Hg per year and a decrease in valve area of 0 to 0.3 cm2 per year. Again, marked individual variability in the rate of hemodynamic progression Figure 22-19 Change in maximal aortic jet velocity (Vmax ) and pressure gradient during follow-up in 45 patients. (From Faggiano P, Ghizzoni G, Sorgato A, et al: Am J Cardiol 1992;70:229–233.) was observed ( Fig. 22-19 and Fig. 22-20 ). Although Doppler- echocardiographic studies have the advantage of larger patient numbers and potentially less selection bias (a repeat echocardiographic study is likely to be requested more often than a repeat cardiac catheterization), many of these studies are retrospective, with the data extracted from ongoing clinical databases. Thus, patients with rapid progression, those developing symptoms, or those requiring surgical intervention may be overrepresented. Conversely, repeat studies may not have been performed in clinically stable patients. The results of more recent prospective studies may avoid some of these biases.[61] [128] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 10 It is important to remember that as the disease progresses, increasing obstruction to left ventricular outflow most often is reflected by both a decrease in valve area and an increase in jet velocity and pressure gradient. However, if there is a concurrent decrease in transaortic 488 TABLE 22-4 -- Hemodynamic Progression of Valvular A Mean Follow Clinical up Status at Type of Measurement Patients, Interva Study Entry Study Method N yr Bogart et 2 cardiac Retrospective Invasive 11 4.9 al[116] caths Cheitlin et 2 cardiac Retrospective Invasive 29 4 al[117] caths Wagner 2 cardiac Retrospective Invasive 50 3.5 and Selzer caths [120] Jonasson Calcific AS Retrospective Invasive 26 9 et al[118] Nestico et 2 cardiac Retrospective Invasive 29 5.9 al[119] caths Davies et 2 cardiac Retrospective Invasive 47 al[121] caths Otto et al Asymptomatic Prospective Doppler 42 1.7 [90] Roger et al AS on echo Retro cohort Doppler 112 2.1 [123] Thoreau et AS on echo Retrospective Doppler 25 4.8 al[122] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 10 Faggiano AS on echo Prospective Doppler 45 1.5 et al[124] Peter et al AS on echo Retrospective Doppler 49 2.7 [126] Brener et AS on echo Retrospective Doppler 394 6.3 al[125] Otto et al Asymptomatic Prospective Doppler 123 2.5 [128] Bahler et AS on echo Retrospective Doppler 91 1.8 al[60] Palta et al AS on echo Retrospective Doppler 170 1.9 [127] Roshenhek AS on echo Prospective Doppler 128 1.8 et al[61] with V max >4.0 m/sec AS, aortic stenosis; AVA, aortic valve area; ∆P, pressure gradient; Vmax , volume flow rate, a decrease in valve area alone may be seen with no change in jet velocity or transaortic gradient. A decrease in transaortic volume flow rate may occur secondary to comorbid disease, such as increasing mitral regurgitation or myocardial infarction, but also may occur late in the disease course of isolated aortic stenosis as left ventricular stoke volume decreases because of the onset of subtle systolic dysfunction (Fig. 22-21) . Conversely, some patients may have an interval increase in jet velocity and pressure gradient with no change in valve area if transaortic stroke volume is increased because of systemic factors (e.g., anemia, fever, pregnancy) or increasing aortic regurgitation. At this point, it is not clear whether the rate of hemodynamic progression in an individual patient is either predictable or "steady." In fact, it is most likely that the rate of progression is nonlinear; that is, a fairly slow rate of Figure 22-20 Maximal aortic jet velocity (Vmax ) is plotted for the initial mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 10 and final Doppler echocardiographic studies in 42 asymptomatic patients. Group means are indicated by the symbol . (From Otto CM, Pearlman AS, Gardner CL: J Am Coll Cardiol 1989; 13:545–550.) progression may change to a rapid increase in severity when the opposing forces of left ventricular ejection and leaflet stiffness can no longer be balanced. Predictors of Hemodynamic Progression Factors that predict the rate of hemodynamic progression in an individual patient have not been well defined. Clearly, valve anatomy is an important factor in disease progressive, since most patients with a bicuspid stenotic valve require surgical intervention at a younger age than patients with degenerative aortic stenosis.[114] Gender also is important, since the ratio of men to women with aortic stenosis is approximately 2:1. Other factors associated with the rate of disease progression are the severity of aortic stenosis when initially seen (more severe disease 489 Figure 22-21 A 32-year-old man had asymptomatic valvular aortic stenosis with a jet velocity of 5.0 m per second and a continuity equation valve area of 1.2 cm2 (A and B). Over the next year, he developed the onset of exercise intolerance and early symptoms of aortic stenosis. Repeat examination showed a decrease in aortic jet velocity to 4.5 m per second (C) in association with a decreased transaortic volume flow rate (D). Aortic valve area had decreased to 1.0 cm2 . Two-dimensional echocardiography showed normal left ventricular systolic function, but ejection fraction had decreased from 72% to 60%. leads to symptoms more rapidly than milder disease) and age (older patients have more rapid disease progression than younger patients). Clinical factors such as elevated serum lipid levels, hypertension, smoking, and diabetes have been found to be associated with aortic stenosis.[129] In addition, a recent study found that smoking, hypercholesterolemia, and elevated creatinine and calcium levels were associated with more rapid disease progression.[127] However, further studies are needed to confirm these results. Two recent studies suggested that the amount of aortic valve calcium is an important determinant of disease progression.[60] [61] Despite using different grading scales to evaluate valve calcium, both of these studies found that the rate of disease progression was more rapid when mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 10 more valve calcium was present. These studies also confirmed previous observations that the rate of disease progression is highly variable for individual patients. Given the continued uncertainty regarding which factors predict progression in an individual patient, it is prudent to follow patients with aortic valve thickening closely, monitoring for early symptoms of valve obstruction. Periodic echocardiographic examinations also are warranted, particularly for any change in symptoms or functional status. Uncertainty as to the rate of hemodynamic progression in an individual patient complicates the decision as to whether concurrent aortic valve replacement should be performed in patients with only moderate aortic stenosis who are undergoing coronary artery bypass surgery. Some surgeons recommend "prophylactic" valve replacement, since otherwise reoperation may be needed in less than 5 years.[130] Symptomatic versus Asymptomatic Aortic Stenosis The clinical course of the patient with aortic stenosis changes dramatically once symptoms supervene. The 490 Figure 22-22 (Figure Not Available) A, Event-free survival in hemodynamically severe aortic stenosis (triangles) or aortic regurgitation (circle) in severely symptomatic (solid lines and solid symbols) and asymptomatic or mildly symptomatic (dashed lines and open symbols) patients. B, Effective survival in hemodynamically severe aortic stenosis (triangles) or aortic regurgitation (circles) in severely symptomatic (solid lines) and asymptomatic or mildly symptomatic (dashed line) patients. (From Turina J, Hess O, Sepulcri F, Krayenbuehl HP: Eur Heart J 1987;8:471–483.) asymptomatic patient (regardless of hemodynamic severity) has a low risk of sudden death with an actuarial survival rate no different from that of age- matched normal subjects[89] [91] [131] [132] (Fig. 22-22 (Figure Not Available) and Fig. 22-23 ). In contrast, the symptomatic patient has a grim prognosis, with a 5-year actuarial survival rate of only 12% to 50% without surgical intervention. These data were derived from studies of patients who refused surgical intervention.[89] [91] , [111] , [131] [133] [134] [135] In patients with severe, symptomatic aortic stenosis, predictors of survival include the transaortic gradient or velocity, left ventricular systolic function as assessed qualitatively on echocardiography, age, and gender.[136] Of note, patients with a higher transaortic gradient have a better prognosis, most likely mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 10 because when severe stenosis is present, a low gradient indicates a low transaortic stoke volume. In any case, valve surgery for relief of stenosis remains the appropriate treatment for symptomatic patients, even the elderly.[137] [138] Only rarely does severe comorbid disease result in an unacceptably high operative morbidity and mortality. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/193.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 8 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Role of Echocardiography in Clinical Decision Making Timing of Intervention in the Symptomatic Patient Calcific aortic valve disease is prevalent in the elderly.[139] [140] Most of these patients have a systolic murmur on auscultation, but not all are symptomatic. The first step in the clinical decision making process for the timing of intervention in a patient with valvular aortic stenosis is a careful history as to whether symptoms (angina, exertional dizziness, exercise intolerance, or heart failure) are present or absent ( Table 22-5 ; ; Fig. 22- 24 ). Most clinicians defer intervention until definite symptoms are present, since the risk of sudden death is very low in the asymptomatic patient.[89] [91] [131] , [132] The presence of moderate or severe valve calcification in combination with a rapid increase in jet velocity over time (i.e., rapid progressors) identifies a subgroup of asymptomatic patients with a very poor short-term prognosis who are likely to develop symptoms soon.[61] If the patient has symptoms that may be due to aortic stenosis, the next step is to confirm the anatomic diagnosis and quantitate the degree of valve obstruction by Doppler echocardiography. The most appropriate standard of reference for the diagnostic utility of echocardiography in the management of symptomatic aortic stenosis patients is survival and functional status (not catheterization results), as our goal is to predict clinical outcome correctly.[16] Based on this reference standard, aortic jet velocity alone is a simple and useful initial diagnostic test. When jet velocity is very high (>4.0 or 4.5 m per second), severe stenosis is confirmed.[140] [141] [142] Some patients with mixed moderate aortic stenosis and aortic regurgitation will have a jet velocity over 4 or 4.5 m per second even though valve area is in the range of 1.0 to 1.5 cm2 . Comparing Doppler data with subsequent clinical outcome suggests that these patients benefit from valve replacement if symptoms of valve disease are present.[40] Decision making in patients with mixed aortic stenosis and aortic regurgitation is confounded by the need to |
take the degree of left mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 8 ventricular dilation and systolic dysfunction into account as well as the severity of valve obstruction (see Chapter 4) . When jet velocity is very low (<3.0 m per second), severe stenosis is unlikely and valve replacement is not needed.[140] [142] Of course, exceptions do occur in clinical practice and an occasional patient may be seen with a jet velocity less than 3.0 m per second and a valve area less than 1.0 cm2 in association with severely reduced left ventricular systolic function. Similarly, this numerical approach applies only to the symptomatic patient in whom valve replacement is being considered. A high jet velocity in an asymptomatic patient certainly does not mandate surgical intervention. The use of two break points (upper and lower) allows both severity and specificity to be maximized but leaves an intermediate group in whom further evaluation is needed. When the jet velocity is 3 to 4 m per second, calculation of valve area and assessment of the degree of coexisting aortic regurgitation are helpful in clinical decision making. If the valve area is 1.0 cm2 or less and the patient has symptoms of aortic stenosis, valve replacement is indicated. If the valve area is greater than 1.5 cm2 , valve 491 Figure 22-23 Cumulative life table incidence of death in aortic stenosis patients. Asymptomatic persons (closed circles) had a significantly better survival with respect to all-cause mortality, cardiac death, and sudden death than symptomatic patients (open circles). (From Kelly TA, Rothbart RM, Cooper CM, et al: Am J Cardiol 1988;61:123–130.) TABLE 22-5 -- Clinical Decision Making in Adults with Symptomatic Ao Stenosis Lower Upper V V max max Break Break Diag Patients, End Point, Point, Accu Study N Method Point m/sec Midrange m/sec % Otto 104 Split sample Surgical <3.0 AVA, AR >4.0 9 1988 findings [40] plus 1 yr mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 8 mortality Oh 100 Comparison Aortic Single AVA >4.5 6 1988 with cath data stenosis value [141] severity at cath Galan 510 Observational, Actual <3.0 AVA >4.5 9 1991 retrospective outcome [3] (AVR) Shah 93 Blinded Actual <3.0 AVA >4.0 9 1991 decision re: outcome [142] AVR (AVR) AR, aortic regurgitation; AVA, aortic valve area; AVR, aortic valve replacement; V , maximum aortic jet velocity. max replacement is unlikely to be helpful. When the valve area is between 1.0 and 1.5 cm2 , valve replacement may be indicated if there is at least moderate coexisting aortic regurgitation. Again, clinical decision making is problematic in this patient group. One prudent approach in the mildly symptomatic patient is to repeat the Doppler echocardiographic study after a reasonably short time interval (3–12 months). Evidence of disease progression will tip the balance toward intervention, whereas a stable examination and the absence of worsening symptoms argues for further waiting with close clinical follow-up. In clinical practice, the basic echocardiographic examination of a patient with valvular aortic stenosis includes measurement of maximum aortic jet velocity (with optional gradient calculations); continuity equation valve area; assessment of the degree of coexisting aortic regurgitation; evaluation of left ventricular size, hypertrophy, and systolic function; evaluation of the degree of mitral regurgitation; and estimation of pulmonary artery pressures. All of these parameters are included in the clinical decision- making process, along with any other specific measurements needed in an individual patient. Aortic Stenosis with Decreased Left Ventricular Function In some patients it is unclear whether valve opening is restricted due to excessive leaflet stiffness or whether there is only mild leaflet sclerosis with limited motion due to low transaortic stroke volume (Fig. 22-25) . mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 8 There have been two basic research approaches to resolving the problem of distinguishing severe aortic stenosis with consequent depressed left ventricular systolic function from only mild to moderate stenosis with reduced leaflet motion due to intrinsic left ventricular dysfunction: (1) a flow-independent measure of stenosis severity or (2) a load-independent measure of left ventricular systolic function. Although significant progress has been made with both of these approaches, as discussed earlier, neither approach has provided a clear answer. A pragmatic clinical approach to this patient group is to (1) look at the valve, (2) look at the patient, (3) look at the options, and (4) consider further diagnostic evaluation (Table 22-6) . Direct assessment of the degree of leaflet thickening and calcification by fluoroscopy, transthoracic or transesophageal echocardiography, or, if 492 Figure 22-24 Flow chart for clinical decision making in aortic stenosis. AR, aortic regurgitation; AVA, aortic valve area; AVR, aortic valve replacement; F/U, follow-up; Vmax , maximum velocity of aortic jet. Figure 22-25 A 61-year-old man presented with heart failure symptoms. Echocardiographic examination showed a moderately calcified valve with reduced leaflet opening (A) and reduced systolic function (ejection fraction, 20%) in association with marked left ventricular dilation as seen in the apical four-chamber view (B). Transaortic stroke volume was reduced as shown by pulsed Doppler echocardiographic examination of left ventricular outflow velocity in an anteriorly angulated four-chamber view (C). The aortic jet velocity (D) was 3.0 m per second corresponding to a maximum gradient of 36 mm Hg and a mean of gradient of 22 mm Hg. Continuity equation valve area was 0.9 cm2 . After multiple readmissions for heart failure on medical therapy, the patient underwent aortic valve replacement. Postoperatively, there has been no change in left ventricular function and persistent symptoms of heart failure are present. Ao, aorta; AS-jet, aortic stenosis jet; LA, left atrium; LV, left ventricle; LVOT, left ventricular outflow tract; RA, right atrium; RV, right ventricle. 493 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 8 TABLE 22-6 -- Clinical Decision Making: Aortic Stenosis with Decreased Left Ventricular Function 1. Look at the valve Severely calcified versus Flexible leaflets 2. Look at the patient LV dysfunction due to end-stage ischemic disease or cardiomyopathy versus LV dysfunction due to aortic stenosis 3. Look at the options Risk of surgery Comorbid disease Outcome without surgery 4. Evaluate stenosis severity at two different flow rates (dobutamine or exercise): Increased transaortic flow rate Increased AVA suggests flexible valve leaflets No change in AVA suggests stiff, rigid valve leaflets No change in transaortic volume flow rate Severe AS versus unresponsive myocardium? AS, aortic stenosis; AVA, aortic valve area; LV, left ventricular. necessary, direct inspection at the time of surgery often is very helpful. A heavily calcified valve suggests that valve replacement will be beneficial, whereas thin, flexible leaflets argue against valve surgery. Additional clinical information about the patient may clarify the problem. If left ventricular systolic dysfunction is due to aortic stenosis, improvement is expected after valve replacement. However, if left ventricular dysfunction is due to end-stage ischemic disease or a primary cardiomyopathy, little improvement is expected after aortic valve surgery. Next, the therapeutic options and expected outcomes can be estimated for the individual patient. If the risk of surgery is acceptable or if the patient is having surgery for coexisting coronary artery disease, the threshold for valve replacement is reasonably low. If the risk of valve replacement is excessively high because of comorbid disease, medical therapy may be mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 8 appropriate. If the patient has failed aggressive medical therapy, surgical intervention may be indicated, even if the risk is high. If the clinical decision still remains unclear, evaluation of stenosis severity at two different flow rates may be helpful. With mild to moderate aortic stenosis, augmentation of transaortic volume flow rate with exercise or a positive inotropic agent (e.g., dobutamine) will result in a significant increase (>0.2 cm2 ) in valve area as the flexible leaflets open to a greater extent. Conversely, with critical aortic stenosis, valve area will change little despite increased transaortic volume flow due to stiff, rigid valve leaflets. However, an increase in aortic valve area can be seen in some patients with surgically confirmed severe aortic stenosis, which therefore does not exclude fixed valve disease.[143] If the ventricle fails to respond to inotropic stimulation (i.e., no increase in cardiac output), interpretation is more difficult.[50] [144] [145] The failure of volume flow rate to increase may be due to limitation of flow by a severely stenotic valve or may be due to an unresponsive myocardium. In some patients, it may be preferable to evaluate stenosis severity at baseline and after several weeks of therapy to optimize preload and afterload, rather than using maneuvers to acutely increase volume flow rate. Instead of assessing changes in valve area, another approach is to calculate the end-systolic wall stress to fractional shortening relationship and compare the patient's data with those of published series[101] to assess whether improvement after valve replacement is likely. Unfortunately, despite meticulous diagnostic evaluation, outcome is likely to be poor in patients with aortic stenosis and low output, regardless of the therapy chosen.[146] [147] [148] [149] [150] Patients with reduced systolic function and a history of a prior myocardial infarction experience a particularly poor outcome following valve replacement.[151] A recent study that included patients with a low transvalvular gradient in addition to impaired systolic function found that the ejection fraction improved in the majority of patients following surgery, but that the 30-day mortality rate was 21%.[152] Evaluation of the Asymptomatic Patient Undergoing Noncardiac Surgery In the asymptomatic patient with valvular aortic stenosis undergoing noncardiac surgery, echocardiography allows (1) assessment of disease severity, (2) monitoring of left ventricular function before, during, and after the procedure, and (3) alerting the clinician to the need for invasive mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 8 hemodynamic monitoring. Many of these patients, even with severe obstruction, can be managed without valve replacement if loading conditions are optimized preoperatively and careful invasive monitoring is continued in the postoperative period.[153] [154] Common postoperative complications include pulmonary edema or congestive heart failure associated with tachycardia that usually resolves quickly with rate control and diuresis. Similar considerations apply to the management of the pregnant patient with aortic valve disease (see Chapter 31) . Optimizing the Surgical Approach Once the decision has been made to proceed with relief of stenosis, the echocardiographic examination plays a key role in choosing the optimal surgical approach. Valve replacement remains the standard therapy for relief of valvular aortic stenosis. The optimal valve size and type typically are selected in the operating room based on direct measurement of the annulus by the surgeon. Echocardiographic prediction of prosthetic valve size has been only fair because of the limited number of valve sizes and the goal of implanting a larger valve when possible to improve hemodynamics. [155] For homograft valve replacements, an estimate of the optimal size is more important than for mechanical valves, so that the correct size will be available at the time of surgery.[156] For homograft aortic valves, diastolic left ventricular outflow tract diameter correlates best with implanted valve size. Note that the diastolic outflow tract diameter measurement averages 2 mm smaller than the systolic measurement (which is used in valve area calculations). A dilated aortic root commonly is seen as a result of poststenotic dilation and, in some cases, may be large enough to merit root replacement. In patients with a 494 small aortic annulus, an enlarging procedure may be considered or a specific valve chosen to avoid suboptimal hemodynamics postoperatively. Recognition of a subvalvular membrane, which can be mistaken for valvular stenosis on echocardiography, will alter the surgical approach and may allow resection of the membrane without valve replacement. Coexisting hypertrophic cardiomyopathy, although rare, is important to recognize to avoid postoperative dynamic subaortic obstruction. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 4 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Echocardiographic Evaluation after Valve Replacement for Aortic Stenosis Evaluation of the Valve Replacement Surgical procedures that preserve the native aortic valve have not yet been successful for treatment of valvular aortic stenosis,[157] nor has percutaneous balloon valvuloplasty shown long-term benefit in adult patients. |
[136] A mechanical or stented tissue prosthetic valve is most often implanted after removal of the stenotic valve leaflets. The fluid dynamics of prosthetic valves, evaluation of valve function, and other postoperative complications are discussed at length in Chapter 23 , Chapter 24 , and Chapter 25 . Newer surgical approaches to treatment of valvular aortic stenosis include the development of stentless tissue valves[158] [159] [160] [161] [162] [163] and the use of aortic valve homografts.[157] [164] [165] Both these valves types offer the advantages of improved hemodynamics compared with conventional valves, the absence of the need for chronic anticoagulation, and the hope of increased durability. Some centers also have reported success with the pulmonic valve autograft procedure in young adults, as well as adolescent patients.[166] [167] [168] In this procedure, the patient's stenotic aortic valve is replaced with his or her own native pulmonic valve. A homograft then is used in the pulmonic position. Potential advantages of this procedure include optimal hemodynamics and low thrombogenicity. In addition, tissue viability of the pulmonic autograft provides the possibility of tissue growth and repair, which are particularly important features in adolescent patients. In one series including patients up to age 35 years, event-free survival rate after the pulmonic autograft procedure was 90% at 7 years.[166] Events included reoperation for either aortic or pulmonic valve dysfunction, significant aortic regurgitation, and death. More recently, echocardiographic follow-up of 100 patients undergoing the pulmonic valve autograft procedure was reported.[169] The reintervention rate was 2% at a mean follow-up period of 33 months, with a range of 6 months to 7 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 4 years. A unique complication of the pulmonic autograft procedure is the development of homograft failure, either from stenosis or regurgitation. With homograft stenosis, patients typically develop progressive dyspnea approximately 3 to 6 months following surgery, at a time when continued physical recovery from the surgical procedure would be expected. Tissue from these failed explanted homografts show a prominent inflammatory cell infiltrate and therapy has thus focused on suppressing the heightened immune response with oral steroids. When a course of oral steroids fails to control the disease process, reoperation may be required. Since stentless tissue valve, homografts, and pulmonic autografts appear similar to a native aortic valve on echocardiographic examination,[160] [165] it is important that details about the surgical procedure be available at the time of the echocardiographic examination. Doppler findings for these valves also are similar to findings in native valves except that antegrade velocities may be slightly higher. Pulmonic autografts tend to have some degree of regurgitation early postoperatively, which typically decreases over the next several months, presumably due to collagen synthesis and increased structural stability of the valve in response to the increased mechanical stress on the valve leaflets. Other Hemodynamic Changes Postoperatively If left ventricular end-diastolic pressure has been chronically elevated preoperatively, as the ventricle remodels and filling pressures normalize, there may be a corresponding decrease in pulmonary artery pressures. If pulmonary pressures are elevated because of coexisting lung disease, little change is expected postoperatively. Moderate pulmonary hypertension (pulmonary artery pressures of 31 to 50 mm Hg) occurs in approximatly 50% of patients evaluated preoperatively with right heart catheterization.[170] However, the presence and magnitude of pulmonary hypertension do not appear to be related to the severity of aortic stenosis. It remains unclear whether preoperative pulmonary hypertension is related to postoperative survival, because studies have yielded conflicting results. [171] The effect of aortic valve replacement on coexisting mitral regurgitation remains controversial. In theory, mitral regurgitant severity should decrease given the "afterload reducing effect" of aortic valve replacement.[172] However, the magnitude of this effect may be small, particularly if there is anatomic abnormality of the mitral valve apparatus.[173] When significant mitral regurgitation accompanies severe aortic stenosis, it is prudent to consider a surgical intervention to reducing mitral regurgitant severity at mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 4 the time of aortic valve replacement. Intracavity gradients due to dynamic obstruction at the midventricular level are seen in one quarter to one half of aortic stenosis patients in the early postoperative period.[174] [175] The severity of obstruction varies from trivial to severe, and clinical evidence of hemodynamic compromise may be seen in some patients. Patients with small hypertrophied and hyperdynamic ventricles at baseline are more likely to have obstruction postoperatively. [176] Typically, obstruction is manifested as a late-peaking systolic velocity curve, which is similar to the pattern seen in hypertrophic obstructive cardiomyopathy. However, the level of obstruction is at the midventricular or papillary muscle level, rather than subaortic, and systolic anterior motion of the mitral valve is not seen. Obstruction is dynamic in that the presence and severity of obstruction varies from day to day (peaking at the third postoperative day) and in that obstruction can be provoked or increased 495 by maneuvers that decrease left ventricular preload or increase contractility. Echocardiographic recognition of midcavity ventricular obstruction in the postoperative period affects clinical management, since intravascular volume loading and avoidance of agents that increase contractility or reduce afterload can result in significant clinical improvement. The echocardiographic finding of dynamic obstruction after aortic valve replacement also has significant prognostic implications. Patients with obstruction have more frequent postoperative complications (hypotension, arrhythmias), a longer hospital stay, and a higher mortality rate than those without obstruction.[175] [176] [177] The Effect of Valve Replacement on the Left Ventricle When left ventricular systolic function is depressed because of valvular aortic stenosis, improvement is seen early in the postoperative period. Predictors of improvement in the ejection fraction include female gender and less severe coexisting coronary artery disease.[103] When measured by quantitative angiography, left ventricular mass and wall thickness decrease substantially in the postoperative period. By 10 months postoperatively, left ventricular mass has decreased by about 30% as compared with the preoperative left ventricular mass, with a further decrease in left ventricular mass observed at studies performed 8 years mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 4 postoperatively. Left ventricular mass may remain elevated in some patients, particularly if the prosthetic valve has suboptimal hemodynamics. Despite the apparent improvement in left ventricular geometry and systolic function seen in most patients, irreversible (or only very slowly reversible) changes in myocardial structure persist late postoperatively, with a relative increase in myocardial interstitial fibrosis as compared with normal and persistent diastolic dysfunction.[178] These myocardial changes, in combination with the mild pressure overload of the prosthetic valve, can result in persistent systolic overload at the myofibrillar level.[93] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/195.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Future Directions Echocardiographic evaluation of aortic stenosis is an established and effective clinical tool. However, to explain the relationship between hemodynamic severity and symptom onset, a flow-independent measure of stenosis severity still is needed. At this point, the most promising research approach to a flow-independent measure of stenosis severity is to determine the change in the degree of valve narrowing measured at two different volume flow rates rather than utilizing data obtained only at rest. Continuity equation valve area and the slope of the maximum velocity/maximum volume flow rate relationship both are potentially useful approaches to this problem. A plausible hypothesis is that early in the disease course of "degenerative" aortic stenosis, increases in volume flowrate result in increased opening of the valve leaflets. As leaflet stiffness increases, this increase in leaflet motion diminishes until, eventually, increases in left ventricular ejection force no longer result in increased leaflet motion. We propose that symptom onset correlates with a stiff and rigid valve that limits the patient's ability to increase cardiac output with exercise. Other investigators have proposed a similar approach measuring stenosis severity at different flow-rates using exercise or dobutamine.[50] [78] [87] Further studies are needed to assess the potential prognostic value of this approach. As studies using Doppler approaches provide additional insight into the natural history of this disease, these data will allow prediction of disease progression in individual patients. In addition, these data will allow sample size calculation and appropriate risk stratification for interventional trials. In the future, these techniques will be used as end points in clinical trials of interventions to prevent or delay progression of "degenerative" valvular aortic stenosis. MD Consult L.L.C. http://www.mdconsult.com mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company 501 Chapter 23 - Fluid Dynamics of Prosthetic Valves Ajit P. Yoganathan PhD Brandon R. Travis PhD Doppler echocardiography has made noninvasive examination of prosthetic heart valve function a clinical reality. Unfortunately, there are still many imperfections in echocardiographic examinations, including acoustic shadowing, reflections caused by implanted valves, and limitations in ultrasound technology. Despite these limitations, a number of important parameters can be calculated or estimated to aid in the assessment of prosthetic heart valve function and performance. Once a valve has been implanted, its function is governed primarily by its hemodynamic characteristics. In order to understand the hemodynamic performance of prosthetic heart valves, it is necessary to have a solid background in the physical laws that govern their function; therefore, the purpose of this chapter is to introduce cardiologists to the governing principles of fluid dynamics, relevant formulations used in prosthetic valve assessment, and fluid mechanical characteristics of specific prosthetic heart valves. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/198.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 8 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Fluid Dynamics With few exceptions, a material can be characterized as a fluid if it deforms continuously under the action of shear stress.[1] Shear stress is defined as a force per unit area applied tangentially to a surface. Viscosity is related to the amount of deformation that a fluid experiences when a shear stress is imposed on it. A constant viscosity fluid, called a Newtonian fluid, is one in which the relationship between viscous shear stress and strain rate is linear, as shown in Equation 1: where µ is the viscosity, usually defined in centipoise (grams/cm·s). The coefficient in this linear relationship is the dynamic viscosity. Equation 1 states the relationship between viscous shear stress (τ), viscosity (µ), and strain rate for flow in the x-direction with the derivative taken in the y- direction, perpendicular to the direction of flow. Blood behaves as a Newtonian fluid in regions of high strain rate. For flow in large arteries, 3.5 cp is often used as a viscosity estimate for blood.[2] Conservation of Mass Conservation of mass governs all materials, and it is the logical starting point for an introduction to fluid motion. Consider an imaginary volume, a control volume, enclosed by a surface through which fluid can flow, as shown in Figure 23-1 . It is not necessary for this control volume to coincide with any physical boundaries; it is purely a tool for the analysis of physical systems. Conservation of mass, or continuity, states that the change in mass within this control volume is equal to the mass of fluid that enters the volume, minus the mass that exits. [3] A very good assumption for cardiovascular applications is that 502 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 8 Figure |
23-1 Control volume for the conservation of mass. V1 and V2 are the inlet and outlet velocities flowing over areas A1 and A2 . ρ, fluid density. blood is incompressible, meaning its density does not vary. Assuming that there are only two surfaces across which fluid flows, surfaces 1 and 2, the velocities (v) and areas (A) can be related by conservation of mass, as shown in Equation 2. pρv1 (t)A1 = ρv2 (t)A2 (2) Conservation of Momentum The principle of conservation of momentum was initially formulated as Newton's second law of motion—mass times the acceleration of an object is equal to the sum of the forces acting on that object. For application to fluid mechanics, it is more convenient to define this in terms of the fluid momentum. The momentum of a fluid is a measure of the mechanical force it is able to transfer and is equal to the product of fluid mass and fluid velocity. A change in momentum of a fluid can only be accomplished by the application of a force. The general form of the principle of conservation of momentum for an incompressible Newtonian fluid is called the Navier- Stokes equations.[3] The forces that merit consideration within the cardiovascular system are pressure, gravity, viscous shear stresses, and turbulent stresses. Conservation of Energy Consider the conservation of energy statement, again using the control volume approach. The change in energy within a control volume is equal to the net rate of energy crossing the surface of the control volume plus the net rate of energy generated within the control volume. Energy loss occurs when the net rate of energy generated within the control volume is negative. In cardiovascular applications, energy loss usually occurs because the viscosity of the fluid converts its kinetic energy to heat. The general equation for energy conservation is difficult to apply to cardiac blood flow; however, with a number of simplifying assumptions a useful relation can be obtained. The Bernoulli equation,[4] as shown in Equation 3, is used mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 8 extensively in noninvasive cardiology: where p is the static pressure and v is the velocity, along the streamline, h is the vertical distance above some reference point, and s is the distance between points one and two along the streamline. This equation can be derived from either the conservation of energy or the conservation of momentum. Each term in Equation 3 has a physical definition that aids in comprehension and application of the Bernoulli equation. The left side of the equation represents the difference in pressure acting on the fluid between the positions one and two. The first term on the right side is called the inertial term and represents the change in fluid acceleration owing to temporal changes in the applied force. The second term on the right side is the kinetic energy associated with the fluid at each location. This term can also be considered the convective acceleration term, which is associated with a change in the velocity of a fluid as it travels from one location to another. The classic example of convective acceleration is the steady flow of fluid through a converging nozzle, such as a funnel. Because of continuity, the velocity is higher at the exit of the funnel than at the entrance, and acceleration occurs even though the flow is steady. The third term on the right side of the equation is the hydrostatic pressure difference, owing to the difference in elevation between the two points. The final term on the right side of the equation is the irreversible loss of mechanical energy or momentum owing to viscous effects. The limitations that arise when using Equation 3 are important to understand. Initially, Bernoulli's equation was derived for inviscid flow, in which there are no viscous effects. Because it is not physically possible to obtain such a flow, the term on the far right was added to account for losses caused by viscous effects. Equation 3 must also be applied between two points that lie along a streamline within a flow field. Streamlines are imaginary lines in a flow field to which the velocity vector is always parallel. In steady flow situations, streamlines can be traced by placing a particle or dye into the fluid and following their motion throughout the flow field. If the flow is unsteady, however, streamlines change from one time to another, and the particle paths no longer coincide with streamlines. Because of the difficulty in defining streamlines, rigorous application of Equation 3 is not possible in cardiovascular flows. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 8 Dimensionless Quantities The structures of cardiovascular flows are governed by chamber geometry and two dimensionless quantities. The first of these quantities, the Reynolds number, is defined as follows: where v is the velocity, µ is the viscosity, ρ is the fluid density, and d is a length representative of the flow regime 503 in question. For flow in a pipe, d is the pipe diameter, whereas for jet flows, it is the diameter of the orifice through which the jet exits. Physically, the Reynolds number represents the ratio of the fluid inertia to the viscous forces acting on a fluid. The other important dimensionless quantity in cardiovascular flows, the Womersley number (α), represents the ratio of the local acceleration a fluid experiences to the viscous forces acting on it. The Womersley number is defined as follows: where ω is the frequency (heart rate) and all other variables are the same for those used in the definition of the Reynolds number. These dimensionless numbers can be used to define a transition regime to turbulence common to all cardiovascular flows occurring in a similar geometry. Turbulence Consider a car traversing a winding road. As long as the car stays below a certain speed, the frictional force between its tires and the road enable the car to follow the path in which its front wheels are aligned. When the car surpasses a certain speed and passes around a large curve, however, the inertia of the car overcomes the frictional force holding the tires to the road. Similarly, flows with large inertia relative to the frictional, or viscous, forces acting on them become turbulent. Under these conditions, a small instability in the flow field (e.g., surface roughness within a pipe) can initiate fluctuations in fluid motion. When these fluctuations propagate to the point where fluid motion can only be described as random fluctuations about a mean velocity, the flow is said to be turbulent. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 8 In steady flows, the tendency of a flow to be turbulent is governed only by the Reynolds number and the chamber geometry. Two geometries that have been studied extensively and have direct applications to cardiovascular fluid mechanics are flow through a straight pipe and flow through a small, circular orifice. Flow through a straight pipe transitions to turbulence at Reynolds numbers of approximately 2000.[5] Flow through small, circular orifices create a phenomenon known as a free jet. For steady free jet flows, which are inherently more unstable than pipe flows, the critical Reynolds number is approximately 1000, with fully turbulent flow occurring at Reynolds numbers greater than 3000.[6] [7] In pulsatile flow, the transition to turbulence depends on the Womersley number and the shape of the flow waveform as well as the Reynolds number and chamber geometry.[8] [9] The critical Reynolds numbers for the transition to turbulence in pulsatile flow is much higher than the corresponding numbers in steady flow. Estimates of transition to turbulence in the ascending aorta by Yoganathan et al[4] (based on work by Nerem and Seed[10] ) indicated that the critical Reynolds number for transition is approximately 8000. It is also important to note that in pulsatile flow, turbulence may not be present during the entire cycle. Because flow acceleration is inherently more stable than flow deceleration, turbulence is more often observed during the deceleration phase of pulsatile flow. [9] Shear Stress Both viscous and turbulent shear stresses, if large enough, can potentially lyse or activate cells of the blood[11] [12] [13] [14] however, the origin, and consequently the scale, of viscous and turbulent shear stresses is different. Viscous shear stresses act on a molecular scale; they arise from the tendency of one molecule to remain near its neighbors. This tendency is quantified in fluids by their viscosity. Because viscous stresses act on a scale much smaller than the diameter of a blood cell, blood cells always experience a viscous shear stress if such a stress is present. In contrast, turbulent shear stresses arise from the inertia contained within the fluctuations of turbulent flow. Turbulent shear stresses act on a scale comparable to the length of the smallest turbulent fluctuations, often much larger than the diameter of a blood cell. Even if a turbulent shear stress is present, a blood cell may not experience this stress if the cell diameter is much smaller than the length scale of the smallest turbulent fluctuations. Boundary Layer Separation mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 8 Due to viscosity, when a flowing fluid contacts a solid body, because of viscosity, the fluid that is immediately adjacent to the body must be the same velocity as the body. For this reason, a boundary layer is formed. The boundary layer is a region in which the velocity changes from zero at the wall to that of the free stream value. Boundary layers are extremely thin but very important, for it is only in this region of the flow that viscous effects are significant. As a fluid moves downstream, viscous diffusion occurs and the viscous effects are felt farther from the wall, and the boundary layer grows. When a fluid flows over a solid body, it must change direction to pass around the body. A pressure gradient is required for this to occur. When an adverse pressure gradient (i.e., a pressure gradient against the flow direction, tending to decrease fluid velocity) is applied, if the magnitude of the pressure gradient is large enough, the fluid within the boundary layer reverses and boundary layer separation occurs. Downstream of the separation point, a region exists in which there may be reversed, turbulent, or disturbed flow. Recirculating or vortical flows are characteristic of this region; they can lead to high particle residence times and oscillatory shear stresses, both of which can have a wide variety of clinical implications, including atherosclerosis.[15] [16] In pulsatile flows, separation can be generated by a geometric adverse pressure gradient or by temporal changes in the driving pressure. Geometric adverse pressure gradients are present behind all prosthetic heart valves because of the small orifice area. As the area increases downstream of a prosthetic heart valve, the velocity decreases, in accordance with the continuity equation. The decrease in velocity is caused by an adverse pressure gradient. Because of the contractile nature of the heart, 504 the blood that flows through it also experiences both acceleration and deceleration during a cardiac cycle. It is during the deceleration phase of a particular flow, when an adverse pressure gradient is present, that boundary layer separation is most likely to occur. Thus, in regions in which there are both geometric and temporal adverse pressure gradients, separation is even more likely. Cavitation Cavitation is the formation of vaporous bubbles resulting from a sudden mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 8 drop in local pressure below the vapor pressure of the fluid. The abrupt closure of a mechanical prosthesis has been shown to induce cavitation in in vitro flow circuits,[17] [18] [19] and a few works have linked cavitation with mechanical valve closure in vivo as well.[20] , [21] The formation and subsequent collapse of cavitation bubbles releases a tremendous amount of energy within a very localized area; cavitation has been known to crack steel turbomachinery. Cavitation during the mechanical valve closure event is thought by some to be responsible for pitting on mechanical prosthesis surfaces[22] and the blood damage induced by mechanical prostheses.[18] The sharp drops in local pressure created by mechanical prosthesis closure lasts less than 2 ms,[18] [19] [20] [21] so the resulting cavitation bubbles collapse soon after they are created. Vaporous cavitation bubbles could act as nucleation sites, however, drawing in blood gasses such |
as nitrogen and carbon dioxide. The resulting gaseous emboli could last much longer than the cavitation event. Indeed, gaseous emboli have been detected in the circulation of patients with mechanical prostheses by transcranial Doppler. [23] Such emboli have been dubbed with the acronym HITS (high intensity transient signals). Pressure Recovery Consider steady flow of fluid through a pipe with a restrictive orifice placed downstream of the pipe entrance. Because of continuity, as the fluid enters the restriction, it accelerates. Assuming that the flow is streamlined when the particle enters the restriction, the velocity increases and the static pressure decreases, according to the Bernoulli equation. Once it exits the restriction and the cross-sectional area increases, the particle's velocity decreases and the pressure increases. The increase in pressure distal to a restrictive orifice is called pressure recovery. If there are no viscous energy losses, the pressure recovers to the value it had at the entrance to the restriction; however, viscous losses always occur, pressure does not recover completely, and irreversible mechanical energy losses occur.[3] Consider two similar steady flow situations. The first geometry is that of a Venturi flow meter, as shown in Figure 23-2 . The second case involves flow through an orifice meter, in which a restrictive orifice is placed in the center of a straight pipe (see Fig. 23-2A) . In the first case, because of the smooth contraction before the Venturi throat and the gradual area expansion downstream, there is no separation and very little energy loss. Most of mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 8 Figure 23-2 A, Orifice meter with pressure drop. B, Venturi meter with pressure drop. the velocity at the Venturi throat is converted back to pressure. For the same flow through the orifice meter, the velocity at the orifice would be approximately the same as the velocity at the Venturi throat. Because of the very rapid area contraction and expansion surrounding the orifice, however, a large separation region forms downstream and energy is lost. Pressure measurements at the location of the greatest contraction within each model would yield approximately the same value, which could lead one to believe that the energy losses in both models are identical. If the pressure is measured further downstream, however, it is evident that the Venturi meter has a much smaller energy consumption than the orifice meter, owing to downstream recovery of pressure. The same concepts may hold true for stenoses within the cardiovascular system. In the Venturi model, the peak velocity and the smallest pressure occur at or very near to the throat of the model, whereas in the orifice meter, because fluids cannot turn sharp corners, the peak velocity occurs slightly downstream of the orifice. The location at which this occurs is called the vena contracta because the area that the fluid passes through is less than the orifice area. Therefore, according to the Bernoulli and continuity equations, the maximum pressure drop across a prosthetic valve occurs at the location of the vena contracta and not at the valve orifice. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/199.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 6 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Application of Fluid Mechanics to Prosthetic Heart Valves Pressure Drop The pressure drop (∆P) across a prosthetic valve is related to the energy losses caused by its presence. Pressure 505 drops across natural valves can be measured with invasive catheter techniques; however, it is both difficult and dangerous to pass a catheter through a prosthetic valve. Fortunately, the Bernoulli equation can provide a noninvasive estimate of the pressure drop across prosthetic or natural valves. Neglecting the viscous effects and applying Equation 3 at mean conditions, so that the integral term vanishes, yields Equation 4: Point 1 is proximal to the valve and point 2 is at the orifice. If the velocity upstream of the valve is much smaller than at the valve, v1 can be neglected and Equation 5 is obtained: If the velocity is measured with continuous wave Doppler ultrasound (in meters per second), the pressure drop can be obtained from this equation in millimeters of mercury. When measuring pressure distal to prosthetic valves, it is important to note whether or not the recovered pressure is measured. It is especially important when using continuous wave Doppler ultrasound to evaluate prosthetic heart valves. Continuous wave Doppler ultrasound measures the highest velocity, which occurs at the vena contracta. Consequently, the Doppler-derived pressure drops are always based on the pressure at the vena contracta, before pressure recovery occurs. Thus, one is likely to mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 6 overestimate the transvalvular pressure drop because pressure recovery is not considered. Although Doppler ultrasound may overestimate transvalvular pressure drops, however, they are extremely useful in patient diagnosis. A study by Marcus et al[24] has shown that Doppler-derived pressure drops measured across small-diameter prosthetic mechanical valves (Medtronic-Hall and St. Jude) correlate just as strongly with fluid mechanical energy losses as the recovered pressure drops measured by catheterization. Pressure drop and recovery through prosthetic valves can be significant factors affecting the pressure within the left ventricle. A larger pressure drop across a prosthetic valve requires a larger systolic pressure in the left ventricle to drive flow through the circulation. Because it has been shown that left ventricular pressure is the primary determinant of myocardial oxygen consumption,[25] it is imperative that the pressure in the left ventricle is minimized when dealing with prosthetic valves. Numerous studies detailing the effects of recovery on pressure drop measurements for both natural and prosthetic heart valves have been published, and this topic continues to be an area of active research.[26] [27] [28] [29] [30] [31] [32] [33] [34] [35] Valve Area Cardiologists have used a variety of methods to determine the forward flow area of a valve. Because of acoustic anomalies caused by prosthetic valves and the limited spatial resolution of echocardiography, it is often impossible Figure 23-3 Control volume in the left ventricle for determining aortic valve area. V1 and V2 are the inlet and outlet velocities flowing over areas A1 and A2 . to measure the valve area directly. Applying a control volume analysis to a prosthetic valve in the aortic position (Fig. 23-3) and rewriting Equation 1, however, allows for estimation of the mean area over which fluid flows, as shown in Equation 6: The integral is taken with respect to time over the systolic flow period, v is 1 the velocity upstream of the aortic valve, and v2 is the velocity at the vena mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 6 contracta. A is the area of the vena contracta or the effective valve area and 2 A is the area at the upstream face of the control volume, measured by 1 echocardiography. Inherent to Equation 6 is the assumption that the spatial velocity profile is uniform over the entire orifice area; however, because the velocity profile is nonuniform in mechanical prostheses, it is difficult to apply Equation 6 accurately. By extending the control volume from the left ventricular outflow tract to encompass the entire left ventricle (Fig. 23-4) , it is possible to use this technique to determine the mean mitral valve area. The time-velocity integral of both the mitral and the left ventricular outflow tract positions must be calculated over the entire cardiac cycle. It is only necessary to integrate the velocity at the mitral valve during diastole and that of the aortic valve during systole, because these are the only times in which there is flow through the valves. If regurgitation is not present in either valve, Equation 6 can be applied and the effective area of the mitral valve can be obtained. When aortic regurgitation is present, the velocity and area at the light ventricular outflow tract can be used instead for calculation of effective mitral orifice area. Another method for determining valve area can be 506 Figure 23-4 Control volume in the left ventricle for determining mitral valve area. V1 and V2 are the inlet and outlet velocities flowing over areas A1 and A2 derived using the Bernoulli equation and conservation of mass. A contraction coefficient (Cd ) can be defined as the area of the vena contracta divided by the area of the valve orifice (Ao ).[3] The continuity equation for flow through an orifice, including the contraction coefficient, appears in Equation 7, where Q is the flow rate and v is the velocity at the vena contracta: Q = Ao vCd (7) Substituting Equation 5 into Equation 7 and solving for velocity yields an mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 6 equation that can be used to determine the effective orifice area of a cardiac valve: The constant was determined by using the density of blood (ρ = 1050 kg/m3 ) and converting the units to those convenient for biomedical use. The effective area will be square centimeters, if the root mean square systolic or diastolic flow rate (Q ) is in cubic centimeters and the mean rms systolic or diastolic pressure drop (∆P) is measured in millimeters of mercury. Another method that has been developed involves measuring the pressure half-time of an orifice to estimate the orifice area. The pressure half-time (P ) is the time required for left ventricular pressure to decrease to half of t/2 its peak value. An empiric relation between the pressure half-time and the area of the mitral valve (Amv ) has also been established. It was based on observations that changes in the mitral pressure drop with time were constant for a particular orifice area[36] [37] The constant 220 was empirically determined,[38] but this equation has been shown to be dependent on a number of factors other than the valve area, including the severity of aortic regurgitation and ventricular wall properties. This equation is ineffective for prosthetic heart valves, limiting its application.[39] [40] Regurgitant Flow Rate Because mechanical prosthetic valves are fairly rigid, they are unable to form tight seals when closed. Consequently, regurgitant jets are present in prosthetic valves under normal conditions, although the amount of regurgitation is usually small. Normal regurgitant flow is characterized by a closing volume during valve closure and leakage after closure (see Figure 23-11) . Regurgitant flow is often characterized by the regurgitant volume. The regurgitant volume is the total volume of fluid through the valve per beat owing to the retrograde flow. It is equal to the sum of the closing volume and the leakage volume. The closing volume is the volume of fluid flowing retrograde through the valve during valve closure. Any fluid volume accumulation after valve closure is caused by leakage and is mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 6 referred to as the leakage volume. These quantities are dependent on valve size, increasing with increasing valve diameter. Typically, the regurgitant volume is higher for mechanical valves than for bioprosthetic valves; however, prosthetic valves can exhibit substantial regurgitation when they malfunction. To distinguish normal from abnormal valve function, it is important to differentiate between normal regurgitant volume and additional regurgitation owing to disease. Fluid mechanical analysis of this problem has provided two different techniques that at least partially fulfill this requirement. Turbulent Jet Theory Using free turbulent jet theory, Cape et al[41] [42] [43] (and later Sugawara et al [44] ) were able to derive relations for the regurgitant flow rate based solely on Doppler ultrasound measurements. Turbulent jets have a number of unique characteristics. Upon entering a chamber they spread radially, pulling or entraining stationary fluid with them. Initially, though, the jet has a core of fluid that is not affected by the stationary fluid. This potential core has the same velocity as the jet at the orifice and persists for a few orifice diameters downstream, as shown in Figure 23-5 . Once the core vanishes, the jet reaches a state that is amenable to theoretical analysis. It is important to recognize, however, |
the assumptions inherent in this theoretical analysis. Unsteady flow effects are neglected, and the analysis assumes that the jet enters a stationary fluid and does not impinge on solid boundaries. In the heart, regurgitant jets are unsteady, often impinge on the walls of the heart, and always encounter incoming forward flow. Additional work has been performed that treats jets in confined and impinging geometries; these geometries more closely resemble the chambers of the left heart. Burleson et al [45] [46] constructed a dimensional analysis model of valvular regurgitation based on the center line velocity decay of the jet and the width and length of the receiving chamber. Their equation has been shown to 507 Figure 23-5 Free jet center line velocity decay showing jet velocity (v) plotted versus distance (x). be accurate for a number of in vitro geometries and conditions.[45] [47] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 6 Proximal Flow Convergence The principle of conservation of mass was also applied in the region proximal to the valvular orifice to measure regurgitant volume.[48] [49] [50] [51] When fluid enters a regurgitant orifice it must accelerate to reach a peak velocity at the throat of the orifice. If the orifice is circular, this acceleration region should be axisymmetric about the center of the orifice. Thus, upstream of the regurgitant orifice, a series of concentric isovelocity contours hemispherical in shape can be defined within the flow field. This physical argument is the basis for the proximal flow convergence method of quantifying regurgitant flow rate. If a control volume is constructed to coincide with a hemispherical contour and the regurgitant orifice, as shown in Figure 23-6 , the same amount of fluid that enters the volume from an isovelocity contour exits the control volume through the regurgitant orifice. The control volume statement is represented mathematically in Equation 9. Q = (2πr2 )V (9) o r The term within parentheses is the surface area of the hemispherical control surface. Vr is the velocity measured with color Doppler echocardiography and r is the distance at which the velocity is measured. Q is the flow rate at o the regurgitant orifice. Because of its simplicity and ease of application, this technique has received a great deal of attention, especially for mitral regurgitation. The effects of regurgitant orifice motion,[52] orifice geometry variation,[53] [54] [55] [56] and ultrasound machine settings[53] have all been addressed with both in vitro and in vivo investigations. In addition, its application to prosthetic valve regurgitation has also been considered.[57] Studies in our laboratory have found that isovelocity contours from regurgitant orifices can be described better by a hemielliptical shape than by a hemispherical shape, yielding more accurate estimations of regurgitant flow rate in vitro.[58] [59] Unfortunately, rigorous in vivo validation of the proximal flow convergence technique is difficult. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/200.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Hemodynamic Characteristics of Native Valves In order to effectively analyze flow through prosthetic heart valves in the mitral or aortic positions, it is important to understand the conditions under which natural valves function. Figure 23-7 illustrates typical pressure and flow waveforms for healthy individuals at both the aortic and the mitral valves. During systole, the pressure difference required to drive the blood through the aortic valve is on the order of a few millimeters of mercury. Diastolic pressure differences across the aortic valve are much larger than systolic, the pressure usually being about 80 mm Hg. The valve closes near the end of the deceleration phase of systole with very little reverse flow. The blood flow through the mitral valve is biphasic during diastole, as shown in Figure 23-4 . The first peak, the E wave, is due to ventricular relaxation, whereas the second peak, the A wave, is caused by contraction of the left atrium; therefore, all valves in the mitral position open and close twice during each cardiac cycle. It is also evident that all cardiac valves are closed during both isovolumic contraction and isovolumic relaxation. Measurements of the velocity profile just distal to the aortic valve have been performed with Doppler echocardiography in normal subjects.[60] The peak systolic velocity is Q = (2πr2 )V . (12) o r Figure 23-6 Proximal isovelocity surface area schematic. Vr is the velocity on a hemispheric shell defined by the radius (r) with surface area A1 . A2 is the regurgitant orifice area and Vo is the peak regurgitant jet velocity. 508 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 Figure 23-7 Pressure and flow waveforms for the left heart. 1.35 ± 0.35 m per second and the velocity profile at the level of the aortic valve annulus is relatively flat; however, there is usually a slight skew toward the septal wall (<10% of the center line velocity) caused by the orientation of the aortic valve relative to the long axis of the left ventricle. This skew in the velocity profile has been shown by many experimental techniques, including hot film anemometry,[61] [62] Doppler ultrasound,[60] and magnetic resonance imaging.[63] The flow patterns distal to the aortic valve also play an important role in proper valve function. During systole, vortices form behind each leaflet in the sinus region. In vitro studies have attempted to relate these vortices to effective valve closure.[64] [65] It has been shown that the ventricular vortices are unnecessary for valve closure; however, they do ensure that the valve closes quickly, reducing leakage.[66] The velocity profile at the mitral valve has been determined in detail in pigs and should be comparable to the velocity profile in humans because of the similarity in cardiac anatomy.[67] Again there is a slight skew to the profile, but there does not seem to be a preferred orientation. It is dependent on the particular geometry of the mitral valve, the diastolic flow patterns within the left ventricle and the location at which the pulsed Doppler sample volume is placed.[67] When the sample volume was placed at the mitral annulus, the peak early diastolic velocity was 63.6 ± 16.1 cm per second, whereas the late diastolic peak velocity was 53.7 ± 10.8 cm per second.[67] When the sample volume was at the tip of the mitral valve leaflets, the peak early diastolic velocity was 82.9 ± 30.8 cm per second and the peak late diastolic velocity was 39.6 ± 14.2 cm per second. Vortices develop in the left ventricle during diastole as blood enters through the mitral valve. Bellhouse[68] proposed that the vortices helped to close the mitral valve at the end of diastole. Later work has shown that the vortices play a role in early closing of the mitral valve, but late closure is dominated by left ventricular pressure.[69] Because of the restrictive area of prosthetic valves, the peak velocities are usually higher, and the spatial velocity profiles are dramatically different from those in natural valves. The shear stresses in prosthetic valves also are mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 much larger because of the higher velocities and turbulence. The magnitude of the shear stress varies greatly depending on the type of prosthetic valves. It is important to note the differences and similarities between valve types in terms of shear stress magnitudes, peak velocities, and flow patterns so that an effective assessment of prosthetic valve function can be performed. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/201.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 27 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Fluid Mechanics of Specific Prosthetic Valve Designs Prosthetic heart valves have been successfully used in heart valve replacement over the past 40 years. Currently, heart valve prostheses can be classified into two primary categories, mechanical and biologic. Mechanical valves in current clinical use are composed of three basic designs or classifications: ball-and-cage, tilting disc, and bileaflet. The biologic valves can be further classified into three categories: stented, unstented, and homograft valves. Although significant progress has been made in the development of better prostheses through new materials and more physiologic valve designs, several problems associated with prosthetic valves have not been eliminated. Existing problems that can be related to the valve hemodynamics or local fluid mechanics are (1) thrombosis and thromboembolism, (2) hemolysis, (3) tissue overgrowth, (4) damage to endothelial lining, and (5) regurgitation. The presence of high shear stresses can lead to damage of formed blood elements, platelet activation, and initiation of biochemical processes affecting coagulation. Lethal damage to red cells can occur with fluid shear stresses as low as 1500 dyn/cm2 .[11] These levels can be significantly lower (10 to 100 dyn/cm2 ) in the presence of foreign surfaces, such as those presented by a valve prosthesis.[12] [13] Sublethal damage can occur in stress fields as low as 500 dyn/cm2 .[14] In addition, platelet activation and damage have been shown to occur in shear stresses ranging from 100 to 500 dyn/cm2 .[70] The residence time of the cell in the damaging fluid environment is a significant factor in determining lethal stress levels that further complicates the mechanism for damage. Additionally, regions of flow separation and stagnation form local environments suitable for accumulation and growth of thrombi and fibrous or pannus tissue.[71] The fluid mechanic performance of prosthetic heart valves is often assessed mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 27 through in vitro testing to determine transvalvular pressure drops, regurgitant volumes (closure and leakage), distal and proximal velocity fields, 509 and the locations and levels of turbulent stresses. The relationship between valve fluid mechanics and the development of problematic function have been studied by numerous investigators over the past two decades. In vitro studies have concentrated on quantifying local fluid stress levels through state-of-the-art flow measurement techniques such as laser Doppler anemometry,[72] [73] [74] [75] [76] [77] [78] [79] [80] [81] [82] [83] [84] [85] [86] [87] [88] [89] [90] [91] hot film anemometry,[92] [93] [94] and ultrasound velocimetry.[95] The fluid mechanics of the various prosthetic valve designs are discussed in this section. Comparisons between the many valve designs within each classification of prostheses are left to the many references dealing with the assessment of individual valves. Antegrade and retrograde flow fields are described, including turbulence levels, regurgitation, and pressure drop characteristics for the different valve designs. All flow characteristics are referenced from in vitro experiments conducted in our laboratory unless otherwise specified. In most citations, the data are representative of 25- or 27-mm aortic prostheses tested under physiologic pulsatile flow conditions providing a cardiac output (CO) of 5.0 to 6.0 L per minute and a heart rate (HR) of 70 bpm. Exact test conditions (valve size, CO, HR, pressures) are noted for each citation. The measurement of pressure drop is intrinsically related to the distal flow fields of valves. The effect of pressure recovery depends strongly on flow structure and the vessel geometry in which the flow is entering. Stewart et al[29] have assessed the differences in determining transvalvular pressure drops across aortic valves owing to pressure recovery effects, when using standard in vivo techniques such as Doppler ultrasound or cardiac catheterization. Doppler-measured pressure drops are not equal to catheter- measured drops, unless the catheter is placed at the same location where the peak velocity is measured by Doppler, typically the vena contracta of the jet. Pressure recovery is very dependent on valve type, size, orientation, and position (i.e., aortic or mitral), and it is particularly likely with mechanical valves, which exhibit complex jet flow patterns with more than one jet, and in smaller aortic valves at higher flow |
rates. In general, the Doppler technique measured higher pressure drops in mechanical aortic valves, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 27 especially in the larger sizes, than did the catheterization technique. In addition, some valve designs such as the Medtronic Freestyle unstented bioprosthesis and larger size bileaflet and tilting disc mechanical valves require that the upstream approach velocity (i.e., the term v in Equation 4) 1 be measured and used in the modified Bernoulli equation, owing to small pressure drops. When pressure drops are expected to be small, neglecting the approach velocity in the calculations can lead to significant overestimation in the pressure drop. Clinicians should be aware of these effects when interpreting pressure drop data in diagnostic exams. Mechanical Valves The three major mechanical valve designs or classes are the tilting disc, bileaflet, and ball-and-cage. These valves differ primarily in the type and function of the occluder. Although these different designs influence the valvular Figure 23-8 Schematic showing the geometry of commonly used mechanical valve prostheses. fluid mechanics, all three share common flow structures such as well- defined jet flows, wakes with some degree of flow reversal, and turbulent shear layers. The antegrade flow, regurgitant flow, and pressure drop characteristics for each valve design are discussed separately in the following sections. Because the design of a valve can strongly influence the local fluid dynamics, a brief discussion of the pertinent design features of each class of valve is provided. Figure 23-8 illustrates the design features of the three classes of mechanical valve prostheses. Tilting Disc Valves The tilting disc valve has one occluder (disc) generally of a circular cross section. The disc is often mounted such that it is free to rotate about a pivot axis, typically displaced from the disc diameter. Metal struts are used to secure the disc within the valve housing and control its range of motion. Numerous design variations on the tilting disc valve exist. These different designs vary in the pivot mechanism or strut design, the range of disc motion allowed, or in the geometry of the disc, which can range from flat to curved. Typically, the occluder opens to angles between 60 and 80 degrees with respect to the valve annulus. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 27 The tilting disc valve is characterized by two orifices separated by the occluder. The major orifice is the larger open area formed between the disc pivot axis and the housing, as the disc swings distally to the open position. This orifice is free of blockage owing to mounting struts and causes little resistance to transvalvular flow. As the disc opens, the remaining part of the disc, on the other side of the pivot axis, swings in the proximal direction to form the minor orifice. Mounting struts, which can vary from one to two depending on valve design, typically span the minor orifice. Because of the upstream protrusion of the disc into the minor orifice tract and the presence of the mounting struts, a slight obstruction of flow is encountered. Antegrade Flow. Figure 23-9 and Figure 23-10 illustrate the antegrade flow patterns of the Björk-Shiley monostrut and Medtronic-Hall tilting disc valves. The antegrade flow is characterized by a major orifice jet and a minor orifice jet. The major orifice jet is spatially larger than the minor orifice jet. It is semicircular in cross section with 510 Figure 23-9 Velocity and turbulent shear stress profiles downstream of a 27-mm Björk-Shiley monostrut tilting disc valve at peak systole. A and C, Profile through the major and minor orifices at 11 mm downstream. B and D, Center line profile 17 mm downstream across the major and minor orifices (major orifice to the right). peak systolic velocities of approximately 2 m per second in the aortic position. Under comparable flow conditions, most tilting disc valves exhibit similar major orifice jet structures and peak velocity magnitudes. The spatial structure of the minor jet varies depending on the number of struts used to secure the disc. In single-strut designs such as the Björk- Shiley monostrut and the Medtronic-Hall tilting disc, the minor orifice jet appears as two jets separated by a well-defined wake behind the strut. The flow on each side of the strut is nearly symmetric with similar spatial structure and velocity magnitude. Valves with two struts display a minor orifice jet structure consisting of a strong central jet bounded by two weaker jets. The adjacent weaker jets are separated from the central jets by the wakes of the struts. Their velocity magnitude is roughly 30% to 40% of the velocity magnitude of the central jet. The peak velocities of the minor orifice jet are typically of the same magnitude or slightly less than the peak mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 27 velocity in the major orifice jet in nearly all tilting disc designs. Wake regions are observed behind the valve struts and disc. These wake regions are areas of flow separation with significant velocity defect and nearly stagnant flow. Wake regions persist for 10 to 20 mm downstream of the valve annulus. Owing to the opening angle of the disc, the major and minor orifice jets are directed toward the wall on the major orifice side of the valve, following the occluder. In the aortic position, this results in a region of separated flow in the sinuses located below or near the minor jet at peak systole. Because of the strong major orifice jet and the orientation of the disc with respect to the flow, strong secondary flow structures are encountered downstream of the valve. These secondary flows form a pair of counter-rotating vortices or helical motions. The vortices are generated by the high-momentum fluid in the major jet wrapping around the sides of the disc and flowing into the low-momentum, separated flow regions immediately behind the disc. Flow over the disc generates vortex shedding similar to that observed with flow over a delta wing airfoil. Turbulent stresses associated with the titling disc design are located in the jet shear layers and in the wakes of the discs and struts. The turbulent shear stress profiles for the monostrut and Medtronic-Hall valves are shown in Figure 23-9 511 Figure 23-10 Velocity and turbulent shear stress profiles downstream of a 27-mm Medtronic-Hall tilting disc valve at peak systole. A and C, Center line profile 15 mm downstream across the major and minor orifices (major orifice to the right). B and D, Profile through the major and minor orifices at 13 mm downstream. and Figure 23-10 . Peak turbulent shear stresses, in the aortic position, can range from 1500 to 3500 dyn/cm2 depending on the particular tilting disc design. These stress levels were measured 10 to 15 mm downstream of the valve housing and may be even higher closer to the valve. Large stresses persist almost into the aorta, indicating that a significant volume of the fluid is occupied by the turbulent shear layers, which may be relevant in that sufficiently long residence times may exist for formed blood elements exposed to turbulent stresses. Table 23-1 summarizes the peak velocity and turbulent shear stress levels for many of the 27-mm aortic valves in clinical use. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 27 Normal Regurgitant Flow. The tilting disc design shows slightly lower regurgitant volumes than the bileaflet design, owing to reduced closing and leakage volumes (Fig. 23- 11) . Ranges for the regurgitant volume of the tilting disc valve vary from approximately 5.5 mL per beat for 19- and 20-mm valves to 9 mL per beat for 29-mm valves. Table 23-2 and Table 23-3 list the regurgitant volumes for several prosthetic valve designs. The leakage flow in mechanical valves is often in the form of small-scale regurgitant jets. In the tilting disc design these jets emanate from small gaps around the perimeter of the valve between the disc and the valve housing. [76] [96] , [97] Baldwin et al[96] measured the gap width of a Björk-Shiley monostrut valve with Delrin rings and obtained widths of approximately 75 µm, which varied nonuniformly around the valve perimeter. These leakage jets were believed to be advantageous because of the potential for washing of the perimeter of the valve housing 512 TABLE 23-1 -- Peak Systolic Velocity and Turbulent Shear Stress Levels for Common 27-mm Aortic Valve Prostheses † Peak Turbulent Peak Shear Measurement Velocity Stress Valve Type Valve Location (cm/s) (dyn/cm2 ) Ball-and-cage Starr-Edwards 1260 12 mm 220 1850 downstream Tilting disc Björk-Shiley 7 mm 200 3400 convexo-concave downstream 11 mm 200 1800 downstream Björk-Shiley 8 mm 200 1250 Monostrut downstream 11 mm 200 800 downstream Medtronic-Hall 13 mm 200 1500 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 27 downstream Omnicarbon 14 mm 225 2000 downstream Bileaflet St. Jude Medical 13 mm 210 1500 Standard downstream Duramedics 13 mm 210 2300 downstream Carbomedics 12 mm 228 1520 downstream Stented Carpentier-Edwards 15 mm 370 4500 bioprostheses Porcine 2625 downstream Carpentier-Edwards 15 mm 200 2000 Porcine 2650 downstream Carpentier-Edwards 17 mm 180 1000 Pericardial 2900 downstream Hancock MO Porcine 10 mm 330 2900 250 downstream Hancock II Porcine 18 mm 260 2500 410 downstream Ionescu-Shiley 27 mm 230 2500 Standard Pericardial downstream Hancock Pericardial 18 mm 170 2100 downstream Nonstented Medtronic Freestyle * Leaflet tips 125 bioprostheses 10 mm from 100 tips St. Jude Medical Leaflet tips 150 TSPV * 10 mm from 125 tips †Data obtained at 5 L/min CO, 70 bpm HR, and 120/80 mm Hg aortic pressure. *Data obtained from in vitro Doppler ultrasound measurements. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 27 during closure. Other studies have shown that the regurgitant jets are of a significant velocity magnitude, ranging from 2 to 5 m per second, and turbulent stresses are several times greater than in the antegrade flow field. Measurements in the regurgitant jets of the Björk-Shiley valve indicate that peak turbulent shear stresses are as high as 10,000 dyn/cm2 .[96] Turbulent scales in these jets are estimated to be of the same order of magnitude as the size of red cells and may result in higher rates of hemolysis than in the antegrade turbulent fields. Pressure Drop Characteristics. To minimize the workload on the heart, a prosthetic valve should not impose resistance to forward flow. In general, prosthetic Figure 23-11 Regurgitant, closing, and leakage volumes of a valve in the aortic position. valves impose more forward flow resistance than do natural valves. Prosthetic valves are often characterized by their pressure drop or through their effective orifice areas (Equation 8), which can be used to estimate the resistance a valve imposes on forward flow across it. The effective orifice area (Aeff ) is an index of how well a valve design uses its primary or internal orifice area. Another measure of a valve's resistance to forward flow is the performance index (PI), the ratio of A to the valve sewing ring eff area. The PI provides a measure of how well a valve design uses its total mounting area, the area the flow would see without the valve. Although the Aeff is a function of the valve size, the PI attempts to normalize for valve size, providing a more uniform measure of a valve's resistance characteristics independent of the size and nearly independent of the flow rate. The tilting disc design presents a relatively streamlined configuration to the flow and thus shows relatively low gradients. Tilting disc valves typically show a PI ranging from 0.4 to 0.65. A and PI for several prosthetic valve eff designs in clinical use today are provided in Table 23-2 and Table 23-3 . Orientation. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 27 The orientation of the tilting disc valve in the mitral position has been studied in vivo by Jones et al.[98] These authors made comparisons of the orientations of the major orifice jet of tilting disc valves with respect to the left ventricular geometry. The studies indicated that the preferred orientation for tilting disc valves in the mitral position is with the major orifice oriented toward the left ventricular free wall, as opposed to the septum. Greater intraventricular turbulence was observed with a septal orientation of the major orifice than with a free wall orientation. Orientation of the major orifice toward the septal wall produced large areas of velocity reversal, |
directed against the minor orifice. In contrast, 513 TABLE 23-2 -- In Vitro Hemodynamic Data for Common Aortic Valve Prostheses * Regurgitant EOA Size Volume † Valve Type Valve (mm) (mL/beat) (cm2 ) PI Ball-and-cage Starr-Edwards 1260 27 5.5 1.75 0.30 25 4.3 1.62 0.33 21 2.5 1.23 0.36 Tilting disc Björk-Shiley convexo- 27 8.5 2.59 0.45 concave 25 7.3 2.37 0.48 21 5.5 1.54 0.45 Björk-Shiley Monostrut 27 9.2 3.34 0.58 25 7.6 2.62 0.53 23 6.9 2.00 0.48 21 5.9 1.45 0.42 19 5.5 1.07 0.38 Medtronic-Hall 27 9.6 3.64 0.64 25 8.4 3.07 0.62 23 7.3 2.26 0.54 20 6.2 1.74 0.51 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 27 Bileaflet St. Jude Medical 27 10.8 4.09 0.71 Standard 25 9.9 3.23 0.66 23 8.3 2.24 0.54 21 6.8 1.81 0.52 19 6.8 1.21 0.43 St. Jude Medical 29 13.5 4.98 0.75 Regent 27 12.3 4.40 0.77 25 11.2 3.97 0.81 23 10.3 3.47 0.83 21 9.0 2.81 0.81 19 7.6 2.06 0.73 17 6.3 1.56 0.69 Carbomedics 27 7.5 3.75 0.65 25 6.1 3.14 0.64 23 6.5 2.28 0.55 21 3.4 1.66 0.48 19 3.0 1.12 0.40 Sorin Bicarbon ‡ 27 3.06 0.71 25 2.39 0.69 23 2.07 0.73 21 1.54 0.67 19 0.97 0.55 Stented Carpentier-Edwards 27 <3 1.95 0.34 bioprostheses Porcine 2625 25 <2 1.52 0.31 21 <2 1.28 0.37 Carpentier-Edwards 27 <2 2.74 0.48 Porcine 2650 25 <2 2.36 0.48 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 27 21 <2 1.38 0.40 19 <2 1.17 0.41 Carpentier-Edwards 27 <3 3.70 0.64 Pericardial 2900 25 <2 3.25 0.66 21 <2 1.88 0.54 19 <2 1.56 0.55 Hancock Porcine 242 27 <3 2.14 0.37 25 <2 1.93 0.39 23 <2 1.73 0.42 21 <2 1.31 0.38 19 <2 1.15 0.41 Hancock MO Porcine 25 <2 2.16 0.44 250 23 <2 1.94 0.47 21 <2 1.43 0.41 19 <2 1.22 0.43 Hancock II Porcine 410 27 <2 2.36 0.41 25 <2 2.10 0.43 23 <2 1.81 0.44 21 <2 1.48 0.43 Ionescu-Shiley 27 <3 2.35 0.41 Standard Pericardial Mosaic Porcine 29 <3 3.15 0.48 27 <2 2.81 0.49 25 <2 2.11 0.43 23 <2 1.74 0.42 21 <1 1.54 0.44 Mitroflow Pericardial 29 <4 3.71 0.56 23 <3 2.12 0.51 19 <2 1.34 0.47 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 12 di 27 Nonstented Medtronic Freestyle 27 <4 3.75 0.65 bioprostheses Porcine 25 <4 3.41 0.69 23 <3 2.69 0.65 21 <2 2.17 0.63 19 <2 1.84 0.65 EOA, effective orifice area; PI, performance index. *5 L/min CO typical, 70 bmp HR, 120/80 mm Hg aortic pressure. †EOA Computed from Equation 8. ‡Values from Badano L, Mocchegiani R, Bertoli G, et al: J Am Soc Echocardiogr 1997; 10:632–643. 514 TABLE 23-3 -- In Vitro Hemodynamic Data for Common Mitral Valve Prostheses * Regurgitant EOA Size Volume † Valve Type Valve (mm) (mL/beat) (cm2 ) PI Ball-and-cage Starr-Edwards 1260 30 1.99 0.28 28 1.66 0.27 26 1.56 0.29 Tilting disc Björk-Shiley Standard 31 3.40 0.45 29 6.7 2.79 0.42 25 2.15 0.44 Björk-Shiley convexo- 29 10.1 2.96 0.45 concave 27 8.3 2.28 0.40 25 2.03 0.41 Medtronic-Hall 31 10.0 3.53 0.47 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 13 di 27 29 10.0 3.53 0.53 27 8.9 2.73 0.47 25 7.2 2.23 0.45 Bileaflet St. Jude Medical 31 13.1 3.67 0.48 Standard 29 10.9 3.40 0.51 27 9.7 2.81 0.49 Stented Hancock Porcine 342 35 <4 2.72 0.28 bioprostheses 33 <4 2.54 0.30 31 <4 2.36 0.31 29 <4 2.11 0.32 27 <2 1.77 0.31 25 <2 1.63 0.33 Hancock II Porcine 33 <4 2.66 0.31 31 <3 2.29 0.30 29 <3 2.05 0.31 27 <2 1.78 0.31 25 <2 1.59 0.32 Carpentier-Edwards 27 <2 2.03 0.35 Porcine 6650 Carpentier-Edwards 27 <2 2.68 0.47 Porcine 6900 Carpentier-Edwards 31 <4 2.58 0.39 Porcine 6625 Ionescu-Shiley Standard 31 <5 3.00 0.40 Pericardial 27 <2 1.77 0.31 25 <2 1.61 0.33 Mosaic Porcine 33 <4 2.38 0.28 31 <3 2.26 0.30 29 <3 2.02 0.31 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 14 di 27 27 <2 1.71 0.30 25 <2 1.55 0.32 Nonstented Mitral Valve Allograft ‡ 25 3.38 0.69 bioprostheses 23 1.80 0.43 EOA, effective orifice area; PI, performance index. *5 L/min CO typical, 70 bpm HR. †EOA computed from Equation 8. ‡In vitro measurements at 5 L/min CO. free wall orientation of the major orifice produced more physiologic left ventricular flow patterns. These results have been corroborated in in vitro flow visualization studies conducted in our laboratory, under physiologic flow conditions in an anatomically correct left ventricular model.[99] Studies by Travis et al[100] and Kleine et al[101] have examined the effects of valve orientation on forward flow hemodynamics through mechanical prostheses in the aortic position. Travis et al studied the effects of valve orientation on fluid mechanical energy loss and transvalvular pressure drop in angled in vitro models of the aortic inflow tract. Their study showed that orientation of the disc so that it is parallel to the proximal flow direction when the valve is in the open position minimizes energy loss and pressure drop for the tilting disc valve. Kleine et al used an in vivo pig model to examine the effects of prosthesis orientation on turbulent stresses. These researchers found a minimum in turbulent stress magnitude with orientation of the major orifice to the right posterior aortic wall, which is the area of highest velocities during ejection. Bileaflet Valves The bileaflet design is characterized by two semicircular leaflets typically made of pyrolytic carbon that are hinged to the valve housing. The leaflets divide the flow into three regions, two lateral orifices and a central orifice. The primary differences between the many bileaflet valves are in the hinge design, the leaflet opening angle, and curvature of the leaflets. Hinge design variations are employed to control opening angle and influence the local fluid mechanics, washout, and flow patterns generated in the hinge, which may affect leaflet function and pressure mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 15 di 27 515 drop. Leaflet opening angles vary from 75 to 90 degrees in the bileaflet designs in current clinical use. The bileaflet valves tend to show better bulk flow hemodynamics than the tilting disc or ball-and-cage designs. The characteristic geometry of the bileaflet design is illustrated in Figure 23-8 . Antegrade Flow. The antegrade flow fields of bileaflet designs are characterized by three jets. Two jets emanate from the lateral orifices and one from the central orifice, as illustrated in Figure 23-12 . All three jets tend to show similar peak velocity magnitudes, independent of valve design. Greater forward flow emerges from the lateral orifices, however, than from the central orifice. The cross section of the lateral jets tends to be of a crescent shape, whereas the central jet is nearly planar in cross section. Wakes generated from the leaflets separate the three jets and persist for several centimeters downstream. The triple jet pattern is also discernible in two-dimensional color flow maps, using color Doppler ultrasound techniques as Figure 23-12 Velocity and turbulent shear stress profiles 13 mm downstream of a 27-mm St. Jude Medical bileaflet valve at peak systole. A and C, Center line profile through lateral and central orifices. B and D, Profile through the central orifice only. illustrated in Figure 23-13 . This color Doppler flow map was obtained in pulsatile flow in vitro studies of a 31-mm St. Jude Medical bileaflet valve in the mitral position. The central jet loses its coherence after 2 or 3 cm as the lateral jets grow and merge into the central flow region. The lateral jets do maintain their coherence and relatively high velocity magnitude over a greater distance. The flow is initially well ordered during the early acceleration phase and becomes turbulent before peak systole. Separated regions with flow reversal are generally observed around the perimeter of the housing. The separated regions tend to be asymmetric around the valve with larger spatial dimensions near the hinges than adjacent to the lateral jets. This asymmetric behavior may be related to the increased thrombogenecity of the bileaflet design that occurs in the hinge regions. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 16 di 27 Turbulent stresses are concentrated in the leaflet wakes and in the shear layers alongside the three jets. The bileaflet design exhibits lower turbulent stresses than the 516 Figure 23-13 (color plate.) Two-dimensional color Doppler flow mapping of the downstream triple jet flow fields of a bileaflet valve design under physiologic pulsatile flow conditions. tilting disc and ball-and-cage designs, with peak aortic values ranging from 1000 to 1500 dyn/cm.2 Peak stresses in the mitral position are less because of the lower peak diastolic transvalvular velocities. Three-component turbulent stress measurements have shown that the turbulent stress distribution is similar to that of local two-dimensional jets and wakes.[102] The onset of turbulence can be related to a Reynolds number based on the local flow properties of the jets and wakes and not on a Reynolds number based on global geometry, such as the size of the annulus or the diameter of the aorta. Understanding this turbulence structure may also provide potential leaflet design changes to minimize stress levels. As a result of this similarity with jet and wake structures, computational techniques may be able to use low Reynolds number turbulence models developed for jet and wakes. Peak aortic velocity and turbulent stress levels for clinically used 27-mm bileaflet valves are provided in Table 23-1 . Normal Regurgitant Flow. Retrograde flow characteristics for the bileaflet design are similar to those for the tilting disc valve. Regurgitant volume characteristics are summarized in Table 23-2 and Table 23-3 . The bileaflet design shows slightly larger regurgitant volumes than the tilting disc valve. Leakage flow through the bileaflet valve design occurs primarily through the pivots. In addition, leakage is also observed around the periphery and from the gap between the two leaflets. Figure 23-14 illustrates typical two-dimensional color Doppler flow mapping images of these regurgitant jets. Velocity and turbulence measurements, obtained both within the pivots and 1 mm upstream of the valve housing in the aortic position, indicate that the major jets persist through nearly all of diastole. The mean velocity magnitudes in the jets are on the order of 2 or 3 m per second with turbulent shear stress mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 17 di 27 levels exceeding 3000 dyn/cm.2 These high turbulent stresses, when coupled with a relatively stagnant adjacent flow regime, could lead to thrombus formation. Such a region of stagnation was noted in the pivots of the Medtronic Parallel valve. This design was voluntarily withdrawn from the market after a high incidence of thrombosis was noted in clinical trials. Explant data revealed that this thrombus was located preferentially within the inflow region of the valve pivots. Ellis et al,[103] Gross et al,[104] and Healy et al[105] subsequently performed extensive laser Doppler velocimetry measurements, computational simulations, and flow visualization studies that linked the thrombus formation within the Medtronic Parallel pivot to a persistent stagnation region at the same location. In contrast, in studies of bileaflet prostheses that have clinically acceptable rates of thrombosis, such as the St. Jude Medical Standard and Regent valve designs, no persistent regions of stagnation were found within the pivots.[106] [107] Pressure Drop Characteristics. The bileaflet design in general has lower pressure drops than do any of the three mechanical valve designs, although the pressure drop of the Medtronic-Hall tilting disc valve is comparable to that of the St. Jude Medical Standard valve. [82] Recent bileaflet prosthesis designs, such as the St. Jude Medical Regent valve, have incorporated narrower sewing cuffs and a thinner, reinforced valve orifice to increase the Aeff and PI for a given valve size. These values as well as data from other bileaflet valve designs are tabulated in Table 23-2 and Table 23-3 . Orientation. The bileaflet valve is mounted in one of two orientations in the mitral position. The first position is the anatomic position, with the leaflet hinge plane of the valve oriented in a direction perpendicular to the plane of the aortic outflow and mitral inflow tracts. The leaflets pivot in a similar plane as that of the native mitral valve leaflets. The second position is the antianatomic position, with the valve mounted such that the leaflet hinge plane is rotated 90 degrees from the |
anatomic position. The orientation of the St. Jude Medical bileaflet valve in the mitral position has been studied in in vitro flow visualization experiments conducted in our laboratory. The results of these studies indicate that the antianatomic Figure 23-14 (color plate.) Two-dimensional color Doppler flow mapping of the regurgitant jet flow field of a bileaflet valve design mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 18 di 27 under physiologic pulsatile flow conditions. 517 position provides better flow patterns along the posterior wall of the ventricle. Potentially better lateral flow expansion in the plane perpendicular to the plane of the aortic outflow and mitral inflow tracts is also observed. The anatomic position, however, provides adequate flow patterns within the left ventricle with slightly narrower lateral expansion of the inflow jets. Van Rijk-Zwikker et al[108] investigated the effects of orientation of the Carbomedics bileaflet valve in in vivo pig studies. Two-dimensional echocardiographic and color Doppler measurements were analyzed to determine the influence of valve orientation on valve function and the transvalvular flow patterns within the left ventricle. The 90-degree, antianatomic orientation was found to be superior to the anatomic orientation of the valve. The anatomic orientation resulted in diastolic backflow directed toward the valve, which may lead to asymmetric motion of the valve leaflets. The antianatomic position produced diastolic backflow patterns that enter the left ventricular outflow tract. Minimal interference with the function of the leaflets is expected from these flow patterns. The studies of Travis et al[100] and Kleine et al[101] examined the effects of aortic bileaflet valve orientation as well as tilting disc valve orientation on forward flow hemodynamics. Travis et al found that orienting the leaflets of the open valve parallel to the proximal flow direction resulted in decreases in energy losses and pressure drops in vitro. Kleine et al found that turbulence created by bileaflet valves was minimal when one of the lateral orifices faces the right posterior wall of the aorta. Ball-and-Cage Valve The ball-and-cage valve is characterized by a silicone ball mounted into a wire cage, as illustrated in Figure 23-8 . The Figure 23-15 Center line velocity and turbulent shear stress profiles 30 mm downstream of a 27-mm Starr-Edwards ball-and-cage valve at peak systole. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 19 di 27 only ball-and-cage valve in use today is the Starr-Edwards 1260. The cage is constructed from three wire struts separated by 120 degrees. The struts emanate from the valve housing and converge at the distal end of the valve, the apex of the cage. The ball is free to travel along the cage, typically over a 1- to 2-cm distance. Antegrade Flow. The flow fields of these valves consist of annular jets that emerge from around the occluder or poppet. In the aortic position, the jets are initially directed toward the wall of the aorta where they impact and then follow the contour of the aortic wall. Peak systolic velocities in the aorta are comparable to those encountered in the other valve designs, approximately 2 m per second at peak systole. The annular jets show rapid development early in systole during the acceleration phase of flow. A gradual divergence and growth of the jet is observed with increasing displacement downstream, where the jet maintains its structure over a considerable axial distance. Velocity profiles at peak systole are shown in Figure 23-15 , 30 mm downstream of the valve. Large mean velocity gradients are observed alongside the annular jet, with values exceeding 1500 L per second. The flow field in the mitral position is similar to the jet structure in the aortic position; however, the jet peak velocities are lower, the jet decays more rapidly, and greater lateral expansion of the jet occurs in the ventricle. The ball generates a large wake in the central part of the flow field that starts in early systole and grows into a region of reverse flow lasting from peak to end-systole. The lateral extent of this region of reverse flow is on the order of 8 to 10 mm distal to the apex of the cage. Peak reverse velocities can be as high as 20 to 25 cm per second. These regions of large separation are responsible for the thrombogenecity of these valves.[109] The ball in these types of valves is often observed to fluctuate at the apex, which is most likely caused by flow instabilities within the wake or vortex shedding from the ball. This 518 phenomenon increases the lateral extent of the wake and produces an increase in the relative velocity between the ball and the model wall and an increase in pressure drop across the prosthesis. The turbulent stresses are concentrated in the large velocity gradients associated with the annular jets of these valves. Turbulent shear stresses as mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 20 di 27 high as 1900 dyn/cm2 have been measured downstream of these valves in the aortic position. High turbulent stresses are observed through most of systole over a significant length downstream of the valve. The rapid turbulent stress generation indicates a quick temporal development of the jet and prolonged perseverance of the jet structure. Immediately adjacent to the ball, peak turbulent shear stresses are estimated to be as high as 3500 dyn/cm2 . The large wall shear stresses associated with the ball valve could cause damage to the endothelial lining of the aorta. The turbulent stresses measured in the annular jets are more than sufficient to cause lethal damage to red blood cells, as well as platelet damage and activation. Coupled with the large separated region behind the ball, thrombus formation on the apex of the cage is likely and has been documented in the medical literature. Normal Regurgitant Flow. The normal regurgitant flow of the ball-and-cage design is composed mainly of the closing volume flow. The seating of the ball valve is generally very good with little or no leakage flow. Typical values of the regurgitant volume are roughly 5 mL per beat for the 25- and 27-mm valve sizes. These values are also provided in Table 23-2 and Table 23-3 . Pressure Drop Characteristics. These valves typically show larger pressure drops than do the tilting disc and bileaflet designs. The PI and A of the Starr-Edwards valve range eff from 0.36 and 1.62 cm2 for 25-mm size valves to 0.3 and 1.71 cm2 for the 27-mm valve. Typical values of the A and PI are tabulated in Table 23-2 eff and Table 23-3 . The large wake region is principally responsible for the large pressure drop across the valve. Figure 23-16 Center line velocity and turbulent shear stress profiles 17 mm downstream of a 27-mm Carpentier-Edwards pericardial valve at peak systole. Bioprostheses The most common bioprosthetic valves are composed of three biologic leaflets made from the porcine aortic valve or bovine pericardium. They are mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 21 di 27 constructed similarly to the natural aortic valve. The annular ring is cloth covered and molded to function similarly to the aortic annulus. Metal or polymeric stents provide support to the leaflets at their commissures in the stented design, whereas the leaflet commissures in nonstented aortic valves must be attached to the native aorta for support. The clinically available designs vary mainly in the support structure and in the leaflet material and construction. All trileaflet bioprostheses, however, open to a centrally located orifice with respect to the valve annulus and mimic the open geometry of the normal aortic valve but with a smaller orifice area. Tissue valves are less thrombogenic than mechanical valves and thus do not require anticoagulant treatment; however, tissue valves exhibit higher pressure gradients than do most commonly used mechanical valves, particularly in the small sizes that exhibit stenotic characteristics. These valves also suffer from calcification of the leaflets, material fatigue leading to valve failure because of leaflet rupture or tearing, or both. Calcification of the tissue is often a precursor to leaflet rupture and tearing, as these are often observed adjacent to calcified lesions. Stented Valves Antegrade Flow. All stented bioprosthetic valves have central jet type flow fields as illustrated in Figure 23-16 and Figure 23-17 . The newer generation porcine valves and most pericardial valves create flatter velocity profiles than do the earlier porcine valve designs. Flatter velocity profiles 519 Figure 23-17 Center line velocity and turbulent shear stress profiles 15 mm downstream of a 27-mm Carpentier-Edwards 2625 porcine valve at peak systole. result in more evenly distributed downstream flow fields and lower turbulent shear stress levels. Early designs, such as the Carpentier-Edwards porcine model 2625 and the Hancock I porcine valves, generated asymmetric jet profiles. The jets were directed slightly away from the stent in a plane that bisected one leaflet and the stent opposite that leaflet, as illustrated in Figure 23-17 . Peak aortic velocities exceed 3 m per second at peak systole for normal flow conditions. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 22 di 27 The newer porcine designs, such as the Carpentier-Edwards porcine 2650, and the pericardial valves produce jets that are wider and have more blunted profiles. These jets exhibit a more axisymmetric velocity profile with large mean velocity gradients (viscous stresses) alongside the jets. Peak velocities range from 2 to 3 m per second under normal flow conditions in the aortic position. These jets still show a slight laterally directed motion similar to the older porcine valve designs, but it is not as pronounced. In in vitro experiments, stagnant flow can be observed throughout systole between the outflow surfaces of the valve leaflets and the flow model wall. In earlier valve designs, these stagnation regions were larger and exhibited regions of flow reversal. Stented bioprosthesis stagnant regions can be amplified in conditions of low cardiac output, in which one of the three leaflets may fail to open fully. Flow stasis can lead to deposition of thrombogenic elements on the outflow surfaces of the leaflets. In all stented valve designs, the turbulent shear stresses are confined to narrow regions in the shear layers of the central jets. Peak turbulent shear stresses in the aorta ranged from greater than 2000 dyn/cm2 to greater than 4500 dyn/cm2 in the early valve designs. The pericardial and newer porcine aortic valve designs exhibit lower stress levels, in the range of 1000 to 2500 dyn/cm.2 Additionally, turbulent shear stresses show a more confined spatial structure along the jet shear layers in the newer valve designs, as shown in Figure 23-15 . Turbulent shear stress levels are high enough to cause hemolysis and platelet activation. Considering the location of peak stresses adjacent to the regions of reverse flow, it may be speculated that the tissue valve would also be prone to thrombogenic events or tissue overgrowth of the sewing ring. Normal Regurgitant Flow. All tissue valves exhibit some degree of regurgitant flow in the closing volume. Leakage volume is essentially zero in properly functioning valves. The closing volumes, however, are generally lower in bioprostheses than in the mechanical prostheses. The lower closing volumes are caused by more rapid closure of the valve leaflets for tissue valves compared with the occluders of the mechanical valve designs. Regurgitant volumes are on the order of 1 mL per beat for most tissue valves. The Ionescu-Shiley pericardial valve, however, has closing volumes ranging from 2.5 to 6.5 mL per beat, depending on valve size and position (aortic or mitral). Typical values of the regurgitant volumes for several bioprosthetic valves are given in Table 23-2 and Table 23-3 . Regurgitant jets are normally nonexistent mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 23 di 27 and the presence of such a jet indicates valve incompetence. Pressure Drop Characteristics. All stented porcine tissue valves are mildly stenotic compared with the natural valve in large sizes, and they are moderately to severely stenotic in the small sizes. Porcine valves in small sizes exhibit a higher degree of stenosis than do comparably sized mechanical valves. As a result, the PI of common stented porcine tissue valves ranges from 0.3 to 0.4, compared with values around 0.6 to 0.7 for similarly sized mechanical valves. This stenotic behavior is due in part to the construction of the leaflets, the stiffness of the fixed tissue, and the man-made commissures. The stents also act to restrict the motion of the leaflets somewhat during opening. Typical A ranges from 1.3 to |
2.5 cm2 for 21- to 27-mm porcine aortic eff valves, respectively.[110] The new generation of stented pericardial valves (e.g., Carpentier-Edwards, MitroFlow), however, have pressure drop characteristics comparable to the St. Jude Medical Standard and Medtronic- Hall mechanical valve designs in all sizes. For example, the Carpentier- Edwards aortic pericardial valves (sizes 27 to 19 mm) have Aeff values ranging from 3.7 to 1.56 cm2 . The Aeff and PI values for several tissue 520 valves, both porcine and pericardial, are listed in Table 23-2 and Table 23- 3 . Nonstented Valves Nonstented aortic valve prostheses are composed of a natural porcine valve and usually some length of the intact aorta. The original right and left coronary arteries are also ligated with short remnants to aid in reimplantation of the patient's coronaries. In vitro testing of nonstented aortic bioprostheses requires a compliant test chamber capable of simulating the human aortic root. Hemodynamic data show that aortic nonstented valves have pressure drops comparable to mechanical prostheses. [111] [112] [113] During the past few years, several investigators have begun testing and using mitral valve heterografts.[114] These mitral heterografts typically use fixed valves with or without intact papillary muscles. These new mitral replacements can be considered to be nonstented bioprostheses. Currently, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 24 di 27 quantitative in vitro testing of the flow fields of these valve designs is limited; however, our laboratory has begun assessing the hemodynamic characteristics of these mitral replacements. A study by Jensen et al[115] has shown that the fixation of porcine mitral heterografts in glutaraldehyde reduces orifice area and increases total regurgitation in these valves. Although no mitral valve replacements are currently approved in the United States, one design is in clinical trials in Europe. This valve, the St. Jude Medical Quattro valve, is fashioned from pericardium and offers reasonable hemodynamics. Mitral heterografts have the potential for better hemodynamic performance, reduced thrombogenesis, and improved left ventricular function. Antegrade Flow. Currently, quantitative data on the antegrade flow fields for both aortic and mitral nonstented tissue valves are under study. Ultrasound Doppler results for a 27-mm Medtronic Freestyle valve[111] indicate that the flow accelerates uniformly through the valve with an apparent uniform and flat profile downstream of the valve. Doppler-measured peak velocities at the leaflet tips ranged from 75 to 125 cm per second at cardiac outputs from 3.0 to 5.0 L per minute. The peak velocities decreased to a range of 60 to 100 cm per second at 5 to 10 mm from the leaflet tips over the same range of cardiac outputs. There is no appearance of a jet with steep velocity gradients, as is observed in stented bioprostheses. Similar results were obtained from ultrasound Doppler measurements conducted with a 29-mm St. Jude Medical TSPV valve design. Normal Regurgitant Flow. The nonstented aortic valves exhibit regurgitant volumes that are comparable to closing volumes of valves exhibiting similar A . Good eff coaptation is observed with little or no leakage. Nonstented mitral valve heterografts tested in our laboratory exhibited comparable closing volumes to unfixed natural valves tested in the same flow loop. Good coaptation was observed with no leakage. The function of mitral heterografts is strongly dependent on the implantation technique, which is expected when considering the complicated function of the mitral complex compared with the aortic valve. Pressure Drop Characteristics. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 25 di 27 The unstented Medtronic Freestyle valve has a lower pulsatile pressure drop than comparably sized stented valves. In the 25 and 27 mm size Freestyle valves, Aeff was comparable to the St. Jude Medical Standard bileaflet valve, whereas in smaller sizes it was comparable to the St. Jude Medical Regent valve. The Medtronic Freestyle and Mosaic porcine valves use the exact same tissue, treated with the same processes. The Aeff of a 23- mm Medtronic Freestyle stentless valves, however, was found to be similar to that of a 27-mm stented Mosaic valve. Thus, removal of bioprosthetic valve stents definitely creates less forward flow obstruction and significantly improves overall hemodynamic performance. The Aeff for several sizes of the Medtronic Freestyle porcine valve are listed in Table 23-2 and Table 23-3 . Because of the added complexity of the unstented design and the increased factors governing selection and style, optimal flow performance of these valves both in vitro and in vivo depends on the type of valve configuration used for a particular patient geometry and on the proper sizing of the valve. Improper selection of style and size can compromise hemodynamic performance of the valve. In vitro tests of the Medtronic Freestyle valve indicate that the Aeff can be optimized by using a valve one size larger than the size of the simulated aorta. Thus, a 23-mm valve should be used in a 21-mm aorta. Total root or an inclusion cylinder valve geometry technique showed better A results than partially or fully scalloped valve eff configurations. Pressure drops for mitral valve heterografts are generally higher than normal mitral valves, owing to stiffening of the valve tissue resulting from fixation. Homograft Valves Homograft valves are cryopreserved human valves, and they have been used for more than two decades in the aortic position. With the advent of improvements in surgical techniques and viable mitral heterografts, a mitral homograft is also a possibility. Aortic homografts are typically implanted as a complete valve, annulus, and aortic section. As a result, the effective annulus area is reduced from the original aortic valve annulus before replacement. Mitral homografts consist of intact mitral valves with annulus, papillary muscles, and chordae tendineae. Antegrade Flow. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 26 di 27 The flow field characteristics of the homograft aortic valves are similar to those of the natural valve, although peak velocities are slightly higher because of a reduced Aeff resulting from the smaller area of the outflow tract. Peak velocities, however, are smaller in homograft valves than those observed in other prosthetic designs for comparably sized valves. The aortic homograft shows excellent hemodynamics over the entire size range in contrast to the stented bioprostheses, which show increased stenosis in the smaller valve sizes. Studies conducted in our lab indicate that sheep allograft mitral valves and untreated normal mitral valves have excellent hemodynamics compared with that of stented valves.[115] The unfixed mitral valves exhibit both qualitatively and quantitatively similar forward flow characteristics to those observed clinically for normal human mitral 521 Figure 23-18 Planar two-dimensional transmitral flow patterns in the left ventricle during diastole. Images were obtained from in vitro planar flow visualization experiments of natural, untreated mitral valves. (From Lefebvre XP, He S, Levine RA, Yoganathan AP: J Heart Valve Dis 1995;4:422–438.) valves. The qualitative left ventricular flow fields during diastole are illustrated in Figure 23-18 . This figure shows the in vitro flow patterns for the natural mitral valve using a two-dimensional planar flow visualization technique outlined in Lefebvre.[99] These experiments were conducted in an anatomically correct left ventricular model constructed of polished transparent acrylic. The models were manufactured so that the native mitral valve complex, including papillary muscles and chordae tendineae, could be implanted and tested under normal physiologic conditions. Figure 23-19 illustrates the model and relationship of a native valve mounted in the model. Normal Regurgitant Flow. As with other bioprosthetic valves, the homograft valves exhibit small closing volumes. Properly functioning homograft valves should exhibit little or no regurgitation caused by leakage. The mitral homografts show the same dependency of implantation technique on overall hemodynamics. Proper implantation of the valve complex including proper alignment of the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 27 di 27 papillary muscles with the valve annulus results in superior function with no regurgitation other than normal closing volume. Pressure Drop Characteristics. The homograft valves show low pressure drops with large A compared eff with mechanical and stented valves. Vetter et al[116] conducted in vitro tests of 23- and 25-mm mitral homograft valves at physiologic conditions of 5 L per minute CO and 70 bpm HR to measure the pressure drop and A eff characteristics of these valves. Measured pressure drops ranged from 10.4 to 3.4 mm Hg for the 23- and 25-mm valves, respectively. The corresponding Aeff ranged from 1.8 to 3.4 cm2 . These values are comparable to 25- and 27-mm Hancock 342 and Hancock II bioprostheses, indicating a significant improvement in hemodynamics for similar valve size. Typical values for the Aeff and PI of homograft valves are listed in Table 23-2 and Table 23-3 . MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/202.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Future Directions We foresee that the future direction of prosthetic valve research will follow several courses: tissue-engineered bioprosthetic valves; invention of novel tissue fixation techniques; improved mechanical valve design; improved in vitro, computational, and animal testing protocols; and development of noninvasive diagnostic capabilities. Conceptually, tissue-engineered valves would hold the most promise for a near-perfect valve replacement. The goal of this research is to grow living human aortic valves in the laboratory, preferably using the patient's own tissue. Potential advantages involve total acceptance of the living tissue, with hemodynamic and cellular function similar to the normal human aortic valve, resulting in a lifetime equal to that of native valves. Tissue xenografts are currently fixed in glutaraldehyde, which stiffens the compliance of the valve material and hinders hemodynamic performance. [115] Other fixative techniques may improve hemodynamic performance or increase the functional lifetime of xenografts. For mechanical valves, the focus will be on reducing their thrombogenic properties. This goal could possibly be achieved by development of biocompatible surface coatings and materials, or by changing valve geometry to improve closure and leakage flow through these valves. [117] A first step in this research should be to improve understanding of blood element damage, thromboembolic events, and thrombus formation. As we enrich our understanding of these topics, in vitro evaluation techniques and in vivo diagnostic capabilities should also improve. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/203.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Acknowledgments The work reported from our laboratory has been supported by grants from the Food and Drug Administration, Figure 23-19 The anatomically correct left ventricular in vitro model used in the testing of nonstented and homograft mitral valves. (From Lefebvre XP, He S, Levine RA, Yoganathan AP: J Heart Valve Dis 1995;4:422–438.) 522 the American Heart Association, the heart valve industry, and generous gifts from Tom and Shirley Gurley and the Lilla Boz Foundation. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/204.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company 525 Chapter 24 - Echocardiographic Recognition and Quantitation of Prosthetic Valve Dysfunction Miguel Zabalgoitia MD After more than 3 decades of clinical experience, the search for the "ideal" artificial heart valve continues with increasing interest. Thirty years ago, prosthetic valves were limited to the ball-and-cage mechanism; since then, single and double tilting discs and several stented and nonstented biologic devices have been introduced. Each of these valves is accompanied by individual ultrasonic and hemodynamic characteristics (see Chapter 23) , making the roles of the |
echocardiographer and sonographer understandably more complex. The optimal management of patients with prosthetic valves requires serial assessment of valve function and left ventricular performance. Symptoms of fatigue, dyspnea, and exercise intolerance may be caused by valve dysfunction or a variety of comorbid conditions. Doppler echocardiography is the imaging modality of choice in evaluating patients with known or suspected prosthetic valve dysfunction because it provides information regarding valve structure, hemodynamics, native valve status, and left ventricular function.[1] [2] [3] Since its clinical introduction more than a decade ago, transesophageal echocardiography (TEE) has been widely mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 accepted as a tool that allows superior anatomic and functional assessment of native and prosthetic valves.[4] [5] [6] TEE now is a routine diagnostic procedure in assessing prosthetic heart valves. Three-dimensional (3D) echocardiography is an evolving new technology with a wide range of potential clinical applications, and evaluation of prosthetic heart valves, particularly tissue valves, may be one of them. Other available methods for assessing prosthetic valves include cardiac catheterization with angiography for both hemodynamic and structural information. Cardiac catheterization also provides the opportunity to perform fluoroscopy in the case of metallic valves. The potential use of magnetic resonance imaging in assessing prosthetic valve function has been suggested by a comparative study detecting pathologic prosthetic regurgitation.[7] Further studies are needed to determine the most appropriate clinical setting for this imaging modality. Nowadays, it is impossible to ignore the impact that economics has on our daily practice. Evaluation of cost and effectiveness of diagnostic testing is complex; it involves the test itself and the treatment strategies that follow. [8] In this regard, one must answer the following questions: Do the test results affect the decision-making process?; Do the test results lead to the treatment of choice?; What is accuracy of the testing?; What is the cost?; and What is the morbidity due to the test? Although a detailed ultrasound cost analysis of prosthetic heart valves is lacking, the subject offers a useful frame of thought, and the answer to each of the above-mentioned questions is clearly favorable. In fact, the perception of most clinicians is that Doppler echocardiography in patients with prosthetic heart valves is a highly cost-effective tool. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/206.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 6 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Prosthetic Heart Valve Classification Several types of prosthetic heart valves, divided into mechanical and biologic categories based on their primary 526 TABLE 24-1 -- Classification of Prosthetic Heart Valves Mechanical Ball-and-cage (Starr-Edwards) Single tilting disc (Medtronic-Hall, OmniScience) Double tilting disc (St. Jude Medical, Carbomedics) Biologic Heterograft stented (Hancock, Carpentier-Edwards) Heterograft nonstented for aortic valve (Toronto SPV, Medtronic Freestyle, and CryoLife-O'Brien) Heterograft nonstented for pulmonic valve (CryoLife-Ross) Homografts (aortic, pulmonic, and mitral) manufacturing material, are available for implantation. Table 24-1 lists the most common prosthetic heart valves currently used in clinical practice. Mechanical Valves Ball-and-Cage. The first successful valve replacement used a ball-and-cage design, [9] [10] and after several modifications, only the Starr-Edwards valve has endured with an estimated usage of more than 200,000. It consists of a Silastic ball mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 6 with a circular sewing ring and a cage formed by metal arches located around the sewing ring (Fig. 24-1) . The silicone rubber ball retracts toward the apex of the cage as antegrade blood flows through the valve orifice and between the ball and the stents. [11] Single Tilting Disc. A single disc tilting valve consists of a circular sewing ring with a circular disc eccentrically attached by lateral or central metal struts. Medtronic- Hall, Figure 24-1 Mechanical heart valves. Starr-Edwards (S-E), Medtronic- Hall (M-H), OmniScienct (Omni), and St. Jude Medical (SJM). Björk-Shiley, and OmniScience are representatives of this group. The first successful low-profile design was the Björk-Shiley, introduced in 1969,[12] with an estimated usage of 360,000. The Björk-Shiley valve has been discontinued from the United States market. When the pyrolytic carbon disc opens, blood flows through two unequal (major and minor) orifices and the disc opens with an angle ranging from 60 to 80 degrees, which favors closure by a backflow mechanism (see Fig. 24-1) . This angle results in resistance to flow around the disc and stagnated flow behind the disc, a site of potential thrombus formation. Double Tilting Disc. Bileaflet valves have two semicircular pyrolytic carbon discs attached to the valve ring by two small midline hinges. St. Jude Medical and Carbomedics are the prototypes of this group (see Fig. 24-1) . The bileaflet design was introduced by St. Jude Medical in 1977 and has been used over 600,000 times. Mechanical valves are extremely durable with overall actuarial survival rates ranging from 94% ± 2% at 10 years for the St. Jude Mechanical valve to between 60% and 70% at 10 years for the Starr-Edwards valve.[13] [14] [15] Primary structural abnormalities are very rare,[16] [17] [18] and most valve malfunctions are caused by perivalvular leak, endocarditis, and thrombosis. Chronic anticoagulation is required in all patients with mechanical valves to prevent valve thrombosis and embolic events. With adequate mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 6 anticoagulation, the rate of thrombosis is 0.6% to 1.8% per patient-year for bileaflet valves.[13] [19] [20] Biologic (Tissue) Valves Stented Bioprostheses. Porcine valves currently in use are the Hancock and Carpentier-Edwards. The leaflets are treated with glutaraldehyde to reduce antigenicity, but they are less pliable than normal human valves.[21] The Carpentier-Edwards porcine valve has a stent made from a single piece of wire and the three leaflets are mounted above the sewing ring, allowing a larger orifice area and a better hemodynamic profile. Both porcine bioprostheses have a similar macroscopic appearance, but they are easily distinguishable by their radiographic appearance; Hancock appears as a circular ring whereas Carpentier-Edwards appears as a crown. The Ionescu-Shiley bioprosthesis from bovine pericardial tissue was discontinued after 10 years of use because of dehiscence.[22] The Carpentier-Edwards pericardial (Perimount) valve is currently available, but unlike the Ionescu-Shiley, which used retention sutures to attach the leaflets, the Perimount valve is mounted within the stent to maximize cusp opening and to reduce abrasion between tissue and stent. The long-term results with this valve are very encouraging. A major advantage of bioprosthetic valves is the low rate of thromboembolism (1.6% per patient-year) in the absence of chronic anticoagulation[23] however, stented heterograft valves are subject to progressive calcific degeneration and failure typically after 6 to 8 years of implantation.[24] [25] [26] [27] [28] [29] Calcific degeneration is faster in children, young adults, and patients with abnormal calcium metabolism.[30] [31] In several large series, the rate of degeneration for porcine valves was 3.3% per patient-year and a freedom 527 from valve failure rate for aortic valves was 78% ± 2% and for mitral valves was 69% ± 2%.[23] [32] [33] After 10 years, the rate of deterioration accelerates abruptly with freedom from valve failure rates of 49% ± 4% for aortic and 32% ± 4% for mitral prostheses.[32] Using the porcine bioprosthesis in patients over 70 years of age, a 90% freedom from valve replacement at 12 to 15 years has been reported.[33] [34] This finding may be related to a decreased rate of degeneration in elderly patients or an increased rate of death from other than valve-related causes in the group of mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 6 patients who did not outlive their prostheses. Nonstented Bioprostheses. Nonstented heterografts are expected to improve hemodynamics and long- term durability while retaining the fundamental advantages of tissue valves. The goals are to return the patients to their own baseline conditions as is feasible, prolong survival, and improve quality of life. The absence of the stent and sewing cuff make it possible to implant a larger valve for a given annular size, resulting in a greater effective orifice area. A nonstented bioprosthesis uses the patient's aortic root as the valve stent, absorbing the motion stress induced during the cardiac cycle and leading to better hemodynamic performance. Nonstented bioprostheses include the Toronto SPV,[35] [36] Medtronic Freestyle,[37] [38] [39] [40] and CryoLife-O'Brien.[41] [42] [43] There are several variations within the same valve, depending on the patient's needs and the surgeon's preference. These variations include the full root technique with reimplantation of the coronary arteries, the root inclusion technique with preservation of the native coronary arteries, or the subcoronary technique. Figure 24-2 depicts a subcoronary implantation. Removal of the stent appears to eliminate much of the stress that promotes calcification and valve deterioration. Nonstented bioprostheses typically are manufactured from intact porcine aortic valves processed at very low fixation pressures. Moreover, some valves (i.e., Medtronic Freestyle) are treated with the anticalcificant amino-oleic acid, which may further decrease calcific deposits. The addition of a layer of polyester fabric around the graft adds support and aids implantation.[44] [45] Nonstented valves have been used primarily in the aortic position in men older than 60 years of age. The reported operative mortality rate for patients with nonstented valves is 3% to 6%,[46] [47] but these figures are probably affected by patient selection. Postoperative complications at 12 months appear to be low, with endocarditis reported at 1% to 2%, thromboembolism at 2% to 3%, and hemorrhage at 1.5%.[44] [46] [47] There have been no reports of primary structural failure, and the reported survival rates have been as high as 91% ± 4% at 6 years.[44] [47] [48] The CryoLife-Ross valve is a pulmonary nonstented bioprosthesis made of three noncoronary porcine cusps used to correct congenital defects involving the pulmonic valve, and they can also be used during the Ross procedure as described later. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 6 Homografts. Homografts are antibiotic-sterilized, cryogenically-preserved valves harvested from cadaveric human hearts.[49] Their major advantages are relative resistance to infection, lack of need for chronic anticoagulation, and excellent hemodynamic profile, most notably in Figure 24-2 Drawing of a nonstented aortic valve (Toronto SPV) at the subcoronary position. (Courtesy of St. Jude Medical, Inc., St. Paul, Minn. All rights reserved. Copyright © 2001 St. Jude Medical, Inc. Toronto SPV is a registered trademark of St. Jude Medical, Inc.) smaller aortic root sizes.[50] [51] As illustrated in Figure 24-3 (Figure Not Available) , homografts have been developed for the aortic, pulmonic, and even for mitral valves. The technical aspects of homograft preparation and the meticulous and highly skilled freehand surgical technique required for implantation in some cases have limited their use on a routine basis. Typically, homografts are inserted without a stent, using the patient's natural fibrous annular tissue for support. Ross Procedure. The pulmonic autograft (or Ross procedure), first described in 1967,[52] consists of replacing the abnormal aortic valve with the native pulmonic valve of the same patient, then placing a nonstented homograft or porcine bioprosthesis in the pulmonic position. The operation is technically demanding; the pulmonic valve is removed with healthy tissue above and below the valve insertion. This procedure requires some reconstruction of the right ventricular outflow tract. In addition, the coronary arteries are reimplanted into the pulmonary artery trunk that serves as the new aortic root. Although the Ross procedure involves two valve operations (aortic valve autograft and pulmonic valve nonstented allograft) to correct one diseased valve, it provides optimal hemodynamics and echocardiographic performance and low valve-related complication rates.[53] The main long- term problem with this operation has been degeneration and failure of the right-sided valve caused by obstruction in the distal segment of the homograft conduit.[54] [55] Early 528 Figure 24-3 (Figure Not Available) Drawing of cardiac anatomy depicting the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 6 availability of homografts for the pulmonary, aortic, and mitral valves. (Courtesy of CryoLife, Kennesaw, Ga.) autograft failure (<6 months) most often is due to technical errors or persistent endocarditis, and late failures generally are due to aortic annulus dilation, endocarditis, or valve degeneration.[56] [57] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/207.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina |
1 di 7 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Fundamental Principles Pertaining to Prostheses Modified Bernoulli Equation Blood flow velocity through a narrow orifice is related to the pressure difference between two chambers as described by the Bernoulli principle used to convert flow velocity (m/sec) to pressure gradient (mm Hg). The modified Bernoulli equation used in prosthetic valves is the same as that used in native valves: Pressure gradient = 4(V )2 MAX where VMAX is the maximal (peak) velocity across the valve orifice. It is important to recognize that the modified Bernoulli equation neglects the effects of acceleration and viscous losses, and yet it has proved to be remarkably accurate when compared with catheter-derived pressure gradients when both are obtained simultaneously.[58] [59] [60] [61] [62] [63] When the left ventricular outflow tract velocity (V ) is greater than 1 m per 1 second, such as in patients with concomitant aortic regurgitation, V should 1 be subtracted from VMAX . Maximal instantaneous and mean gradients should be calculated for aortic valves, and mean gradient should be calculated for mitral valves. A high gradient in the setting of anemia, tachycardia, or sepsis does not necessarily indicate stenosis; conversely, an upper normal limits gradient in the setting of severe left ventricular dysfunction may indicate significant stenosis. Pressure Recovery Recording valve gradients that appear to be an "overestimation" when compared with those at catheterization may result from distal pressure recovery, which refers to the conversion of kinetic energy present at the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 7 valve level to pressure energy distal to the valve.[64] [65] When flow passes through the prosthesis, components of velocity and momentum are directed centrally, causing the flow stream to contract distally for a short distance. This point of maximal constriction is called vena contracta and occurs downstream distally from the anatomic location of the prosthesis. As the jet expands and decelerates beyond the vena contracta, the associated turbulence results in an increase in aortic pressure or pressure recovery. Under these circumstances, when the aortic pressure is measured in the upper ascending aorta (distal to the vena contracta), the pressure difference between the left ventricle and the aorta is less than the aortic pressure measured at the vena contracta. The degree of pressure recovery may be as high as a mean of 10 mm Hg in small St. Jude Medical valves challenged under physiologic flow rates. The magnitude of pressure recovery is greater with larger valve areas and with smaller aortic roots; therefore, patients with severe prosthetic stenosis and poststenotic aortic root dilation may show less pressure recovery than patients with mild to moderate stenosis and normal aortic root diameter. Pressure recovery and vena contracta are important concepts to keep in mind when Doppler- and catheter-derived pressure gradients are being compared. Because continuous wave Doppler measures velocity at the level of the vena contracta (physiologic variable) and catheterization measures the difference between left ventricle and the fully recovered static pressure in the aorta, catheter-derived data must be interpreted with caution. Failure of the invasive technique to record the gradient at the vena contracta level may explain some of the reported discrepancies.[66] Continuity Equation An important limitation of Doppler velocities (and pressure gradients derived thereof) is that they are flow volume rate dependent. When transvalvular flow is decreased, such as in patients with significant left ventricular systolic dysfunction, Doppler velocities may only be moderately elevated despite severe obstruction. Thus, comparisons may be confounded by interval changes in flow volume rate. For these reasons, estimation of valve areas, in addition to mean pressure gradients, should be routinely calculated. The equation of continuity can be used to estimate aortic and mitral valve areas. Figure 24-4 illustrates how to apply the continuity equation in aortic prostheses: mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 7 AVA = (A × VTI )/VTI LVOT LVOT TRANSPROSTHESIS 529 Figure 24-4 Effective orifice area (EOA) calculation for an aortic valve prosthesis. The left panel corresponds to the outflow tract (subvalvular) velocity, also known as V1 . The middle panel corresponds to the prosthesis velocity, also known as V2 . The right panel corresponds to the parasternal long-axis view, showing the outflow tract diameter (arrows). Ac, aortic closure; AO, aorta; Ao, aortic opening; LA, left atrium; LV, left ventricle; RV, right ventricle; subvalve, subvalvular; vel. int., velocity integral. where ALVOT is the cross-sectional area of the outflow tract at end-systole measured just underneath the prosthesis from the parasternal long-axis view. VTI is the velocity time integral proximal to the valve as seen LVOT from an apical view using pulsed wave Doppler. One must be careful placing the sample volume immediately adjacent to the aortic prosthesis from the apical five-chamber view while avoiding the region of subvalvular acceleration. The Doppler wave form should be smooth with minimal spectral broadening and a well-defined peak. VTITRANSPROSTHESIS is the velocity time integral across the prosthesis using continuous wave Doppler. Because the direction of the jet may be eccentric, all acoustic aortic windows (apical, suprasternal, and right parasternal) should be carefully examined to detect the highest velocity signal. Continuity equation valve areas have been compared with invasively obtained data for bioprosthetic[67] [68] [69] and mechanical valves.[70] [71] The largest source of variability is the accurate and reliable measurement of the left ventricular outflow tract. When this diameter is difficult to obtain from the precordial window, TEE offers an excellent alternative for calculation of aortic valve area.[72] For mitral valve area (MVA), the continuity equation is as follows: MVA = (AVA × VTIAORTIC )/VTITRANSPROSTHESIS where AVA is the cross-sectional aortic valve area as measured from the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 7 parasternal long-axis view, VTI is the velocity time integral across AORTIC the native aortic valve, and VTI is the velocity time TRANSPROSTHESIS integral across the mitral prosthesis.[73] Because the continuity equation is based on the principle of conservation of mass, it assumes that flow across the mitral prosthesis and that across the second valve are equal. Thus, in patients with greater than mild mitral regurgitation, the preferred method to estimate valve area is the pressure half-time. In the presence of aortic regurgitation, the pulmonic valve area and flow can be used in lieu of the aortic valve. The limiting step in using the pulmonic valve is the accurate and reproducible measurement of the right ventricular outflow tract diameter from the precordial approach. An important advantage of the continuity equation is its relative independence from valvular gradient and chamber compliance.[74] Data acquisition for the continuity equation, however, is more cumbersome than the pressure half-time. Doppler Velocity Index The Doppler velocity index (DVI) is a dimensionless ratio of the left ventricular outflow tract to prosthesis velocities: DVI = V /V LVOT TRANSPROSTHESIS Because it is independent of valve size, this index can be particularly helpful when the cross-sectional area of the outflow tract cannot be obtained. Because the velocity proximal to the valve is subtracted from that across the prosthesis, the patient serves as his or her own control, 530 with flow being the main dependent factor. The higher the index, the larger the area; the lower the index, the smaller the area. Index values calculated from 25 patients with normally functioning St. Jude Medical aortic valves were 0.39 ± 0.07, range 0.28 to 0.55. In a small group of patients with severe stenosis of St. Jude Medical aortic valves requiring reoperation, the DVI was 0.19 ± 0.05, range 0.12 to 0.27, which was significantly different from normal values at the 0.05 level.[75] Valve Resistance Resistance is the quotient of gradient and flow (R = ∆P/Q). This mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 7 hemodynamic parameter suggested by Ford et al[76] is an alternative to the Gorlin formula in assessing severity of native aortic stenosis. It can be calculated from echo-Doppler data as follows: Resistance = 1.33 ∆P (ET/SV) where ∆P is the mean pressure gradient in mm Hg, ET is the ejection time in seconds, and SV is the stroke volume in mL per minute. The ratio of mm Hg to mL per minute is converted to dyne-sec-cm5 when multiplied by 1.33. In conditions characterized by variation of flow, valve resistance remained more constant than the Gorlin estimated area. In considering valve resistance, however, one must recognize that most data have been derived from native valve stenosis, not from prostheses; no information is available during changing flow conditions, such as exercise; and there is virtually no clinical data in prosthetic mitral valves. Saad et al[75] studied two groups of patients with prosthetic aortic malfunction (predominant stenosis versus predominant regurgitation) and compared them with a control group. Effective orifice area (continuity equation), Doppler velocity index, and valve resistance were all very helpful in separating the groups. It is unclear, however, whether valve resistance per se added clinically significant information beyond that derived by valve area and Doppler velocity index. An important role of valve resistance in artificial valves may be in patients with small aortic valve areas, relatively low flow velocities, and severe left ventricular systolic dysfunction, to differentiate severe prosthetic valve stenosis from a low cardiac output state, which has been shown to be useful in patients with native aortic stenosis.[77] Pressure Half-Time The pressure half-time is the time required for the peak velocity to decline by a factor of 1 divided by the square root of 2, and it can be helpful in separating normal from obstructed prostheses. The pressure half-time is dependent on several factors, including atrial and ventricular compliance, ventricular stiffness, and, of course, the actual effective orifice area (EOA). Pressure half-time is used to calculate the EOA of mitral and tricuspid valve prostheses based on the inverse relationship between pressure half- time and valve area[78] EOA (cm2 ) = 220 / pressure half-time (msec) mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 7 Validation of this method with invasive data has showed good correlation. Kapur et al[79] compared mitral valve areas derived by pressure half-time with those derived by the Gorlin formula in 32 patients with mitral valve prosthesis and found correlations of 0.94 and 0.79 for bioprosthetic and mechanical valves, respectively. In contrast, Wilkins et al,[59] using simultaneous catheterization and Doppler techniques in 11 patients with mitral prosthesis, found poor correlation. This method relies on the constant, 220, which was originally derived for native rheumatic mitral stenosis. Application of this constant to the wide variety of valve types and sizes cannot be expected to yield predictable results.[3] The continuity equation is an excellent alternative to the pressure half-time to calculate mitral valve area. [80] Leakage Backflow Prosthetic mechanical valves have a normal regurgitant volume known as leakage backflow that occurs when the valve occluder has already been seated and blood leaks into the proximal chamber between and around the occluder assembly. In theory, this "built-in" regurgitation prevents stasis and thrombus formation by a "washing" mechanism. The jets of leakage backflow are characterized by being short in duration, narrow, symmetrical (bileaflet valves), and having low velocities (nonaliasing) encoded in a homogeneous color—red or blue, depending on the transducer location (assuming Nyquist limit >0.53 m/sec). [81] [82] The normal regurgitant jets in the Carbomedics valve are larger than those of the St. Jude Medical. Abnormal jets, on the other hand, are longer in duration, wider, larger, asymmetrical across the valve midline, frequently eccentric ("hugging the wall"), extending far into the receiving chamber, and display a mosaic pattern reflecting high-velocity, turbulent flow. A jet with an unusual angle (i.e., one anteriorly directed toward the atrial appendage) is also typical of a paravalvular leak. Figure 24-5 depicts the typical appearance of a normal backflow in a bileaflet mitral valve (see Fig. 24-5A) . In contrast, a larger, wider, eccentric jet "hugging" the left atrial lateral wall characteristic of severe perivalvular regurgitation is seen (see Fig. 25-5B) . Table 24-2 highlights the differences between physiologic leakage backflow and pathologic regurgitant |
jets. TABLE 24-2 -- Physiologic Leakage versus Pathologic Regurgitation of mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 7 Mechanical Prosthesis Pathologic Jet Feature Physiologic Leakage Regurgitation Size Short and narrow Large and wide Symmetry Symmetrical (bileaflet valves) Asymmetrical Aliasing No (low velocity) Yes (high velocity) Eccentric No Yes 531 Figure 24-5 (color plate.) TEE longitudinal views of a normal CarboMedics valve in the mitral position (A). Two symmetrical regurgitant backflow jets are seen within the left atrium (LA). These jets are low velocity, nonaliased, and encoded in red. In contrast, a pathologic periprosthetic leak is seen in an abnormal valve (B). The jet is high velocity, mosaic in color, and eccentric, and it encircles the left atrial wall (open arrow). The normal regurgitant backflow jets (solid arrows) are also seen. See Table 24-2 for differentiation of physiologic versus pathologic jets. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/208.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 11 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Echocardiography of Normal Prosthetic Valve Function In general, the same principles used in native valves are applicable to artificial valves. Echocardiography has some limitations related to reverberations and shadowing from the interface between ultrasound and the foreign material composing the valve.[83] Intense reverberations projected behind the prosthesis can mask normal structures or instead create artifacts, leading to a misdiagnosis. Table 24-3 describes common limitations and technical errors or "pitfalls" as well as suggestions on how to overcome or minimize their impact. A complete examination should include estimation of pressure gradients and valve area, degree of normal or TABLE 24-3 -- Echocardiography of Prosthetic Valves: Pitfalls Technical Limitations or Pitfalls Suggestions Acoustic shadowing Use window in which ROI is not obscured by the valve's artifact. Consider TEE. Failure to detect peak Image from multiple windows. velocity Under- or Include proximal velocity in continuity equation if overestimation of it is >1 m/sec. valve gradient or effective orifice area Consider pressure recovery. Use mean valve gradient, not "peak-to-peak" or maximal instantaneous gradient. Unexpectedly high Consider high cardiac output setting, i.e., valve gradient or small tachycardia, anemia, sepsis. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 11 effective orifice area Calculate DVI and valve resistance. Compare to previous echo study. Consider prosthesis-patient mismatch. Consider valve thrombosis (TEE?). Consider pannus formation (TEE?). DVI, Doppler velocity index; ROI, region of interest; TEE, transesophageal echo. abnormal regurgitation, left ventricular size and function, native valve structure and function, and calculation of the pulmonary artery systolic pressure. M-mode recording may assist in evaluating disc or leaflet excursion, whereas color M-mode recording may assist in timing regurgitant jets. Two-dimensional (2D) imaging should begin by identifying the sewing ring, the occluder mechanism, and the surrounding area. The ball or disc is often indistinctly imaged because of echo reverberations. The leaflets of normal tissue valves should be thin with an unrestricted motion. A very helpful and frequently overlooked parameter for evaluation of prosthetic valves is comparison with prior studies. The importance of a timely baseline postoperative study cannot be overemphasized. In our institution we routinely perform an ultrasound examination prior to hospital discharge, or in the patient's first clinic visit. This initial study establishes the baseline gradients and area, the postoperative ventricular systolic function, and the systolic pulmonary artery pressure for that particular patient, at that particular time. This anatomic and hemodynamic profile is subsequently used whenever prosthetic dysfunction becomes a concern. How often "routine" echocardiographic follow-up studies should be performed is a controversial topic. Table 24-4 lists the recommended schedule for early and long-term follow-up of prosthetic heart valve evaluation. Follow-up for nonstented bioprostheses and homografts clearly should be different from stented bioprostheses, because nonstented bioprothesis deterioration rates are lower. The effective orifice area is not the sewing ring orifice; it is the remaining area not occupied by the valve occluder assembly. Normally functioning mechanical and stented bioprostheses, therefore, have higher velocities than native valves. The smaller the size of the bioprosthesis, the smaller the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 11 effective orifice area, and the higher the flow velocities. For homografts and the newest nonstented bioprostheses, the hemodynamic profile is near normal. Table 24-5 and Table 24-6 provide the normal range of in vivo velocities for mechanical and bioprosthetic valves in the aortic and mitral positions, respectively. 532 TABLE 24-4 -- Recommended Doppler Echocardiography Follow-up in Patients with Prosthetic Heart Valves Patient Category Recommendation EARLY POSTOPERATIVE Any type of valve Baseline study in all patients LONG-TERM FOLLOW-UP Stented Bioprosthesis Clinically normal Every 2 years for the first 6 years, then every year for 4 years, then every 6 months Patient-prosthesis mismatch Once a year Chronic renal failure Once a year Nonstented Bioprosthesis and Homografts Clinically normal Every 2 or 3 years Mechanical Valves Clinically normal Every 2 or 3 years Patient-prosthesis mismatch Once a year Echocardiographic Features by Valve Type Ball-and-Cage. The Silastic ball produces multiple echoes from its leading edge, obscuring other aspects of its structure. Flow through a normally functioning ball-and- cage valve is characterized by turbulence created by the high-profile ball in the center of the blood stream and by the eddies created as flow circulates retrogradely (Fig. 24-6) . Consequently, when compared with single and mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 11 double tilting disc valves, the hemodynamic performance of the ball-and- cage valve is less, with higher pressure gradients. This hemodynamic profile increases its intrinsic thrombogenicity because of blood cell damage.[15] Color flow in a normal ball-and-cage valve includes low- velocity closure backflow (2 to 5 mL per beat).[11] [84] Single Tilting Disc. Figure 24-7 illustrates a single tilting disc valve in the mitral position. The left panel illustrates the typical antegrade flow through the major and minor orifices in the correct orientation (major orifice toward the lateral aspect, away from the outflow tract) as opposed to the incorrect orientation seen on the right panel. Typical flow velocity of a single tilting disc valve is TABLE 24-5 -- Normal Doppler Values for Aortic Prostheses ‡ Peak Mean Area Velocity Gradient Area Mean Range Type (m/sec) (mm Hg) (cm2 ) (cm2 ) Starr-Edwards 3.1 ± 0.5 24 ± 4 * * Björk-Shiley 2.5 ± 0.6 14 ± 5 * * St. Jude Medical 3.0 ± 0.8 11 ± 6 * * Medtronic-Hall 2.6 ± 0.3 12 ± 3 * * OmniScience 2.8 ± 0.4 14 ± 3 * * Hancock 2.4 ± 0.4 11 ± 2 1.8 1.4–2.3 Carpentier- 2.4 ± 0.5 14 ± 6 1.8 1.2–3.1 Edwards Aortic 1.8 ± 0.4 7 ± 3 2.2 1.7–3.1 Homograft Toronto SPV † 2.2 ± 0.4 3 ± 4 2.2 2.0–2.8 Freestyle † 2.2 ± 0.4 3 ± 4 2.2 2.0–2.8 O'Brien † 2.2 ± 0.4 3 ± 4 2.2 2.0–2.8 ‡Data from references [5] [11] [14] [18] [19] [23] [38] [40] [41] [46] [51] [58] [67] [68] [69] [75] [88] [90] [95] and [103] . *Insufficient data available. †Nonstented bioprostheses. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 11 Figure 24-6 A, Normal diastolic intracavitary flow pattern. B, Disturbed antegrade flow across a ball-and-cage valve. Note the high-profile ball located in the center of the blood stream, creating turbulence and eddying as flow changes direction. around 2 m per second. Flow through the minor orifice consists of two jets separated by a well-defined wake behind the tilting disc but with a velocity similar to the major orifice. The appearance of the disc is characterized by echoes produced by its motion. Color flow in these valves includes a small amount of normal backflow (5 to 9 mL per beat), originated from small gaps around the perimeter of the valve. [85] [86] Hixson et al[81] have reported that the Medtronic-Hall valve has a large central regurgitant backflow that can extend back into the left atrium with aliasing, whereas the peripheral jets are nonaliasing, low-velocity flow. Double Tilting Disc. Figure 24-8 illustrates the anatomic orientation of a bileaflet valve in the mitral position during diastole and normal mitral inflow. The blood flow is near-laminar with a path similar to the laminar flow of the native valve. In the opening position, the hemidiscs appear as parallel lines with a short angle between them. Imaging of the normal valve includes the sewing ring and two distinct echoes in the opening position and a wide obtuse angle in the closing position. Identification of the two hemidiscs may be problematic with the standard approach of transthoracic echocardiography (TTE), particularly in the aortic position. However, multiplane TEE at the upper and midesophageal level can better visualize the hemidiscs for aortic and mitral positions. 533 TABLE 24-6 -- Normal Doppler Values for Mitral Prostheses * Peak Mean Area Velocity Gradient Mean Area Range Type (m/sec) (mm Hg) (cm2 ) (cm2 ) Starr-Edwards 1.8 ± 0.4 4.6 ± 2.4 2.1 1.2–2.5 Björk-Shiley 1.6 ± 0.3 5.0 ± 2.0 2.4 1.6–3.7 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 11 St. Jude Medical 1.6 ± 0.3 5.0 ± 2.0 2.9 1.8–4.4 Medtronic-Hall 1.7 ± 0.3 3.1 ± 0.9 2.4 1.5–3.9 OmniScience 1.8 ± 0.3 3.3 ± 0.9 1.9 1.6–3.1 Hancock 1.5 ± 0.3 4.3 ± 2.1 1.7 1.3–2.7 Carpentier- 1.8 ± 0.2 6.5 ± 2.1 2.5 1.6–3.5 Edwards Homograft 1.8 ± 0.4 6.4 + 3.0 2.2 1.9–2.9 *Data from references [5] [14] [58] [59] [69] [73] [80] [88] and [103] . In normally functioning bileaflet valves, color demonstrates a small amount of normal backflow (5 to 10 mL per beat) designed to decrease the risk of thrombosis by a "wash out" mechanism. TEE visualization of the bileaflet valve depends on the image orientation in the parallel or perpendicular position of the discs in relation to the sound beam. In the parallel position, the discs appear in profile as two lines. Color may reveal up to three distinct jets: two at the edges of the valve directed upward and outward; one centrally located and directed straight up. In the perpendicular position, the leaflets reflect dense reverberations into the ventricular cavity and color reveals a semicircular flare on the atrial aspect. As the probe is pulled or advanced, the central flare becomes narrower. [81] [82] The Carbomedics is a newer version of bileaflet mechanism with recessed pivots that may result in larger regurgitant jets.[87] Stented Bioprostheses. The cross-sectional appearance of porcine valves is that of three cusps and three struts with an echogenic sewing ring. Normal flow pattern is a bell- shaped central flow with a relatively flat velocity profile. Peak flow velocities commonly found in the aortic position are around 2.5 m per second, and in the mitral position are around 1.7 m per second. Mild backflow in normally functioning bioprostheses is less common than in mechanical valves, and it has been reported in up to 10% of the cases.[88] Nonstented Bioprostheses. Careful measurement of the patient's outflow tract or the sinotubular junction is mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 11 Figure 24-7 Single tilting disc mitral prosthesis. A, Correct anatomic disc orientation, allowing the major orifice flow to be directed away from the left ventricular (LV) outflow tract. B, Incorrect anatomic disc orientation, in which the major orifice flow is directed toward the LV outflow tract, creating turbulence. an important contribution of ultrasound in determining nonstented valve size.[89] After implantation, the appearance is of a normal trileaflet valve, with increased echogenicity in the annular region from the layer of fabric supporting the graft. [90] Reported hemodynamics are very encouraging with nearly-natural transvalvular gradients resulting in significant reduction in afterload and wall stress.[46] [47] [48] Ventricular remodeling through regression of cardiac hypertrophy may be an important predictor of survival after valve replacement, and hypertrophy regression as early as 6 months after valve replacement has been reported with nonstented valves.[91] Homografts. Preoperative or intraoperative TEE measurement of the aortic annulus has been used to select the correct homograft size.[51] The 2D imaging of the nonstented homograft is similar to the native aortic valve, with increased echoes at the level of |
the annulus resulting from the retaining sutures as the only hint that a new valve has replaced the native valve. Homograft failure commonly results from progressive aortic insufficiency; valve stenosis is rare.[92] [93] Long-term outcome with homograft valves is complicated by differences in harvesting, sterilization, and preservation, as well as differences in the surgical techniques applied. In the Ross procedure, TEE plays an important role in providing accurate measurement of the right ventricular outflow tract for choosing the homograft size. In addition, color flow Doppler within the left and right ventricular outflow tracts provides essential information regarding aortic and pulmonic regurgitation, respectively. For Figure 24-8 Double tilting disc mitral valve. A, Normal mitral inflow. B, Mitral inflow across a double tilting disc valve, with flow passing through three separate orifices, creating a near-normal flow pattern. 534 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 11 these reasons, in our institution intraoperative TEE is routinely performed during the Ross procedure. Valved Conduits and Composite Grafts. Valved conduits have been used most often in the repair of congenital heart disease. Reestablishing flow from the right heart to the pulmonary artery is often performed with a bioprosthesis. The echocardiographic evaluation should include definition of the anatomic relation of the valve conduit to the heart and the flow velocity through the proximal and distal aspects of the conduit. Careful Doppler evaluation of the entire conduit is necessary because stenosis can occur at either end or anywhere along the conduit. The extracardiac course of the conduit can result in variable angles and directions of flow; therefore, color Doppler may be helpful in defining the location of high-velocity flow. Additional windows from the subcostal, subclavian, and right parasternal windows may be necessary to align the Doppler beam. Composite grafts for left-sided valves are most commonly seen in patients with aortic valve and aortic root diseases such as connective tissue disorders (e.g., Marfan's syndrome), leading to aortic aneurysm or dissection. Complications include pseudoaneurysm of the ascending aorta caused by dehiscence, which can occur at the annulus, at the distal anastomosis with the native aorta, or at the coronary artery reimplantation site.[94] TTE is essential for serial follow-up. TEE can provide additional views of the aortic valve and ascending aorta and should be considered in the evaluation of symptomatic patients or in those in whom the precordial imaging suggests an aneurysm or pseudoaneurysm formation. Echocardiographic Features by Valve Position Aortic. Gradients and areas should be measured and averaged from at least three (sinus rhythm) to five (atrial fibrillation) beats. A clear understanding of the differences among peak gradient, maximal instantaneous gradient, peak-to- peak gradient, and mean gradient is essential to avoid confusion when they are compared to those derived by catheterization. The peak gradient obtained by Doppler closely correlates with the maximal instantaneous gradient derived by catheterization. The mean gradient obtained with either technique correlates very closely with each other. When Doppler and fluid- filled pressure gradients are recorded at the same time in the catheterization mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 11 suite, the degree of concordance is superb.[58] [59] [79] For example, Burstow et al[58] found excellent correlation for the mean gradient (tissue valves, r = 0.93; mechanical valves, r = 0.96) when data were recorded simultaneously; however, when they were not simultaneous, the correlations fell slightly (tissue valves, r = 0.85; mechanical valves, r = 0.87). Values derived with the continuity equation have correlated well with prosthesis size.[95] [96] Peak velocities as high as 3.5 to 4.0 m per second have been recorded in normally functioning prosthetic mechanical aortic valves. These high-flow velocities exist briefly at valve opening; however, the mean gradient usually falls within the normal range. The mean pressure gradient, therefore, and not the peak pressure gradient, Figure 24-9 (Figure Not Available) Simultaneous catheterization and Doppler recordings in a Starr-Edwards prosthesis (A) and a Braunwald-Cutter prosthesis (B) in the mitral position. Note the excellent pressure gradient correlations. (From Burstow DJ, Nishimura RA, Bailey KR, et al: Circulation 1989;80:504–514.) should be used in making clinical decisions, and it is the one to be reported for subsequent comparative studies on the same patient. If the mean pressure gradient is abnormally elevated, prosthetic valve stenosis should be suspected and TEE (or fluoroscopy) should be considered. Mitral. Echocardiographic assessment of mitral prostheses includes calculation of the mean pressure gradient and the effective orifice area. Similar to aortic prostheses, the mitral mean pressure gradient correlates very well with the mean gradient derived at the time of catheterization when both data are recorded simultaneously. As illustrated in Figure 24-9 (Figure Not Available) , the mean pressure gradient is the average of multiple gradient calculations across the Doppler spectral envelope. Assessment of mitral regurgitation is often difficult because reverberations shadow the left atrium. The parasternal long-axis view may be helpful in eccentric jets; however, for accurate determination of mitral regurgitation, multiplanar TEE is the method of choice. This approach is ideally suited for assessing the mitral valve because of its close proximity to the left atrium and the use of high-frequency transducers. The exact appearance of the mitral mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 11 535 valve depends on the valve's orientation and the degree of left atrial enlargement. During the examination, the valve sewing ring should be carefully searched at the midesophageal and transgastric levels. The left atrium and its appendage should be searched for spontaneous echo contrast and thrombus because they may be present in patients with prosthetic mitral valves even if they are in sinus rhythm and have normal left ventricular function.[97] Evaluation of pulmonary venous flow may be important in assessing severity of regurgitation. Tricuspid. Data with tricuspid valve prostheses are far more limited than data with left-sided valves. In many respects Doppler evaluation is similar to mitral prostheses. The prosthesis should be imaged from all available views (parasternal short-axis, parasternal right ventricular inflow, apical four- chamber, and subcostal views). Bioprostheses are preferred over mechanical valves because of their high thrombogenic potential in this position. Because flow across the right-sided chambers increases with inspiration, one should expect mild variations in the peak E wave velocity; therefore, three (sinus rhythm) to five (atrial fibrillation) beats should be taken for an average. Severe tricuspid regurgitation is frequently caused by dilation of the native annulus; therefore, annular rings are nowadays preferred over prosthetic valves to correct hemodynamically significant tricuspid regurgitation. TEE plays an important role in these cases by confirming annular dilation as the origin of the regurgitation and not an intrinsic leaflet abnormality. Pulmonic. Prostheses in this position are relatively uncommon in part because percutaneous balloon valvuloplasty Figure 24-10 Step-by-step recommended approach for evaluating a patient with suspected prosthetic valve dysfunction. Note that auscultation and TTE examination are the initial steps. TEE and cinefluoroscopy are intermediate steps; cardiac catheterization is the last. is an effective tool in hemodynamically significant stenosis.[98] When a surgical intervention is needed, valvotomy is frequently used to palliate the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 11 valve, and later in life a bioprosthesis can be used. As with the native pulmonic valve, the bioprosthesis is best seen from the parasternal short- axis and subcostal views. The more commonly used TEE views include the basal short-axis and the longitudinal views, which may be helpful in choosing the appropriate homograft size. Color flow Doppler examination within the right ventricular outflow tract is essential to document any residual regurgitation. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/209.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 15 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Echocardiography of Prosthetic Valve Dysfunction Figure 24-10 illustrates the recommended step-by-step approach in patients with suspected prosthetic valve dysfunction. A careful clinical examination has no substitute. TTE should always be included in the initial assessment. If a high gradient is detected, additional tests may be needed, including TEE and cinefluoroscopy. Cardiac catheterization and angiography provides important hemodynamic and pathologic confirmation in many cases; however, its use should be restricted to patients in whom TEE and cinefluoroscopy have not provided a definitive diagnosis.[5] For mechanical valves, cinefluoroscopy renders a better means to evaluate the actual valve opening and closing motion. It is clearly indicated whenever valve thrombosis is suspected. One needs to determine the valve's rotational 536 Figure 24-11 Radiographic side view of a bileaflet valve. In the opening position (A), the two discs form a 10-degree angle, whereas in the closing position (B), they form a 120-degree (<25 mm) or 130-degree (>27 mm) angle, depending on valve size. C, Photograph of a bileaflet mechanical valve in the opening position. orientation by positioning the imaging intensifier in a view perpendicular to the valve plane. The right anterior oblique cranial view is frequently used for this purpose, although occasionally a left anterior oblique caudal view may be needed. Depending on the valve type and radiographic characteristics (i.e., radiolucency, radiopacity), the discs appear as dense lines inside the circle formed by the valve housing mechanism. The fluoroscopic side view renders important information in determining the closing angle degree. To achieve the side view, the image intensifier mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 15 should be moved longitudinally 90 degrees and rotated transversely to a position in line with the valve leaflets. For the St. Jude Medical valve, the opening angle between the two parallel lines should be 10 degrees (Fig. 24- 11A) . In the closing position, the two lines form a wide obtuse angle in the form of a "V" (see Fig. 24-11B) ; for valves less than 25 mm the angle should be 120 degrees, and for valves greater than 27 mm it should be 130 degrees. A complete cinefluoroscopic examination can be performed in 15 minutes or less. Figure 24-12 Radiographic representation of a bileaflet valve in the opening position. A, A "frozen" leaflet. By cinefluoroscopy, only one leaflet moves during the cardiac cycle. B, Normal appearance as rotated 90 degrees. In the typical case of thrombosis of a double tilting disc prosthesis, only one leaflet may be moving, indicating leaflet entrapment. Figure 24-12 shows still frames recorded during cinefluoroscopy in a patient with valve thrombosis and entrapment. The opening (A) and closing (B) positions of a St. Jude Medical valve clearly indicate that the right-sided leaflet (near the patient's spine) remains "frozen" during the entire cardiac cycle, indicative of leaflet entrapment by the thrombus. Primary Mechanical Failure Dysfunction from an intrinsic valve problem is known as primary mechanical failure. This complication is rare in the use of current mechanical valves. The Starr-Edwards valve had a rare intrinsic problem called ball variance, in which changes of the ball resulted in emboli either from ball material or thrombi formed on the irregular or cracked ball.[99] [100] Figure 24-13 illustrates a classic example of ball variance with a crack seen across the 537 Figure 24-13 Pathologic specimen showing ball variance in a Starr- Edwards valve. Notice the crack seen across the midportion of the ball and a large thrombus entrapped between the ball and the cage. midportion of the ball and a large thrombus trapped between the ball and mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 15 the cage. Disc embolization from single or double tilting disc valves is rare. The older version of the Björk-Shiley valve had several reported cases of fractured struts resulting in disc embolization. The Björk-Shiley valve is no longer available in the United States, but this valve was implanted in thousands of patients who continue to require follow-up. Monostrut (available in Europe), a new Björk-Shiley valve, is designed so the inflow and outflow struts are machined from a single piece of alloy.[18] Disc fracture has been reported in 3 Medtronic-Hall and in 10 St. Jude valves.[18] Stented bioprostheses on the other hand, may undergo primary failure called calcific degeneration. This type of valve failure is characterized by restricted cusp motion leading to stenosis or cusp tears, which then leads to regurgitation and different |
degrees of mixed lesions.[101] [102] Flail cusp owing to leaflet tears is associated with severe regurgitation; therefore, the echocardiographic detection of a flail cusp has important therapeutic implications. Figure 24-14A illustrates the TEE image at the midesophageal level of a patient with a flail cusp in a stented bioprosthesis. Figure 24-14B shows the explanted bioprosthesis depicting the flailed cusp. A musical or "cooing" sound has been reported with pulsed Doppler in patients with perforated or torn leaflets, which result in a striated, "shuddering" appearance to the signal, referred to as harmonics. [103] [104] [105] Leaflet thickening in the absence of endocarditis most likely represents milder degrees of calcific degeneration; however, a thickened and often irregular appearance can also be seen in endocarditis. In patients with "fibrocalcific" changes on their cusps, the differentiation between calcific degeneration and endocarditis should be based on the clinical context.[103] [106] Thrombosis Thrombosis occurs almost exclusively in mechanical valves, leading to predominant stenosis with or without some regurgitation. Figure 24-15 illustrates a thrombosed Beall valve (disc-in-cage) in the mitral position in a patient presenting in pulmonary edema; in addition, a large left atrial thrombus is sitting in the posterior aspect of the left atrium. The onset of symptoms may be gradual or sudden, and its incidence does not vary significantly Figure 24-14 TEE, horizontal four-chamber view, demonstrating a flail cusp (FC) in a mitral stented bioprosthesis (A). The patient presented to the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 15 hospital with progressive dyspnea on exertion, orthopnea, and fatigue. Ten years earlier, his mitral valve was replaced with a Hancock bioprosthesis. B, The excised valve with one of the cusps flailed and the other two with signs of degeneration. LA, left atrium; LV, left ventricle; RA, right atrium. 538 Figure 24-15 Prosthetic valve thrombosis in a Beall valve. A, Parasternal long-axis view from a patient with a disc-in-cage prosthesis (c) in the mitral position. A large thrombus (th) is noted in the posterior left atrial (LA) wall. B, The excised valve with a large thrombus obstructing the disc motion. AO, aorta; RV, right ventricle. among different mechanical valves, except when the valve is in the tricuspid position. The low flow rate through the right-sided chambers is the most likely predisposing factor for the thrombosis rate as high as 20%, [107] limiting the use of mechanical valves in this position. Echocardiography should focus on determining the range of occluder motion. Several views should be used to determine the plane of maximal excursion. Bileaflet valves present a unique problem because thrombosis can affect only one hemidisc (see Fig. 24-12) . TEE is a sensitive and accurate tool for diagnosing prosthetic valve thrombosis and for evaluating the efficacy of thrombolytic therapy in the emergency room.[107] [108] [109] [110] Although reoperation is frequently recommended in these patients, thrombolysis has been used many times in critically ill patients who are not otherwise candidates for reoperation. Emergent surgery for acute valve thrombosis has a perioperative mortality of 30% to 40%, with the risk linked to the preoperative New York functional class, status of the left ventricular systolic function by echocardiography, urgency of operation, and concomitant coronary artery disease.[111] [112] [113] Thrombolytic therapy is a logical alternative to surgery in these high-risk patients. Numerous reports of the use of thrombolytics in acutely thrombosed mechanical valves have been published mostly in the form of case reports. [107] [109] [110] Table 24-7 includes the four largest series, representing nearly 90% of the total patients so far reported.[114] [115] [116] [117] As can be appreciated, the success rate is 81%; however, there are unavoidable complications including systemic emboli in 18% and an overall mortality rate of about 15%. In clinically stable patients with stuck leaflets and no mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 15 high-risk thrombi, thrombolysis is highly successful and safe, both in the primary episode and in recurrence.[117] The best thrombolytic regimen is yet to be established, but streptokinase has been the most commonly used. For patients with high-risk (i.e., large) thrombus, valve replacement is clearly indicated unless the surgical risk is prohibitive. Thromboembolism Despite the routine use of anticoagulants in patients with mechanical valves, thromboembolism remains a major cause of morbidity and mortality. The incidence of thromboembolic episodes, however, has been significantly reduced with anticoagulation to between 1% and 4% per patient per year, and the risk of serious bleeding on anticoagulation is between 1% and 5% per patient per year.[118] [119] [120] According to the two largest trials, there is no difference in embolization with stented bioprosthetic versus adequately anticoagulated mechanical valves.[118] [120] In the decision of valve replacement, one must consider underlying risk factors such as prior thromboembolism, atrial fibrillation, significant left ventricular dysfunction, left atrial enlargement, left atrial appendage thrombus, and hypertension. The single most attractive advantage of bioprostheses is that in most cases anticoagulation is not needed. The increased risk of reoperation noted with stented bioprostheses, however, is a high price to pay for the reduced risk of bleeding through avoiding anticoagulation. Newer tissue valves such as nonstented bioprostheses and homografts may prove to be durable and yet enjoy the benefit of avoiding anticoagulation. An interesting observation described with TEE is fibrin strands. [121] Fibrin strands are commonly located on the atrial aspect of mitral prostheses or on the ventricular aspect of aortic prostheses. As illustrated in Figure 24-16 , their appearance is that of thin structures a few millimeters in length moving independently from the leaflets. Fibrin strands should be distinguished from vegetations or thrombi by their chaotic movement in and out of the imaging plane. They are more commonly seen on mechanical valves, but they also have been reported on tissue valves, and they have been associated with a higher incidence of embolic events.[122] [123] In a study by Isada et al,[122] 539 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 15 TABLE 24-7 -- Combined Data for Patients with Left-Sided Prosthetic V Thrombosis Undergoing Thrombolytic Therapy Complications Deaths No. of Valve Clinical Reference Patients Location Success EMB HEM SURG TOTAL SURG TH Witchitz 12 8M/4A 69% 0 2 5 3 2 et al[114] Lorient 26 15M/11A 89% 5 0 4 4 2 Roudaut et al[115] Shapira et 12 12M 83% 4 3 2 0 1 al[116] Özkan et 36 * 28M/8A 89% 1 3 0 1 0 al[117] Total 86 63M/23A 82% 10 8 11 8 5 A, aortic; Emb, embolic; Hem, hemorrhagic; M, mitral; Surg, surgical; th thombotic or thromboembolic. *36 episodes in 32 patients. fibrin strands were found in 15 (18%) of 83 prosthetic mitral valve patients, and of those 15 patients, 8 (53%) had embolic events compared with 12 (18%) of 68 patients without strands. In contrast, fibrin strands have also Figure 24-16 (color plate.) TEE, horizontal four-chamber view, demonstrating fibrin strands (arrows) on the atrial side of a St. Jude Medical prosthesis (A). Chaotic movement of these structures in and out of the imaging plane characterizes real-time imaging. LA, left atrium; RA, right atrium; RV, right ventricle. Mild mitral regurgitation is noted in the medial aspect of the prosthesis. been detected in otherwise normal prosthetic valves.[121] Further studies are needed to determine the clinical significance of fibrin strands before clinical decisions are made based solely on their presence. Endocarditis mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 15 Prosthetic valves are at a high risk for endocarditis because of their foreign material and abnormal flows. Prosthetic valve endocarditis carries a significant morbidity and mortality. Older series reported a mortality rate as high as 75% with early endocarditis (<60 days) and 45% with late endocarditis (>60 days). In a more recent study evaluating echocardiographic findings and their relation to morbidity and mortality,[124] the presence of an infected prosthetic valve was a major risk factor for death. Five of 11 deaths related to endocarditis occurred in patients with prosthetic valves. The annual rate for late prosthetic endocarditis is estimated at 0.5% per year. [13] [19] , [118] , [120] According to the Veterans Cooperative[118] and the Edinburgh study,[120] there is no significant difference of endocarditis between mechanical and stented bioprosthetic valves; however, when compared with native valves, prosthetic valve endocarditis is more likely to be associated with ring abscess, conduction abnormalities, and a more grave prognosis. [125] Vegetations typically appear as irregular masses of echoes attached to the valve components commonly moving with the blood path. On tissue valves vegetations usually result in leaflet destruction, whereas on mechanical valves they may interfere with the occluder mechanism, resulting in stenosis, regurgitation, or both. Large vegetations (>10 mm) are associated with increased embolic complications.[126] , [127] Figure 24-17 shows a TEE at the midesophageal level in a septic patient with a stented bioprosthesis in the aortic position. The large echodense mass seen within the left ventricular outflow tract is consistent with a vegetation. Differentiation of vegetation from thrombus may be difficult and often impossible. An important hint is that endocarditis more commonly is associated with regurgitant lesions, whereas thrombosis more commonly is associated with stenotic lesions. Either condition, however, can be seen as mobile echodense masses. Thus, such separation primarily should be based on the clinical presentation and bacteriologic results. Rarely, both complications 540 Figure 24-17 TEE at the midesophageal level from the transverse (T) and longitudinal (L) views in a septic patient with a stented bioprosthesis in the aortic position. A large echodense mass in the left ventricular outflow tract is clearly seen (arrows). LA, left atrium; LV, left ventricle; RA, right atrium, RVOT, right ventricular outflow tract. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 15 may be present in the same valve. Figure 24-18 corresponds to a midesophageal view in a septic patient with a St. Jude Medical valve in the mitral position and a bioprosthesis in the tricuspid position. A large vegetation and a thrombus can be seen on the atrial aspect of the mitral valve. Early and accurate identification of septic complications TABLE 24-8 -- Sensitivity (Sens) and Specificity (Spec) of TTE versus TEE for the Diagnosis of Vegetations and Associated Abscesses in Patients with Endocarditis TTE TEE No. of No. of Patients Patients SENS SPEC SENS SPEC Reference Studied with PVE (%) (%) (%) (%) Mugge et al 105 25 58 ‡ 90 ‡ (1989)[127] * Taams et al (1990) 33 12 36 100 100 100 [128] * Daniel et al (1991) 118 34 28 99 87 95 [129] † PVE, prosthetic valve endocarditis; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography. *Identification of vegetations. ‡Insufficient data available, but smaller studies have reported specificity of TEE at 100%. †Identification of abscesses. Figure 24-18 TEE at the midesophageal level from the transverse view in a septic patient with a St. Jude Medical valve in the mitral position and a stented bioprosthesis in the tricuspid position. A large vegetation (veg) and a thrombus (th) are clearly identified within the left atrium. LV, left ventricle; RA, right atrium; RV, right ventricle. in patients with prosthetic valves have a significant impact on the decision- making process. TEE has dramatically improved the diagnostic accuracy in detecting vegetations, abscesses, and other complications associated with mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 15 prosthetic valve endocarditis. [127] [128] [129] [130] Studies comparing TTE and TEE have included both native and prosthetic valves in their analysis. Table 24-8 lists studies comparing the two modalities in which patients with prosthetic valves were included. Although prosthetic valves are not analyzed separately, the data clearly favors TEE as a superior imaging modality; therefore, TEE should be performed routinely in patients with suspected prosthetic valve endocarditis, most notably in patients who fail to improve on therapy. Development of a perivalvular abscess is associated with a grave prognosis and indicates the need for aggressive medical and surgical therapies.[131] [132] Clinical findings suggestive of an abscess include persistent sepsis despite appropriate antibiotics, new or worsening heart failure symptoms, and development of first-degree atrioventricular block or incomplete right bundle branch block. Figure 24-19 illustrates a range of possible outcomes of a prosthetic valve abscess. Rupture may occur into adjacent structures, including the pericardial sac creating cardiac 541 Figure 24-19 A to D, Clinical, electrocardiographic, and echocardiographic characteristics in septic complications of mechanical valves. AV, atrioventricular; CHF, congestive heart failure; RBBB, right bundle branch block. tamponade; however, a rather common outcome is the development of perivalvular dehiscence with |
a tunnel communicating the aorta with the left ventricular outflow tract and consequently severe perivalvular regurgitation. Emergent surgical treatment may be a lifesaving procedure in these acutely ill patients. Echocardiographic findings of perivalvular abscess include valve rocking, periaortic root thickening, or perivalvular echolucency.[133] As noted in Table 24-8 , identification of an abscess is very difficult from TTE; therefore, TEE is mandatory when this complication is clinically suspected. In addition, fistulous tracts connecting the perivalvular space with adjacent structures can be imaged and tracked down with color flow. Figure 24-20 represents the mid- and upper esophageal images in a septic, critically ill patient with a St. Jude Medical aortic prosthesis who presented to the emergency room with acute aortic insufficiency and pulmonary edema; a large perivalvular abscess is clearly noted. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 15 Patient-Prosthesis Mismatch The term patient-prosthesis mismatch refers to the clinical setting in which the prosthesis is structurally normal but the hemodynamic data are consistent with a greater stenosis than expected for the valve type and size. [134] [135] The mismatch occurs because the valve area is relatively insufficient to fit the patient's body surface area. A given valve area perfectly acceptable for a small relatively inactive subject may be inadequate for a larger physically active individual. This problem is usually seen in patients with small aortic annulus sizes and in whom the valve replacement was performed because of native valve stenosis rather than regurgitation.[134] From the clinical point of view, the patient fails to improve or may even be symptomatically worse. The long-term implications of this condition are not known. After successful aortic valve replacement, regression of cardiac hypertrophy is commonly detected. Failure to regress 6 months after surgery may be a subtle indication that residual aortic stenosis is present and that the hemodynamic burden persists.[136] [137] In some patients inadequate hemodynamics may be apparent only at higher cardiac output stages (i.e., during exercise). For patients with exertional symptoms suggesting high valve resistances without evidence of a primary valve dysfunction, stress echocardiography (see later) should be considered. The diagnosis of patient-prosthesis mismatch requires exclusion of an intrinsic valve dysfunction, which further emphasizes the need for a baseline postoperative study. Prosthetic Aortic Stenosis The initial suspicion of prosthetic valve stenosis may be the incidental finding of abnormally high flow velocities detected during a routine examination. This finding should prompt careful inspection from the parasternal long- and short-axis views to determine possible causes. In addition to thrombus formation, obstruction also can occur from gradual ingrowth of fibrous tissue called pannus formation. An encapsulated perivalvular abscess may reduce the outflow tract area leading to stenosis. Figure 24-21 shows images from a patient with a homograft and a sterile perivalvular cavity reducing the effective orifice area. In the absence of symptoms and if there is normal valve motion otherwise, close follow-up is probably appropriate. Alternatively, stress echocardiography may be necessary to unmask a truly symptomatic stenosis or to address the patient's or referral physician's concerns. If the valve area calculated from TTE data mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 15 is markedly reduced, 542 Figure 24-20 TEE in a septic patient with a St. Jude Medical aortic valve. A, Partial dehiscence and a large abscess cavity (arrow). B, Cross-sectional view of the same pathology. The abscess cavity is composed of echodense and echolucent material (arrow). AO, aorta; LA, left atrium; LV, left ventricle; RA, right atrium. we commonly reassess the aortic valve area (continuity equation) by combining the diameter of the left ventricular outflow tract accurately determined by TEE at the upper-midesophageal level with the transthoracic velocity time integrals obtained during the same setting. Prosthetic Mitral Stenosis Valve area should be routinely calculated from the pressure half-time or the continuity equation (or both) in patients with suspected prosthetic mitral stenosis. Although an E wave velocity greater than 2 m per second may be indicative of prosthesis stenosis, increased velocities in the absence of a prolonged pressure half-time may be a result of prosthetic regurgitation.[2] Color flow can aid in aligning the Doppler beam parallel to the mitral inflow in obtaining the most representative Doppler signal. Mean valve gradient should be combined with pressure half-time or flow volume determination to differentiate prosthesis stenosis from increased transvalvular volume. As noted earlier, TEE is a very useful tool for detecting thrombosed mitral prosthesis and guiding thrombolytic therapy; thus, TEE should always be performed in patients in whom stenosis is suspected. Prosthetic Aortic Regurgitation The approach to grading prosthetic regurgitation is similar to that of native valves and involves evaluation of several echo-Doppler indices. As with native valve regurgitation, ventricular size and function are important clues to the severity of regurgitation. Normal left ventricular internal dimensions is incompatible with severe chronic Figure 24-21 TTE of a patient with stenosis of an aortic homograft. A, Parasternal long-axis view showing an encapsulated antibiotic-sterilized mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 12 di 15 cavity (C), which reduces the outflow tract diameter (LVOT) in half (arrows). B, Continuous wave Doppler from the five-chamber view in the same patient with elevated velocities up to 4.0 m/sec, maximal gradient of 64 mm Hg, and a mean gradient of 34 mm Hg. The continuity equation valve area was estimated at 0.7 cm2 . LA, left atrium. 543 aortic regurgitation. Jet height and area from the short-axis view have been compared with angiographic grading in native valve regurgitation with excellent correlations of 0.93 and 0.91, respectively.[138] [139] In our laboratory we have found the parasternal long-axis view a more useful view to assess the jet area in relation to the left ventricular outflow tract area. Eccentric valvular or perivalvular jets may overestimate the severity of prosthetic regurgitation because they may be directed perpendicular to the outflow tract, occupying a larger portion of the ventricular outflow tract area. The apical five-chamber view should also be used to determine jet characteristics. The pressure-half time can be helpful in differentiating chronic from acute regurgitation. In general, acute (commonly severe) aortic regurgitation has a rapid slope decay indicative of acute elevation of left ventricular pressures at end-diastole. Although highly specific, this finding is poorly sensitive because the decay slope may be altered by changes in diastolic function, particularly ventricular compliance, heart rate, and rhythm. Thus, patients with severe chronic aortic regurgitation and a compliant left ventricle may have an aortic-ventricular diastolic pressure slope similar to patients with milder degrees of aortic regurgitation. Consequently, in many patients the Doppler diastolic slope decay helps in differentiating acute from chronic regurgitation, but not severe from moderate regurgitation. The intensity of the continuous wave Doppler signal may help in assessing severity of regurgitation. In patients with severe regurgitation, the signal intensity of the forward and regurgitant flows are similar. Unfortunately, such estimation is subject to wide interobserver variations. In addition, signal intensity depends highly on the specific gain settings on different ultrasound systems and even in the same machine. Thus, in our laboratory an intense Doppler signal of aortic insufficiency is a hint that the severity of regurgitation is more than mild. The amount of flow reversal in the descending thoracic aorta also has been correlated with severity. Normal flow reversal in the ascending aorta is confined to the early part of diastole, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 13 di 15 whereas flow reversal that persists throughout diastole is seen in patients with severe regurgitation.[3] [81] TEE may provide important etiologic information such as primary mechanical failure (i.e., flail cusp), ring dehiscence, vegetations, or abscess formation with a paravalvular fistula (see Fig. 24-19D) . Additionally, TEE offers an excellent visualization of the ventricular outflow tract area for severity assessment based on the relation of jet area and ventricular outflow tract area. Finally, evaluation of the ascending aorta for aneurysmal dilation or dissection should be part of the TEE examination in these patients. Prosthetic Mitral Regurgitation Assessment of mitral regurgitation by TTE is problematic because reverberations from the metallic material of the prosthesis commonly obscure the left atrium. This problem is less noticeable with bioprostheses. Nevertheless, the common practice in our laboratory is to turn to TEE every time there is clinical or TTE suspicion of pathologic mitral regurgitation, regardless of the type of prosthesis. Color Doppler demonstrating flow convergence or a clearly visible proximal isovelocity surface area on the ventricular aspect of the valve is suggestive of severe regurgitation. The maximal area of the acceleration signal has been used to assess severity of mitral regurgitation.[140] Similar to aortic insufficiency, the intensity of the continuous wave Doppler signal is related to severity; the more intense the signal, the more severe the regurgitation.[71] Significant regurgitation has a density similar to the antegrade flow signal.[141] A recent evaluation of TTE for evaluating prosthetic mitral regurgitation compared proximal isovelocity surface area, intensity of the Doppler signal, and color Doppler jet within the left atrium.[142] Flow convergence was more sensitive but less specific for predicting significant prosthetic mitral regurgitation. Doppler indices used for severe native valve regurgitation also may be helpful in prosthesis regurgitation, such as increased E wave velocity (>2 m/sec), increased mean gradient (>5 to 7 mm Hg), short pressure half-time (<100 m/sec), and increased time velocity integral (>40 cm).[6] [142] [143] Unexplained, worsening, or new pulmonary hypertension may be indicative of significant regurgitation. TEE has substantially improved the diagnostic accuracy of the jet characteristics for determining severity and etiology of prosthetic regurgitation. [4] [144] Remember that color Doppler is a measure of velocity and not of volume, and although the jet area may be relatively small, mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 14 di 15 eccentric jets may result from severe regurgitation, particularly when they wrap around ("hug") the left atrial wall (Fig. 24-22) . An eccentric jet of severe mitral regurgitation loses momentum and velocity as it contacts the atrial wall despite a large volume, a phenomenon known as the Coanda effect.[145] In our laboratory, we use an eccentric jet as an evidence of severity. In fact, most cases of eccentric regurgitation hugging the lateral wall of the left atrium Figure 24-22 (color plate.) TEE from the transverse plane (0 degrees) illustrating a large, eccentric jet of severe mitral regurgitation. 544 enter into one of the pulmonary veins or into the left atrial appendage, confirming severe mitral regurgitation. Prosthetic valve dehiscence, that is, a separation of the prosthetic sewing ring from the native fibrous ring, is caused by detachment of the retaining sutures. Careful TEE evaluation of the annulus at the midesophageal and transgastric levels can reveal a dropout of echoes; when color Doppler is applied, an eccentric jet may become obvious. Detection of valve dehiscence is important because it usually means severe regurgitation requiring surgical repair or replacement. Figure 24-23 is a set of TEE images illustrating a patient with a Hancock bioprosthesis in the mitral position with dehiscence and severe eccentric regurgitation. The morphology of the pulmonary vein Doppler waveform is dependent on both volume of regurgitation and left atrial properties. Pulmonary vein flow characteristics have been useful in assessing severity of native mitral valve regurgitation. Typically, there is loss of the systolic wave amplitude and eventually reversal of systolic flow as the Figure 24-23 (color plate.) TEE showing dehiscence in a stented mitral bioprosthesis with perivalvular regurgitation. A and C, The dehiscent site (arrows) is seen as a dropout of echoes at the annular attachment. B and D, Eccentric severe paravalvular regurgitation is seen through the dehiscence. LA, left atrium; LAA, left atrial appendage; LV, left ventricle; RA, right atrium; RV, right ventricle. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 15 di 15 severity of regurgitation increases from moderate to severe. These changes should not be interpreted as an absolute measure of regurgitant severity, however. In vivo models suggest that pulmonary venous flow reversal is more likely in acute versus chronic mitral regurgitation because the atrium is less compliant and has a smaller initial volume.[146] In addition, characterization of the pulmonary vein flow in prosthetic mitral regurgitation is lacking, and extrapolation of the data from native to prosthetic valves has not been documented. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/210.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others |
in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Stress Echocardiography in Assessing Prosthetic Valve Function In patients with suspected prosthetic valve dysfunction, one may encounter symptomatic patients in whom the 2D and Doppler imaging indicates normal valve function at rest. Under these circumstances, exercise echocardiography may elicit abnormal hemodynamics indicating valve 545 TABLE 24-9 -- Prosthetic Valve Exercise Doppler Hemodynamics Mean Gradient (mm Hg) * No. of Valve Sizes EXERCISE INCREASE Patients (mm) REST † (%) Aortic Position Carpentier- 4 21 15 ± 3 21 ± 3 70 Edwards Medtronic- 14 21 15 ± 4 24 ± 6 80 Hall Medtronic- 14 21–27 9 ± 4 15 ± 6 83 Hall St. Jude 17 21–27 11 ± 4 18 ± 7 81 Medical Mitral Position Björk-Shiley 11 25–31 4.9 ± 10.3 ± 100 1.8 2.9 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 Starr-Edwards 6 28–32 4.6 ± 12.6 ± 130 1.2 4.1 St. Jude 17 26–32 2.5 ± 5.1 ± 3.5 102 Medical 1.4 Medtronic- 15 26–32 3.0 ± 7.0 ± 2.9 116 Hall 1.1 Data from Tatineni et al,[147] Wiseth et al,[148] and Halbe et al.[150] *Mean ± SD. †Exercise protocols used were symptom-limited treadmill and upright or supine bicycle. dysfunction or patient-prosthesis mismatch. In our laboratory, we prefer supine bicycle ergometry over treadmill because serial hemodynamic data can be obtained at different exercise stages. Normal hemodynamics with stress in these patients excludes valve dysfunction as the cause of the patient's symptoms. Valve gradient, valve area, degree of regurgitation, and systolic pulmonary artery pressure can all be calculated at rest and at peak stress (or immediately afterward). Despite its clinical potential, relatively few stress echocardiographic studies in patients with suspected prosthetic valve dysfunction have been published.[61] [147] [148] [149] [150] Table 24-9 summarizes data available regarding valve gradients at rest and with exercise. Dobutamine provides an excellent alternative for evaluating valve hemodynamics when the patient is unable or unwilling to undergo treadmill exercise or bicycle ergometry.[151] In our laboratory we use a protocol similar to that for ischemic heart disease; that is, we attempt to reach at least 85%, or ideally 90%, of the maximal predicted heart rate according to the patients' age and gender. We start with IV administration of dobutamine at 10 µg/kg per minute and increase sequentially every 3 minutes to 20, 30, and 40 µg/kg per minute. If the Doppler signal intensity of tricuspid regurgitation is weak because of trivial or mild regurgitation, we routinely add a small amount of diluted Optison to enhance signal intensity, allowing calculation of systolic pulmonary artery pressure. In patients with single tilting disc prostheses in the aortic position, peak and mean gradients are higher with the dobutamine stress echocardiography compared with symptom-limited treadmill exercise.[152] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 Evaluation of the patient with decreased left ventricular systolic function and possible prosthetic aortic stenosis is problematic. In 24 adults with native aortic valve stenosis (area ≤ 0.5 cm2 /m2 ), mean gradient less than 30 mm Hg, and ventricular dysfunction (ejection fraction ≤ 0.45), deFilippi et al[153] performed echocardiography at baseline and at peak dobutamine stress to distinguish severe fixed aortic stenosis from flow-dependent (relative) aortic stenosis. Three hemodynamic subsets were identified: (1) fixed aortic stenosis with increased cardiac output and transvalvular gradient and no change in valve area; (2) relative aortic stenosis with increased valve area but no change in gradient; and (3) lack of contractile reserve with indeterminate stenosis because of inability to increase cardiac output.[153] Theoretically, a similar study may be applicable, although not yet proved, in patients with severe ventricular dysfunction and prosthetic stenosis of undetermined severity. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/211.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Three-Dimensional Echocardiography in Assessing Prosthetic Valve Function Current echocardiographic approaches to determination of effective orifice area are based on flow characteristics. Flow characteristics, however, also depend on several factors in addition to the actual orifice area, including ventricular compliance, systolic function, and loading conditions. A classic dilemma is the patient with a mechanical aortic valve with high flow velocities detected in a routine Doppler examination. Is this a normal finding? Is it consistent with pannus formation and therefore with some stenosis? Is this a patient-prosthesis mismatch? An echocardiographic technique that actually allows us to visualize the orifice size would likely improve our diagnostic abilities. Three-dimensional echocardiography involves the acquisition and display of cardiac structures in three spatial dimensions allowing their visualization and analysis as they move in time and space. Figure 24-24 illustrates a commonly used rotational scanning mechanism in which the transducer is rotated at 3-degree increments up to 180 degrees. Dynamic 3D imaging may provide a more realistic representation of prosthetic morphology than 2D images. Recent advances in ultrasound equipment, digital storage, and display techniques have made 3D clinically feasible; however, the clinical potential of 3D imaging has just begun to be recognized, and there are no published data on the use of 3D technology in assessing prosthetic valve function. Figure 24-25 depicts a 3D reconstruction of a St. Jude Medical valve performed in our laboratory. The two hemicircular lateral orifices and the central rectangular orifice are clearly indicated. Mitral annular rings have been reconstructed with 3D 546 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 Figure 24-24 Left, The rotational mechanism for acquisition of two-dimensional images at 3-degree intervals from 0 to 180 degrees. Right, The two- dimensional images are piled up one after another, gated by the electrocardiogram. Figure 24-25 Three-dimensional reconstruction of a St. Judge Medical valve in the mitral position as seen from the left atrium or "surgeon's view." The semicircular orifices (curved arrows) and the rectangular orifice (straight arrow) are seen. 547 technology.[153] Dall'Agata et al[154] used TEE to analyze mitral valve rings in 19 consecutive patients who underwent annuloplasty because of severe regurgitation. Fifteen patients received a Cosgrove-Edwards (flexible) ring and four received a Carpentier (rigid) ring. Imaging acquisition used the rotational technique immediately after the operation and was considered to be adequate in 17 of 19 patients. The authors were able to differentiate values from end-systolic to end-diastolic orifice areas (4.2 ± 1.5 cm2 versus 4.8 ± 1.5 cm2 ; P < .0001) in the Cosgrove-Edwards ring, and no significant change in the Carpentier ring.[154] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/212.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company 551 Chapter 25 - Echocardiographic Recognition of Unusual Complications After Surgery on the Great Vessels and Cardiac Valves William A. Zoghbi MD The surgical approach to treating diseases of the aorta and cardiac valves has evolved dramatically over the past two decades. Concurrent with these developments, echocardiography and particularly Doppler techniques have been refined, allowing a better definition of cardiac structures and flow dynamics. Furthermore, transesophageal echocardiography (TEE) has improved the diagnostic capabilities of sonographic techniques by providing superior imaging of the aorta and cardiac structures, thus increasing the diagnostic impact of echocardiography in patients with diseases of the aorta and cardiac valves. A variety of complications, however, may occur in patients undergoing surgery on the great vessels and cardiac valves. These complications may occur early or late in the postoperative period and include infection, thrombosis, obstruction or dehiscence of prosthetic material, and progression of the underlying disease disorder, particularly in diseases of the aorta. Recognition of diseases of the aorta and of the infectious complications and dysfunction of prosthetic valves has been addressed elsewhere in detail ( see Chapter 23 and Chapter 24 ). This chapter focuses mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 on unusual complications following surgery on the aorta and cardiac valves and the role of echocardiographic techniques in assessing these complications. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/214.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 12 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Unusual Complications Following Surgery on the Aorta Pseudoaneurysms of Composite Aortic Grafts Clinical Setting In patients with aortic aneurysm or those with dissection of the aortic root involving the aortic sinuses and aortic valve, which are not amenable to repair, replacement of the aortic root with a composite graft is now widely accepted. [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] First reported, in 1968, by Bentall and De Bono,[1] and more recently modified since then, [5] , [6] [10] [11] [12] [13] this surgical procedure has significantly prolonged the life expectancy of patients affected with annuloaortic ectasia.[5] [9] [14] Knowledge of this procedure, its variations, and complications is crucial for the echocardiographer, particularly because echocardiography with Doppler has emerged as a powerful diagnostic modality in assessing the function and complications of composite aortic grafts. The original Bentall procedure consists of replacing the aortic root and valve with a composite aortic graft 552 (ascending aortic graft and prosthetic aortic valve). The coronary arteries are reimplanted onto the graft, and the aorta is wrapped around the graft to improve hemostasis.[1] [2] [3] [4] [15] Among the complications of composite aortic grafts is the development of a pseudoaneurysm of the ascending aorta. This pseudoaneurysm occurs secondarily to dehiscence of the suture line at the aortic annulus, the coronary ostia, or the distal graft anastomosis. In patients with composite grafts who underwent the original Bentall procedure, this potentially lethal complication was reported to occur at a rate of 7% to 25%. [3] [16] [17] [18] [19] Modifications of the original method have since been proposed to decrease the incidence of pseudoaneurysm mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 12 formation.[2] [5] [6] [11] [12] [13] In 1981, Cabrol et al[2] modified the operation by introducing a second tube graft connecting the coronary ostia and the main ascending aortic graft (Fig. 25-1) . In 1991, Kouchoukos and co-workers[5] showed that the "open," or "button," technique for reimplantation of the coronary arteries led to a lower incidence of pseudoaneurysms. With the present modifications, the incidence of pseudoaneurysm formation has decreased to less than 6%.[5] [7] [8] [9] [12] [19] [20] [21] [22] The clinical symptoms associated with pseudoaneurysm formation vary. Whereas some patients have nonspecific symptoms or may be completely asymptomatic, other patients may be severely limited by dyspnea and fatigue. Given the possibility of aortic rupture, early diagnosis of aortic pseudoaneurysm is therefore essential. Echocardiography with Doppler and, more recently, TEE have had a significant impact on the detection of pseudoaneurysms and the evaluation of patients with composite grafts.[18] [23] [24] [25] [26] [27] [28] [29] [30] Figure 25-1 (color plate.) Diagram of the surgical reconstruction of the aortic root in a patient with ruptured aortic dissection, using a composite aortic graft (modified Cabrol technique). The native aortic root is excised and replaced with a composite graft. A tube graft connects the aortic graft to the left main coronary artery. A vein graft (dark blue) was used in this case to bypass a stenosed right |
coronary artery. (Courtesy of Dr. Hazim J. Safi.) Echocardiographic and Doppler Findings A normal composite aortic graft is visualized with echocardiography as an echo-dense ascending aortic root, with a prosthetic valve in the aortic position. The maximal diameter of the composite graft depends on the size of the graft. In 27 patients with normal composite grafts evaluated in the author's institution, the diameter of the ascending aorta ranged from 3.2 to 5 cm (mean of 4.2 cm).[18] In patients whose native aorta wrapped the graft, a small echo-free space between the graft and the wall of the aorta was seen in most patients (80%) and usually was small, ranging from 0 to 1.4 cm (mean 0.6 cm).[18] In all cases of normal composite graft, Doppler examination showed no evidence of flow in this small echo-free space and the presence of only trivial aortic insufficiency. Echocardiography can provide important diagnostic information about the presence of the pseudoaneurysm and the site of dehiscence of the surgical anastomosis.[18] [31] [32] [33] The identification of an enlarged ascending aorta with an echo-free space around the aortic graft should prompt investigation mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 12 for the presence of a pseudoaneurysm. Other considerations include a hematoma without pseudoaneurysm or, depending on the clinical setting, the presence of graft infection with abscess formation. The space around the graft may contain varying amounts of echo-dense debris or thrombus. A pseudoaneurysm is diagnosed as an enlarged ascending aorta with an echo- free space between the aortic graft and the wall of the aorta, along with the demonstration of flow into the echo-free space (Fig. 25-2) .[18] [31] [32] In a series of patients with pseudoaneurysms diagnosed in the author's institution, [18] 553 Figure 25-2 (color plate.) Echocardiographic and Doppler findings using transthoracic echocardiography in a patient with a large pseudoaneurysm of the ascending aorta complicating a composite graft. The dehiscence was at the aortic annulus anastomosis. A and C show the extent of the pseudoaneurysm as delineated by the arrows in short-axis (A) and long-axis (C) views. The origin and extent of the systolic jet into the pseudoaneurysm are shown in B and D in the same image planes as in A and C. During diastole (E), blood converges from the pseudoaneurysm toward the aortic annulus and enters the left ventricle (arrow) through the dehiscence, mimicking aortic insufficiency. The corresponding angiographic findings are shown in Figure 25-9 . GR, aortic graft; LA, left atrium; LV, left ventricle; PSA, pseudoaneurysm. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.) the maximal diameter of the ascending aorta ranged from 6 to 14 cm. The maximal echo-free space between the aortic graft and the wall of the ascending aorta ranged from 2 to 7 cm. This space may be eccentric or concentric around the graft. Although most cases of pseudoaneurysms report more than 2 cm of echo-free space surrounding the graft, the demonstration of flow into the space outside the graft is essential for the diagnosis, irrespective of the size of the echo-free space. Once a pseudoaneurysm is suspected, special attention is directed to imaging the ascending aorta, aortic root, the plane of the prosthetic valve, and the coronary ostia from the left and right parasternal and suprasternal windows. In cases of pseudoaneurysms, color-flow Doppler imaging frequently demonstrates evidence of a pulsatile flow jet into the echo-free space between the graft and the wall of the ascending aorta (see Fig. 2) . This finding confirms the entity of pseudoaneurysm, as opposed to the mere presence of blood or fluid collected around the graft (Fig. 25-3) . In mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 12 the author's experience, however, transthoracic color-flow examination may not identify flow in the echo-free space in some patients. In these cases, transesophageal examination clearly demonstrates flow into the pseudoaneurysm (Fig. 25-4) . This limitation is the result of the lower resolution and sensitivity of surface echocardiography combined with posterior shadowing from the graft and aortic prosthesis. Transthoracic and transesophageal echocardiography do provide complementary information regarding the status of a composite aortic graft. If any suspicion arises about the presence of a pseudoaneurysm, a TEE is clearly indicated for further evaluation of the abnormality. Following is a description of Doppler echocardiographic findings observed with composite graft pseudoaneurysms. 554 Figure 25-3 Transesophageal horizontal plane demonstrating a large hematoma (arrows) surrounding a composite aortic graft (G) in a patient early after operation. There was no flow detected around the graft by Doppler echocardiography at any level. Th, Thrombus. The hematoma was secondary to postoperative bleeding complications. Aortic Annulus Dehiscence In cases of dehiscence at the aortic annulus anastomosis, with ensuing communication between the left ventricle and the pseudoaneurysm, color- flow Doppler identifies a systolic jet arising from the paraprosthetic valve area, directed cranially into the pseudoaneurysm ( see Fig. 25-2 and Fig. 25-4 ). Because the jet frequently is eccentric, the imaging plane showing the flow jet in the long axis of the aortic root usually is lateral or medial to the plane showing the aortic graft. Thus, the flow jet and aortic graft may not be seen in the same longitudinal plane (see Fig. 25-2) . The short-axis view at the level of the prosthetic aortic valve demonstrates the jet arising in the Figure 25-4 (color plate.) Transesophageal echocardiographic frames and corresponding color Doppler systolic frames in a patient with composite graft pseudoaneurysm. The transthoracic examination in this patient did not demonstrate flow in the pseudoaneurysm. The upper panels are at the level of the ascending aorta; the lower panels are at the prosthetic aortic valve level. The dehiscence at the aortic annulus is depicted by a mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 12 straight arrow. Color flow Doppler demonstrates flow into the pseudoaneurysm. GR, aortic graft; LA, left atrium; LV, left ventricle; PrV, prosthetic valve; PSA, pseudoaneurysm. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.) paravalvular area and oriented into the pseudoaneurysm. Short-axis views from a more cranial angle demonstrate the orientation of the jet in the pseudoaneurysm in relation to the aortic graft. These considerations apply for both transthoracic and TEE imaging ( see Fig. 25-2 and Fig. 25-4 ). Generally, detection of the dehiscence and flow into the pseudoaneurysm is much easier with TEE than with the transthoracic approach. In most cases of dehiscence at the aortic annulus, continuous-wave Doppler views from the apical window demonstrate two distinct systolic jets: one coursing through the prosthetic valve and another coursing through the left ventricular-pseudoaneurysm communication (Fig. 25-5) . In the author's experience, the maximal velocity and derived pressure gradient through the communication have been higher than those through the prosthesis.[18] The systolic jet through the dehiscence frequently starts before the opening click of the prosthetic valve, and its duration is usually longer than the ejection time through the valve (see Fig. 25-5) . In all cases of dehiscence of the aortic annulus, a diastolic jet is seen in the left ventricular outflow, simulating valvular aortic insufficiency. In these cases, concomitant aortic insufficiency arising from within the valve usually cannot be excluded with confidence; however, with TEE, the mechanism of regurgitation can be much better defined. Continuous-wave Doppler recording of these diastolic jets also shows a short pressure half-time, mimicking severe aortic insufficiency. In some cases, an abrupt termination of diastolic flow before the prosthetic aortic-valve click at the onset of early systolic flow through the communication supports the conclusion that this regurgitation is not occurring through the aortic valve (see Fig. 25-5) . Coronary Artery Dehiscence Coronary artery dehiscence is diagnosed by color-flow Doppler as a jet arising from the level of the coronary ostia or coronary anastomosis and directed into the pseudoaneurysm. Dehiscence 555 Figure 25-5 Continuous wave Doppler from the apical window of the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 12 patient with aortic annulus dehiscence shown in Figure 25-2 . Recordings are obtained from the same position on the chest wall, with minor change in angulation. Compared with the systolic jet velocity through the prosthetic aortic valve, the systolic jet through the ventricular-pseudoaneurysm communication has a higher maximal velocity (Vmax), is of longer duration, and starts (oblique arrow) before the first click of the prosthetic valve (horizontal arrow). The diastolic regurgitant jet into the left ventricle has a steep deceleration slope and ends before the first systolic aortic valve click (upper panel, straight arrow) at the time of onset of systolic flow into the pseudoaneurysm. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.) usually is easier to define in patients in whom the pseudoaneurysm is large because of the more defined spatial distribution of the jet. Various flow patterns may be recorded, as shown in Figure 25-6 . Whether the flow is predominantly systolic into the pseudoaneurysm or systolic and diastolic depends on factors such as the compliance of the pseudoaneurysm and whether a communication exists between the pseudoaneurysm and the left ventricle. Compression of the Composite Graft or Adjacent Structures Compression of the graft may result from hematoma or pseudoaneurysm formation[27] and is most commonly observed with aortic annulus dehiscence. With two-dimensional echocardiography, pulsatile compression of the graft can be seen during systole (Fig. 25-7) , most likely because of the high pressure surrounding the graft and possibly a Venturi phenomenon occurring within the graft. Using continuous-wave Doppler, a high-velocity systolic jet can be recorded, a finding similar to that seen in an obstructed prosthetic aortic valve. Differentiation of the two entities may be difficult; however, visualization of the pulsatile compression of the graft provides a good assessment of the underlying condition. If the pseudoaneurysm is extensive, it may compress adjacent structures. Compression of the pulmonary artery with resultant pulmonary arterial stenosis was recently reported as a complication of a large pseudoaneurysm.[33] Role of Transesophageal Echocardiography The use of TEE clearly is advantageous in the overall definition of complications of composite aortic grafts.[18] , [27] [30] [31] [32] [33] [34] For delineation of pseudoaneurysms, the aortic suture ring is clearly visualized with TEE, thereby enhancing the evaluation of dehiscence at this level with both echocardiography and Doppler techniques. Furthermore, the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 12 anastomosis of the coronary arteries to the aortic graft is better assessed. Evaluation of flow in the potential space between the graft and native wrapped aorta or fibrous tissue (in the case of excision of the native aorta) is improved. Dehiscence at the distal anastomosis of the aortic graft to the aortic arch remains difficult to assess because of limitations of imaging in this area; however, this type of dehiscence is the least frequent and rarely occurs alone. In cases of pseudoaneurysm formation secondary to endocarditis, TEE may detect vegetations that can further substantiate the diagnosis (Fig. 25-8) . In the absence of such a finding, however, exclusion of an infected graft based on echocardiographic examination, or based on any structural imaging alone, is difficult. Because of anterior 556 Figure 25-6 (color plate.) Examples of different velocity patterns observed by continuous wave Doppler in two patients with coronary artery dehiscence. In A, the color jet arising from the left main dehiscence is depicted in the parasternal long- (A1 ) and short- (A2 ) axes by a large arrow. In this patient with concomitant aortic annulus dehiscence, continuous wave Doppler (A3 ) shows increased systolic and diastolic velocities directed from the graft into the pseudoaneurysm. The patient in B has a sole dehiscence at the right coronary anastomosis depicted in short axis (B1 and B2 ). Continuous wave Doppler recording (B3 ) shows flow directed from the graft into the pseudoaneurysm in systole and flow reversal from the pseudoaneurysm into the graft in diastole (small arrows). GR, graft; LV, left ventricle; PA, pulmonary artery; PSA, pseudoaneurysm; RV, right ventricle. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.) shadowing produced from the prosthetic valve and graft, an optimum assessment of the aortic root in composite grafts involves combined transthoracic and transesophageal studies. In cases of suspected pseudoaneurysm formation in which a collection of blood and |
thrombus is seen around the graft, and without demonstration of flow by transthoracic echocardiography or other imaging modalities, a transesophageal study is crucial in providing the diagnosis.[18] Other Imaging Modalities mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 12 Several modalities have been suggested as diagnostic screens for the development of pseudoaneurysm after Figure 25-7 Right parasternal transthoracic echocardiographic images of composite graft pseudoaneurysm demonstrating systolic compression of the graft by the pseudoaneurysm. Gr, graft; PSA, pseudoaneurysm. composite graft surgery, including chest radiography, computed tomography (CT), digital subtraction angiography, and more recently, magnetic resonance imaging (MRI).[3] [17] [35] , [36] Although chest radiography may warn of the possibility, its sensitivity and specificity for the diagnosis of pseudoaneurysm are poor. Computed tomography and MRI are currently recommended as diagnostic imaging modalities for the serial evaluation of composite grafts and progression of the underlying disease to other segments of the aorta. [10] As for diagnosing pseudoaneurysm, although CT scanning or MRI can provide the diagnosis of blood or fluid collection around the graft, whether this finding represents a mere collection of fluid around the graft or is the result of communication with the ventricle, coronary arteries, or aorta may not be adequately differentiated. Until recently, aortography was the most widely used method for diagnosis of pseudoaneurysms and was the primary diagnostic modality for further evaluation of fluid collection around the composite graft.[36] Aortography still is an excellent modality for diagnosing dehiscence of the composite graft at the coronary artery anastomosis and distal graft (Fig. 25-9) ; however, in cases of isolated dehiscence of the graft at the aortic annulus anastomosis, aortography has been found to completely miss the diagnosis of pseudoaneurysm.[18] [27] This is explained by the fact that in these cases, the pseudoaneurysm communicates only with the left ventricle; a contrast injection in the aortic root would therefore not opacify the left ventricle or the pseudoaneurysm. An example of such a case is 557 Figure 25-8 (color plate.) Transesophageal echocardiographic frames (left) and corresponding color Doppler systolic frames (right) in a patient with endocarditis and composite graft pseudoaneurysm secondary to aortic annulus dehiscence. The upper panels are at the level of the prosthetic valve; the lower panels are at the level of the left main coronary artery. Two large vegetations are depicted (top, arrows) near the site of dehiscence. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 12 Systolic flow into the pseudoaneurysm is shown, and the limits of the pseudoaneurysm are indicated (bottom, arrows). Gr, graft; LA, left atrium; LVO, left ventricular outflow; P, pseudoaneurysm; RV, right ventricle; Veg, vegetations. Figure 25-9 Aortograms of the thoracic aorta in two patients with pseudoaneurysm complicating composite aortic graft. A, The pseudoaneurysm around the ascending graft is opacified (arrows). B, Aortogram of the patient whose echocardiographic images are in Figure 25- 2 . In this case with single aortic annulus dehiscence, the large pseudoaneurysm is not opacified. (From Barbetseas J, Crawford ES, Safi HJ, et al: Circulation 1992;85:212–222. Reproduced with permission. Copyright 1992 American Heart Association.) 558 presented in Figure 25-2 and Figure 25-9 . Echocardiography in these cases is superior to aortography in the detection of pseudoaneurysms. Because in most of these cases the prosthetic aortic valve is not crossed at catheterization, opacification of the pseudoaneurysm necessitates a left ventriculogram using the transseptal technique or the levo phase of a pulmonary angiogram. In cases with concomitant dehiscence at the coronary or distal graft anastomoses, or in those with coexisting aortic insufficiency, the pseudoaneurysm may be opacified with aortography. [18] Complications of Aortic Allografts for Replacement of the Aortic Valve and Aortic Root Clinical Setting Allograft or homograft replacement of the aortic root also has provided an effective therapy for diseases of the aortic root and the aortic valve. [37] [38] [39] [40] Three general techniques for insertion have been used: subcoronary valve implantation, a mini- or inclusion-root implantation, and an aortic- root replacement. Compared with composite graft replacement of the aortic root, the use of an allograft is particularly helpful in recurrent complications of the aortic root, especially in the presence of infection. Aortic allografts, therefore, have been performed predominantly in patients with destruction of the aortic root resulting from endocarditis, in patients with congenitally narrowed or hypoplastic aortic roots, in patients with complications involving previous root replacement such as heavy calcifications, and in those for whom anticoagulation is contraindicated. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 12 Among the most commonly reported complications of aortic allografts are calcifications of the root, aortic regurgitation, and infectious complications occurring primarily in patients whose underlying indication for aortic root replacement was endocarditis. Similar to composite aortic grafts, reports of unusual complications include problems with anastomotic sites (dehiscence with pseudoaneurysm formation), problems with coronary artery anastomosis, and possible compression of the graft. [38] [40] [41] [42] Figure 25-10 (color plate.) Transesophageal echocardiographic findings in a patient with systolic compression of aortic homograft secondary to dehiscence at the aortic annulus anastomosis. The upper panels display the dynamic compression of the homograft in short axis. Color M-mode echocardiography at the same level shows the systolic compression of the graft (white arrows) and systolic flow in both the pseudoaneurysm (above the arrows) and the homograft. Continuous wave Doppler recording from the transgastric view depicts the high gradient through the obstruction. The aortic valve was normal. Gr, gradient; H, aortic homograft; LA, left atrium; RV, right ventricle. (From Nagueh SF, Bozkurt B, Li GA, et al: Am Heart J 1996;132(5):1070–1073, with permission.) Echocardiographic and Doppler Findings Data are scarce on the echocardiographic findings in aortic root allografts. [42] [43] A normal aortic root allograft, especially early after surgery, may be difficult to differentiate from a native aortic root. Late after surgery, however, calcifications of the homograft are common and are detected by echocardiography as increased echogenicity in the aortic root. If leaflet degeneration occurs, varying degrees of aortic insufficiency, with or without aortic stenosis, may be present. In a recent study, paravalvular aortic insufficiency and eccentric jets were more common in patients with subcoronary aortic allograft implantation (41%) than in those with root replacement (11%).[43] Some unusual complications may affect the allograft, but these complications have occurred early in the postoperative period and can be detected with intraoperative TEE. Recently, cases have been reported with complications related to anastomosis of the coronary arteries with the allograft.[41] Aliasing by color flow was detected along with ischemia in the distribution of the involved anastomosis (left main or right coronary artery). Other reported complications included dehiscence of the homograft with resultant pseudoaneurysm formation. Compression of the graft by the pseudoaneurysm may occur, simulating valve stenosis (Fig. 25- 10) .[42] With more extensive experience in cardiac imaging of these patients, the spectrum of complications and the role of echocardiography and other imaging modalities in patients undergoing aortic allograft surgery mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 12 will be better defined. Replacement of the Aorta with an "Elephant-Trunk" Procedure In patients with extensive aortic aneurysmal disease or in dissection involving the ascending aorta, arch, and descending aorta, replacement of the aortic arch and varied lengths of the aorta can be a major undertaking. In 1983, Borst et al[44] described a dual-stage technique whereby the ascending aorta and arch are replaced first, leaving a segment of the distal tubular graft in the descending 559 Figure 25-11 (color plate.) Transesophageal imaging of the descending aorta (Desc Ao) (longitudinal plane) in a patient with aortic aneurysm involving the arch and descending aorta following a successful first stage of an "elephant trunk" procedure. The free distal end of the tubular graft is seen in the descending thoracic aneurysm. Color flow Doppler shows flow into the descending aorta arising from the distal end of the graft (Gr). thoracic aorta. Borst coined the name "elephant-trunk" technique for this procedure. [44] At a second stage, the distal aorta is repaired beyond the subclavian artery. Since its original description, few modifications have been applied to the technique.[6] [45] [46] After the first stage of the operation, TEE imaging of the descending aorta shows the free position of the distal tubular graft in the descending aneurysm, with blood flow detected in the graft emptying into the aneurysm (Fig. 25-11) . This finding at this stage is normal and should not be mistaken for dehiscence of the graft. Following a successful first stage of the procedure, the most serious and usually fatal complication is rupture of the remaining descending thoracic aneurysm while awaiting the second stage of the surgery. The author has observed an unusual interim complication of severe hemolytic anemia following the first stage, which resolved after the second stage of the repair. The intravascular hemolysis was caused by insertion of the distal graft into the false lumen during the first operation. Because insertion of the graft into the descending aorta during the first stage is performed blind, some surgeons in the author's institution currently use intraoperative TEE to assess the position of the inserted graft in the descending aorta. Other Complications Progression of aortic disease with further aneurysm formation or dissection mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 12 di 12 in additional segments of the aorta is the most common cause for reoperating on patients with diseases of the aorta.[19] [47] [48] [49] Monitoring the progression of aortic disease after the initial surgery affects prognosis and is crucial in the overall management of these patients. In addition to the complications mentioned earlier, rupture of the great vessels with fistula formation, although infrequent, can occur as a complication of aortic dissection or aneurysm. Communication between the aorta and pulmonary artery is clinically suspected by the findings of a continuous murmur, similar to patent ductus arteriosus or the presence of heart failure. Echocardiographic findings depend on the size of the shunt and may include volume overload of the left ventricle and elevated pulmonary pressures. Doppler echocardiographic findings are those of continuous flow into the pulmonary artery from the aorta. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/215.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 13 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Unusual Complications Following Valve Surgery Left Ventricular Pseudoaneurysm After Mitral Valve Replacement Clinical Setting Rupture of the left ventricle with pseudoaneurysm formation is a rare but serious complication following mitral valve replacement. Overall, the incidence appears to range from 0.5% to 2% in isolated or combined mitral valve procedures. [50] [51] [52] [53] [54] Rupture of the left ventricle may occur immediately after surgery, presenting with hemodynamic collapse, or may present in the delayed postoperative period as a false aneurysm of the left ventricle. Anatomic characteristics and other factors have been described as predisposing to rupture of the ventricle such as heavy mitral or annular calcifications, the operative procedure itself, the number of surgical procedures previously undergone, or other hemodynamic considerations; however, often no clear cause for the pseudoaneurysm formation can be found.[55] The clinical presentation of pseudoaneurysm formation is variable. In the early postoperative period, it can present as poor postoperative progress, chest pain, heart failure, or as the development of a new murmur.[51] [52] [56] Late postoperative presentation may be similar or may be totally asymptomatic. In unusual cases, the pseudoaneurysm can compress the coronary arteries, leading to ischemia or myocardial hibernation.[57] Echocardiographic and Doppler Findings Echocardiographic techniques play a significant role in the diagnosis of left ventricular pseudoaneurysm.[58] [59] A pseudoaneurysm, in contrast to a true aneurysm, is visualized as a saccular or globular chamber communicating with the left ventricle through a narrow and abrupt discontinuity in the ventricular myocardium. Over the past few years, the important role of Doppler echocardiography in the diagnosis of pseudoaneurysms has been increasingly appreciated. The demonstration of flow into the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 13 pseudoaneurysm by pulsed- and color-flow Doppler substantiates the diagnosis and may at times be the only clue for its presence in cases where the origin of the pseudoaneurysm cannot be visualized.[60] |
[61] [62] Doppler echocardiography is crucial in differentiating a pseudoaneurysm from other entities such as pericardial cysts, loculated pericardial effusion, or hematoma, especially in cases in which communication of the cavity with the left ventricle is not seen. As with true left ventricular aneurysm, a pseudoaneurysm demonstrates akinesis or dyskinesis during ventricular systole. Characteristic Doppler patterns can be seen with systolic filling and diastolic emptying of the pseudoaneurysm.[63] In patients with sinus rhythm, filling of the pseudoaneurysm during atrial contraction 560 can also be seen. With the availability of intravenous contrast echo agents that can cross the pulmonary circulation,[64] the administration of contrast can be of important diagnostic value in these situations by identifying whether such a communication exists with the left ventricle and by localizing its site. The use of contrast is particularly helpful when the communication with the ventricle is rather large and blood velocity in the cavity is too low to be clearly detected with Doppler. The location of the pseudoaneurysm can vary in relation to the prosthetic valve. Transthoracic echocardiography can demonstrate its presence and characteristic features; however, because of technical difficulties and imaging in the far field, the pseudoaneurysm may be frequently missed with the transthoracic approach. TEE is currently the echocardiographic method of choice in evaluating patients with suspected left ventricular pseudoaneurysm complicating mitral valve replacement.[63] [65] [66] [67] An example of a pseudoaneurysm complicating mitral valve replacement demonstrated by TEE and missed by transthoracic imaging is shown in Figure 25-12 . Other Imaging Modalities Nonsurgical detection of pseudoaneurysm previously has depended on left ventriculography. Angiography is still important in the diagnosis of pseudoaneurysms in patients in whom the transthoracic examination may be difficult and also provides a spatial distribution of the Figure 25-12 (color plate.) Transverse transesophageal mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 13 echocardiography planes at four levels (A to D) are shown along with contrast left ventriculography in the right oblique view, demonstrating opacification of a left ventricular pseudoaneurysm complicating mitral valve replacement. The approximate locations of the transverse echo planes are schematically shown on the angiogram. A1 and A2 show the maximal extent of the pseudoaneurysm and respective color flow demonstrating flow in the cavity. B and C show the neck of the pseudoaneurysm by color Doppler and its proximity and impingement on the proximal circumflex artery (C, arrows). The most caudal plane (D) is at the level of the prosthetic valve (PrV), which is normal. Ao, aorta; LA, left atrium; LV, left ventricle; PsAN, pseudoaneurysm; RV, right ventricle. (From Baker WB, Klein MS, Zoghbi WA: J Am Soc Echocardiogr 1993;6:548–552.) pseudoaneurysm (see Fig. 25-12) ; however, because of its tomographic nature, TEE can further add to left ventricular angiography in pinpointing the site of origin of the pseudoaneurysm and its relation to adjacent structures for later surgical correction. The intraoperative use of TEE in surgical repair of these lesions can also be crucial when the repair involves areas close to the coronaries, in the assessment of ventricular function immediately postoperatively, and to indirectly detect whether injury occurred in the area of the coronary vessels with the evaluation of regional myocardial function.[63] It is generally agreed that management of patients with pseudoaneurysm formation of the left ventricle necessitates surgical intervention because of the risk of rupture and potential sudden death. Although surgical correction has been carried out almost uniformly in high- risk patients, some authors have advocated continued TEE follow-up in asymptomatic patients.[67] Left Atrial Dissection after Mitral Valve Replacement Clinical Setting Dissection of the left atrium with resultant pseudoaneurysm formation is a rare complication of mitral valve replacement.[68] [69] [70] [71] [72] Predisposing factors for this unusual complication are similar to those for left ventricular pseudoaneurysms and include mitral annulus calcifications, 561 Figure 25-13 Dissection of the left atrium demonstrated with intraoperative transesophageal echocardiography after mitral valve surgery. A, horizontal view; B, 73-degree view. Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle. (From Genoni M, Jenni R, Schmid ER, et al: Ann Thorac Surg 1999;68:1394–1396.) mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 13 external cardiac massage, friable atrial wall tissue, preexisting pericardial adhesions, and technical considerations during surgery. Clinical presentation varies from detection in the operating room with TEE, to the presence of a systolic murmur of mitral regurgitation, heart failure, or an asymptomatic state. Surgical correction is recommended for symptomatic cases or those with severe left atrial compression. Spontaneous healing has been reported in only one case.[70] Internal drainage of the false lumen into the right atrium has been recently proposed in cases where the dehiscence at the mitral annulus is small.[71] Echocardiographic and Doppler Findings On echocardiography, a cavity formation is seen within the left atrium, with a linear echo density consisting of the dissection of the atrial wall. This is best delineated with TEE (Fig. 25-13) .[71] [72] Paraprosthetic valve regurgitation is usually seen, with flow by Doppler entering into the false lumen through the communication.[72] Recording of the jet with continuous- wave Doppler provides various degrees of velocity and duration of flow, depending on the size of the communication, and compliance of the false lumen. Pseudoaneurysm of the Ascending Aorta After Aortic Valve Replacement Clinical Setting False aneurysm of the ascending aorta is a rare but serious complication of aortic valve replacement. Potential factors contributing to this complication include leaking aortotomy suture lines, needle punctures for air-evacuation procedures after surgery, postoperative endocarditis, or friability of the aortic wall.[73] [74] [75] [76] Clinical presentation is variable, including an asymptomatic, incidental finding on chest radiography or echocardiography, symptoms of atypical chest discomfort or dyspnea, and the finding of a continuous murmur because of fistula formation with adjacent cardiac chambers.[73] [74] [75] [76] Surgical repair generally is recommended because these pseudoaneurysms have a high propensity for rupture. Echocardiographic and Doppler Findings Echocardiography shows a typical pseudoaneurysmal cavity arising from the ascending aorta in the vicinity of the prosthetic aortic valve. Usually the aorta is of normal size, and the neck of the pseudoaneurysm is small and mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 13 may be difficult to appreciate on transthoracic echocardiography. TEE enhances imaging and definition of the pseudoaneurysm, which could be lined with thrombus. Color Doppler identifies flow into the cavity in systole, emptying in diastole (Fig. 25-14) . In a typical aortic pseudoaneurysm, there is no associated aortic insufficiency or flow in the cavity. In case of further complications of the pseudoaneurysm, however, continuous flow can be detected at the site of rupture into the right atrium or right ventricle.[75] [76] Similar to other pseudoaneurysms of the aorta, aortography, CT, or MRI also can delineate the pseudoaneurysm 562 Figure 25-14 (color plate.) Echocardiographic and Doppler images of an aortic pseudoaneurysm obtained with transesophageal echocardiography in the 30-degree and 90-degree planes. Flow is seen entering the pseudoaneurysm in systole and emptying in diastole. The corresponding aortogram delineates the extent of the pseudoaneurysm. Ao, aorta; An, pseudoaneurysm; LA, left atrium. (see Fig. 25-14) . In these cases, Doppler echocardiography and aortography can aid surgical correction by more accurately pinpointing the site of rupture and flow into the pseudoaneurysm. Pseudoaneurysm of the Mitral-Aortic Intervalvular Fibrosa Clinical Setting The region of the mitral-aortic continuity or mitral-aortic intervalvular fibrosa (MAIVF) contains mostly fibrous, relatively avascular tissue. Because of its composition, the MAIVF is the weakest segment of the aortic ring,[77] is prone to infection, and is more sensitive to trauma. The roof of the MAIVF is formed of pericardium, and its ventricular side is the posterior portion of the left ventricular outflow tract. Dehiscence in the MAIVF region, secondary to infection, trauma, or even surgical manipulation may result in the formation of an abscess or a pouch between the medial wall of the left atrium and the aorta. An intervalvular pseudoaneurysm ensues when the abscess or pouch communicates with the left ventricular outflow tract.[78] [79] [80] [81] An example of an MAIVF pseudoaneurysm is shown in Figure 25-15 . Most pseudoaneurysms in the MAIVF region occur secondarily to infection and are more common in mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 13 patients with prosthetic valves.[82] Other causes include trauma, surgical trauma, and congenital pseudoaneurysms.[82] [83] [84] Detecting these pseudoaneurysms is important because of their potential complications, which may include rupture into the left atrium or aorta, resulting in mitral or aortic regurgitation, respectively, or even rupture into the pericardial space, with ensuing cardiac tamponade and death.[78] [81] [83] Determining the incidence of MAIVF pseudoaneurysms is difficult. Prior to the use of TEE, the few reports available surfaced at pathology or during angiography. With the advent of TEE, the most sensitive technique for evaluating these lesions, MAIVF pseudoaneurysms were detected in 9% of patients undergoing TEE for suspected aortic valve or ring disease.[82] The clinical presentation varies but is most commonly that of endocarditis, congestive heart failure, valvular regurgitation, or it may be asymptomatic, without a history of endocarditis. Because the pseudoaneurysm is located between the left atrium and aorta, and its origin is in the left ventricular outflow, it is not readily identified at surgery and may be missed. Thus, accurate detection, delineation, and differentiation of MAIVF pseudoaneurysms from ring abscesses is important in overall patient management and in the guidance of surgical correction. Echocardiographic and Doppler Findings Transthoracic echocardiography has been used for the diagnosis of aortic root complications.[85] [86] Its sensitivity, however, recently has been shown to be limited in the evaluation of posterior lesions, particularly in the presence of prosthetic aortic valves; by contrast TEE substantially improves the diagnosis of such lesions.[87] [88] In a series from the author's institution, transthoracic echocardiography detected 43% of a total of 23 lesions affecting the aortic root, whereas TEE identified 90% of the lesions.[82] The importance of the transthoracic approach in detecting anterior ring abscesses cannot be ignored, however, particularly in the presence of prosthetic aortic valves, where TEE may have significant limitations because of shadowing of the prosthesis in the region of the anterior aortic ring. Combining transthoracic and transesophageal imaging, therefore, would allow a comprehensive evaluation of the aortic root and is strongly recommended. In contrast to aortic ring abscesses, intervalvular pseudoaneurysms exhibit a characteristic dynamic feature during the cardiac cycle. Marked pulsatility is observed in most MAIVF pseudoaneurysms, with expansion during early systole and collapse in diastole (see Fig. 25-15) . [82] This mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 13 feature is explained by the fact that the pressure in the pseudoaneurysm reflects left ventricular pressure and 563 that a large portion of the pseudoaneurysm is surrounded by the left atrium. Thus, when left atrial pressure exceeds left ventricular pressure in diastole, the pseudoaneurysm collapses, whereas it expands in systole. This dynamic behavior during the echocardiographic examination is indeed the first clue to the presence of an MAIVF pseudoaneurysm. In contrast, aortic ring abscesses located anteriorly or posteriorly in the aortic root do not exhibit this marked pulsatility, which may be explained by several factors. In walled-off abscesses without detectable flow, pulsatility is not expected. In ring abscesses with systolic and diastolic flow owing to paraprosthetic aortic regurgitation, the pressure remains high throughout the cardiac cycle in these cavities compared with adjacent chambers so that pulsatility is not seen. Although collapsibility provides indirect evidence for the presence of an MAIVF pseudoaneurysm, confirmation of this diagnosis requires visualization of the neck of the pseudoaneurysm in the left ventricular outflow. This communication rarely can be seen by transthoracic echocardiography[82] however, it is usually well visualized with the transesophageal approach. In the author's experience, the size of the neck has ranged from 0.5 to 2.1 cm in diameter. In cases where there is still doubt about whether the cavity communicates with the aorta or left ventricle, the administration Figure 25-15 (See also color plate.) Echocardiographic and color Doppler frames from the transverse plane during transesophageal echocardiography showing a typical simple mitral-aortic intervalvular fibrosa pseudoaneurysm with its location, pulsatility, and flow patterns during the cardiac cycle. Top, Pseudoaneurysm (straight arrow) and communication with the left ventricular outflow (curved arrow) are shown. The pseudoaneurysm begins to expand during early systole, remains distended in late systole, and collapses during diastole. Bottom, Magnified color Doppler views of the area within the box seen in the top middle panel. During early systole, the pseudoaneurysm fills, showing high, |
aliased velocities. Low, nonaliased velocities are seen during the remainder of systole while the pseudoaneurysm remains expanded (middle). During diastole, the pseudoaneurysm empties and collapses. LA, left atrium; LV, left ventricle. of intravenous contrast agents that cross the pulmonary circulation can help resolve this issue. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 13 Color Doppler imaging is crucial in the evaluation of MAIVF pseudoaneurysms. Its application helps to assess whether rupture of this cavity into adjacent chambers has occurred and define its communication. The following are characteristic Doppler features in unruptured and ruptured MAIVF pseudoaneurysms. In the case of unruptured pseudoaneurysms, Doppler evaluation usually is less impressive. Only a brief duration of flow into the pseudoaneurysm occurs during early systole (20–60 msec), at which time pressure between the pseudoaneurysm and left ventricle is equalized, and no further flow is detected by Doppler (see Fig. 25-15) .[82] During diastole, a brief period of flow exiting from the pseudoaneurysm may be seen but frequently can be missed because of its low velocity. In contrast, in pseudoaneurysms that have ruptured, into either the left atrium or aorta, an intense color-flow signal can be seen during the cardiac cycle. In cases of rupture into the left atrium, color Doppler shows holosystolic, intense flow signal in the pseudoaneurysm and eccentric "mitral" regurgitation through the perforation of the pseudoaneurysm, the latter acting as a conduit for blood flow from the left ventricle to the left atrium (Fig. 25-16) . The use of color Doppler actually facilitates 564 Figure 25-16 (See also color plate.) Two-dimensional and color flow transesophageal echocardiography images of a complicated mitral- aortic intervalvular fibrosa pseudoaneurysm with rupture into the left atrium in the setting of endocarditis after mitral valve annuloplasty and aortic valve replacement. The pseudoaneurysm (slender arrow) and its neck (large arrow) are shown. The pseudoaneurysm is septate, has mobile vegetations, and expands significantly in systole. An intense color flow jet in systole is seen through the pseudoaneurysm with subsequent, eccentric regurgitation into the left atrium. Ao, aorta; LA, left atrium; LV, left ventricle. the identification of the rupture site of the pseudoaneurysm by tracking the origin of the regurgitant jet. The ruptured site is rarely seen by transthoracic echocardiography but can be suspected by the presence of eccentric mitral regurgitation arising close to the aortic root. Similar to unruptured pseudoaneurysms, those pseudoaneurysms communicating with the left atrium show systolic expansion and diastolic collapse (see Fig. 25-16) . In cases where rupture of the pseudoaneurysm occurs into the aorta, with or without concomitant dehiscence of the prosthetic aortic valve, aortic insufficiency is detected (Fig. 25-17) . In systole, color Doppler shows mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 13 antegrade flow from the ventricle through both the pseudoaneurysm and the prosthetic aortic valve. In diastole, retrograde flow of "aortic" insufficiency is seen, directed from the aortic root into the pseudoaneurysm and into the ventricle. Other Imaging Modalities Until recently, cineangiography has been the standard for diagnosing aortic root lesions.[89] With the advent of echocardiography with Doppler, and more recently TEE, however, these techniques have rivaled the invasive diagnostic modality. Few cases of MAIVF pseudoaneurysms have been described with angiography.[80] [90] [91] The pulsatility described earlier is also seen on angiography (Fig. 25-18) . In a case series in which patients underwent both diagnostic modalities, MAIVF pseudoaneurysms were more frequently detected by TEE than by aortography.[82] Only 2 of 9 pseudoaneurysms were identified by aortography, both of which had associated aortic insufficiency (Fig. 25-19) . The direct communication between the left ventricular outflow tract and pseudoaneurysm explains the need for a ventricular injection of dye to detect this abnormality. This finding is similar to that described earlier for pseudoaneurysms of composite aortic grafts with a single dehiscence at the aortic annulus anastomosis. Thus, in patients without aortic insufficiency, demonstration of the pseudoaneurysm with angiography requires left ventriculography. Compared with angiography, TEE more clearly delineates the origin of the intervalvular pseudoaneurysms and their communication elucidating 565 Figure 25-17 (See also color plate.) Two-dimensional and color Doppler frames during omniplane transesophageal examination at an angulation of 120 degrees, showing a ruptured mitral-aortic intervalvular fibrosa pseudoaneurysm into the aorta. During systole, blood flows into the pseudoaneurysm and from the pseudoaneurysm into the aorta through small fenestrations (white arrow). Normal flow direction through the prosthesis (black arrow) is also shown. During diastole, blood regurgitates into the left ventricle through the pseudoaneurysm (black arrows). An, pseudoaneurysm; Ao, aorta; LA, left atrium; LV, left ventricle; PrV, prosthetic aortic valve. (From Afridi I, Apostolidou MA, Saad RM, et al: J Am Coll Cardiol 1995;25:137–145. Reproduced with permission from the American College of Cardiology.) the origin of concomitant mitral regurgitation or aortic insufficiency and, therefore, assisting in planning surgical repair.[82] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 10 di 13 Patients with cavitary lesions complicating aortic valve disease, particularly prosthetic valves, require extensive surgical intervention, including in some cases aortic root replacement. Because of the risk of rupture into the pericardium, surgical correction of MAIVF pseudoaneurysm is warranted in most cases. Although the natural history of uncomplicated pseudoaneurysm is unclear, surgical repair was performed in the majority of cases reported. In patients who do not undergo an immediate operation, TEE may be useful in identifying serial changes in the pseudoaneurysm or the development of a rupture into adjacent chambers, which can help plan appropriate therapy. Intracardiac Fistula following Valve Replacement Clinical Setting Intracardiac fistula formation is an uncommon complication following valve replacement surgery. Several types of fistulae may occur following mitral valve replacement, Figure 25-18 Left anterior oblique view during aortography in a patient with mitral-aortic intervalvular fibrosa (MAIVF) pseudoaneurysm and aortic insufficiency. The MAIVF pseudoaneurysm (arrows) shows pulsatility during the cardiac cycle. (From Afridi I, Apostolidou MA, Saad RM, et al: J Am Coll Cardiol 1995;25:137–145. Reproduced with permission from the American College of Cardiology.) including left ventricular–to–right atrial communications and left ventricular–to–coronary sinus fistulae.[92] [93] [94] [95] These complications are attributed mainly to excessive débridement and injury to the mitral annulus during surgery. Concomitant endocarditis, however, may be an underlying mechanism in late postoperative cases. In the early postoperative period, the clinical presentation may include a new systolic murmur, findings of high cardiac output, or a high oxygen saturation in the pulmonary artery; however, this condition may be often misdiagnosed as remnant tricuspid regurgitation or periprosthetic valve regurgitation. Conversely, fistula formation following aortic valve replacement, between the aorta and cardiac chambers, such as left or right atrium or right ventricle, is usually secondary to infectious causes but could also occur in the setting of a ruptured pseudoaneurysm.[75] [76] Findings in these conditions are similar to those of rupture of sinus of Valsalva, including a continuous murmur. Echocardiographic and Doppler Findings mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 13 A left ventricular-to-right atrial fistula mimics tricuspid insufficiency, and differentiating it from the latter may be difficult. A few direct and indirect clues may raise suspicion for this diagnosis. In contrast to most tricuspid insufficiency 566 Figure 25-19 Example of a patient with an unruptured mitral-aortic intervalvular fibrosa (MAIVF) pseudoaneurysm diagnosed with transesophageal echocardiography (TEE), missed at aortography. Top, TEE transverse planes show the MAIVF pseudoaneurysm expanding during systole (left) and collapsing during diastole (right). Communication between the pseudoaneurysm and left ventricular outflow region (arrow) is seen. Bottom, Aortogram during systole and diastole in the same patient appears normal. An, MAIVF pseudoaneurysm; LA, left atrium; LV, left ventricle; PrV, prosthetic aortic valve. (From Afridi I, Apostolidou MA, Saad RM, et al: J Am Coll Cardiol 1995;25:137–145. Reproduced with permission from the American College of Cardiology.) jets, which are directed towards the interatrial septum, the jet from the fistula seen by color Doppler arises near the crux of the heart and is usually directed centrally or toward the free wall of the right atrium. Unconventional imaging planes used to assess the origin of the jet may provide visualization of proximal velocity acceleration on the left ventricular side, raising suspicion for the diagnosis. Recording of jet velocity by continuous-wave Doppler will invariably lead to registering a high-velocity jet, similar to mitral regurgitation. If there is concomitant mitral regurgitation, the jet velocities will be almost equal—this will lead to an overestimation of pulmonary artery pressure when using the modified Bernoulli equation. A close examination of right ventricular function, septal motion, pulmonary flow velocity contour, and pulmonary insufficiency jet, if available, may reveal a discordance between findings of normal pressure by these indices and that derived from the "tricuspid insufficiency" jet, raising suspicion for the diagnosis. Further confirmation may be carried out with TEE aiming at better definition of the origin of the jet. In the case of left ventricular–to–coronary sinus fistula, a high-velocity intense color jet is seen in the coronary sinus, which in these cases is usually dilated. The differential diagnosis includes a coronary artery–to– coronary sinus fistula, where, in contrast, a continuous flow occurs.[96] On the other hand, fistula formation between the aorta and cardiac chambers through a periprosthetic aortic valve abscess rupture is diagnosed as a mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 12 di 13 continuous systolic and diastolic jet into the respective chamber, with a continuous and intense recording by continuous-wave Doppler of high velocity reflecting the high-pressure difference between aorta and the communicating chamber. In the above conditions, the most often used alternative diagnostic modality is contrast cineangiography for demonstrating the communications. Pulmonary Valve Autotransplantation: The Ross Operation In 1967, Ross described the use of an autologous pulmonary valve to replace the diseased aortic valve. The procedure, presently known as the Ross operation, consists of implanting the patient's own pulmonary valve within the aortic root and replacing the pulmonary valve with either an aortic or pulmonary allograft. This procedure is performed predominantly in young adult patients and children with aortic valve disease and offers the advantages of valve viability and potential for growth in young patients, and the elimination of the need for long-term anticoagulation, in addition to increased durability compared with aortic allografts and bioprosthetic valves in this age group.[97] [98] Complications of the Ross operation include the potential for aortic insufficiency because of malalignment of the pulmonic valve in the aortic position, and valve degeneration occurring late after surgery. More recently, replacement of the aortic root with a pulmonary root autograft has been proposed.[99] [100] [101] The potential advantage of this procedure, compared with simple pulmonary valve autograft, is the more optimal alignment and function of the valve leaflets, because the sinuses of Valsalva also are transplanted. Short-term follow-up data from these patients have not revealed significant dilatation of the wall of the pulmonary artery in the aortic position. Over the past few years, more experience with the procedure has been acquired.[40] [102] [103] [104] [105] [106] The incidence of progressive aortic insufficiency has been low and has improved with the root-replacement technique.[40] [107] Annular dilatation of the pulmonary autograft occurs after implantation in the aortic position (20% increase on average).[107] [108] Infrequently, however, aneurysmal or pseudoaneurysmal formation may develop at this site, complicating pulmonary autograft surgery and necessitating reoperation.[109] [110] Progressive stenosis of the allograft in the pulmonary position has been infrequently reported, usually at the distal anastomosis in the pulmonary artery[101] [111] however, reoperating on the pulmonary allograft may be necessary in up to 20% of patients, at 20 years.[40] Echocardiographic techniques are ideally suited for the follow-up and mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 13 di 13 detection of complications in patients with pulmonary valve or pulmonary root autografts.[101] [107] [108] [109] [110] [111] [112] [113] In most cases, transthoracic echocardiography with Doppler is sufficient to evaluate the aortic root and the presence and severity of aortic insufficiency. In suspected complications, TEE improves the definition of aortic root pathology.[109] Similarly, echocardiography can provide serial assessment of allograft function in the pulmonary position. Stenosis at the distal anastomosis has been recently reported with Doppler echocardiography, requiring reoperation in few patients.[101] [111] The transesophageal approach may be needed to evaluate complex lesions or the mechanism of postoperative complications. 567 MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/216.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without |
the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Section 5 - Cardiomyopathies and Pericardial Disease 571 Chapter 26 - Doppler and Two-Dimensional Echocardiographic Evaluation in Acute and Long-term Management of the Heart Failure Patient Jannet F. Lewis MD Background It is estimated that there are 2 million individuals in the United States with a diagnosis of congestive heart failure, and nearly 400,000 new patients are diagnosed each year. Among 652 members of the Framingham Heart Study who developed congestive heart failure between 1948 and 1988, median survival after onset of heart failure was 1.7 years in men and 3.2 years in women.[1] One-year and 5-year survival rates were 57% and 25% in men and 64% and 38% in women, respectively. No significant change in the prognosis of congestive heart failure was identified during the 40 years of observation. However, the course of the disease is not uniformly poor, and considerable variability exists among individual patients. [2] [3] [4] [5] [6] [7] [8] [9] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 Moreover, newer therapeutic interventions, both pharmacologic treatment [10] [11] [12] [13] and cardiac transplantation,[14] [15] [16] promise improved survival in patients with congestive heart failure. Improvement in survival depends in part on the ability to correctly characterize the disease and stratify patients with regard to prognosis to make the most appropriate therapeutic plan. Two-dimensional and Doppler echocardiography have markedly improved our understanding of the pathophysiology of congestive heart failure and have also provided noninvasive techniques for accurate diagnosis of underlying causes, hemodynamic evaluation at baseline and during medical intervention, and important prognostic information to guide further management. This chapter is devoted primarily to the use of two- dimensional and Doppler echocardiography in the evaluation and management of congestive heart failure due to dilated cardiomyopathy. Other diseases associated with heart failure (coronary artery disease, valvular heart disease, other cardiomyopathies) are the subjects of separate chapters. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/219.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Echocardiography in the Diagnosis of Cardiomyopathy 572 The widespread use of echocardiography in the management of patients with suspected or known cardiac disease has facilitated our appreciation of the spectrum of diseases that present with the constellation of signs and symptoms of congestive heart failure. Thus, while many patients with manifestations of decompensated congestive heart failure have reduced left ventricular ejection fraction, congestive symptoms and signs may be present in other conditions.[17] [18] Previous observations in patients undergoing noninvasive assessment of systolic function have shown that as many as 50% of patients with clinically diagnosed congestive heart failure have a normal left ventricular ejection fraction. Most of these patients have systemic hypertension alone or in combination with ischemic heart disease. A substantial minority have nondilated cardiomyopathies, such as hypertrophic or restrictive cardiomyopathy, with heart failure occurring primarily as a consequence of diastolic dysfunction. Echocardiography provides excellent visualization of the left ventricle in most patients and readily distinguishes the three major forms of cardiomyopathy. Dilated cardiomyopathy is characterized by dilated cardiac chambers, most prominently the left ventricle, and reduced ejection fraction[3] [8] [19] , [20] (Fig. 26-1) . Echocardiographic diagnosis of hypertrophic cardiomyopathy is based on identification of severe asymmetric hypertrophy of the left ventricle, usually most marked in the ventricular septum with sparing of the posterior wall, and normal or increased ejection fraction[21] [22] [23] [24] [25] (see Chapter 27) . The disease shows considerable morphologic diversity, however, and recognition of this diversity is essential for diagnosis. Thus, while septal hypertrophy is the most prominent and best-recognized feature of the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 disease, hypertrophy may be confined to the apical segments of the left ventricle[26] [27] or most marked in the posterior free wall.[28] Also, there appear to be definite age-related morphologic differences among patients with hypertrophic cardiomyopathy[29] [30] [31] (Fig. 26-2) . Elderly patients with this disease, compared with younger patients, generally show less severe hypertrophy that is more often localized to the ventricular septum. Restrictive cardiomyopathy, most commonly due to cardiac amyloidosis, may also present with signs and symptoms of congestive heart failure (see Chapter 28) . The disease is characterized by a symmetrically thickened left ventricular wall with a "ground-glass" appearance of the myocardium, and normal left ventricular chamber size and systolic function until the very advanced stages of the disease (Fig. 26-3) . Doppler echocardiographic studies in patients with amyloid heart disease have identified a spectrum of transmitral filling patterns that correlate with the severity of disease and prognosis.[32] [33] Echocardiographic diagnosis of ischemic heart disease is based on identification of segmental wall motion abnormalities ( see Chapter 11 Chapter 12 Chapter 13 Chapter 14 ). In most patients, the distinction between ischemic heart disease and dilated cardiomyopathy is readily apparent. However, in some Figure 26-1 Diastolic (A) and systolic (B) frames in an apical four-chamber echocardiographic view from a 23-year-old man with dilated cardiomyopathy. The left ventricle is dilated and the ejection fraction is markedly depressed. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. patients with severe ischemic heart disease, there may be substantial left ventricular dilation and global systolic dysfunction.[34] Alternatively, patients with nonischemic dilated cardiomyopathy may demonstrate segmental areas of akinesis as well as regions with apparently preserved contractility, usually the basal segments of the inferior and posterior walls. [35] Consequently, in patients with severely depressed left ventricular systolic function, the distinction between nonischemic and ischemic disease may present an important diagnostic problem. Although coronary arteriography provides definitive diagnosis in such cases, other noninvasive modalities such as dobutamine stress echocardiography also give important diagnostic and therapeutic information. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 573 Figure 26-2 Echocardiographic images in a parasternal long-axis view from a 23-year-old woman (A) and a 66-year-old woman (B) with hypertrophic cardiomyopathy. In the younger patient, the ventricular septum (VS) is markedly and diffusely thickened and bulges into the left ventricular chamber. In the older patient, the septum is more modestly thickened (arrowheads), and the ventricular chamber shape appears normal. Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/220.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 15 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Assessment of Dilated Cardiomyopathy by Echocardiography Morphologic Description Cardiac enlargement is a central feature in dilated cardiomyopathy. [3] [19] , [36] However, echocardiographic assessment has demonstrated a spectrum of findings with regard to the degree of chamber enlargement, magnitude of left ventricular dysfunction, myocardial thickness, and size and systolic function of the right ventricle.[8] [20] [37] , [38] For example, although most patients show a marked increase in the size of the left ventricular chamber, Keren et al[38] described a group of patients with "minimally dilated cardiopathy." The cause of lack of dilation is not entirely clear, but pathologic examination shows less myofibrillar loss in these subjects than in patients with more dilation. The prognosis for these patients appears to be similar to the prognosis for those with the more classic form of the disease. The morphologic variability in dilated cardiomyopathy has also been demonstrated at postmortem examination. Benjamin et al[39] found variability in the degree of left ventricular wall thickness and relation of wall thickness to chamber size. A review of clinical records revealed greater wall thickness in long-term survivors than in short-term Figure 26-3 Echocardiographic images from a 62-year-old man with cardiac amyloidosis. The ventricular wall thickness is markedly increased, and the ventricular septum has a typical "ground-glass" appearance. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. 574 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 15 Figure 26-4 Two-dimensional echocardiographic images in an apical four-chamber view from two patients with dilated cardiomyopathy. A, Predominant and disproportionate dilation of the left ventricular chamber can be seen. The right ventricle in this patient appears relatively small. B, More pronounced right ventricular chamber dilation can be seen. Right ventricular systolic function is also depressed in this patient. Pacemaker leads (arrowheads) are present in the right cardiac chambers. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. survivors, and a smaller radius-to-thickness ratio appeared to confer a somewhat protective effect. Similarly, Gaasch and Zile[40] found wall stress to be an important predictor of outcome in patients with dilated cardiomyopathy. Investigations of patients with dilated cardiomyopathy have focused largely on description of the left ventricle. However, right ventricular size and systolic function also vary among patients with dilated cardiomyopathy and have important implications for prognosis and treatment.[9] [41] In a clinical and echocardiographic study of patients with dilated cardiomyopathy, two morphologic subsets were identified: patients with relatively equal degrees of ventricular enlargement, and patients with predominant and disproportionate dilation of the left ventricle but relative sparing of the right [9] (Fig. 26-4) . Severe mitral and tricuspid regurgitation were more common among patients with pronounced right ventricular enlargement. Survival over a mean follow-up period of 28 months was better among patients with primarily left ventricular dilation. Pinamonti et al [42] subsequently reported right ventricular systolic function as a strong predictor of death or cardiac transplantation in 79 consecutive patients with dilated cardiomyopathy followed for a mean of 22 months. Noninvasive Hemodynamic Assessment The hemodynamic parameters assessable by two-dimensional and Doppler echocardiography are listed in Table 26-1 . Assessment of Left Ventricular Systolic Function Left ventricular systolic function in the setting of congestive heart failure has important diagnostic and prognostic implications. In addition, parameters of systolic function may be useful in evaluating the response to therapeutic intervention. The most widely used clinical index of systolic function is ejection fraction (calculated as [end-diastolic volume − end- mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 15 systolic volume]/end-diastolic volume). Left ventricular volume has been assessed by echocardiography on the basis of a number of geometric assumptions (see Chapter 4) . Because the left ventricle commonly loses its normal elliptical geometry in TABLE 26-1 -- Noninvasive Hemodynamic Data Obtainable by Two- Dimensional (2D) and Doppler Echocardiography 2D Doppler Hemodynamic Parameter Alone Alone Both LV diastolic volume X LV stroke volume/cardiac output X X X LV ejection fraction X LA/LV diastolic pressure X Pulmonary artery pressure X RA pressure X X Valvular regurgitation severity X X X LA, left atrial; LV, left ventricular; RA, right atrial. 575 TABLE 26-2 -- Measurement of Stroke Volume/Cardiac Output by Doppler Echocardiography Subjects, Study n r Value * (SEE) Variability, % Method Fisher et al[46] † 15 0.97 (0.23 L/m) Mitral Dubin et al[49] 18 0.87 (11 mL) Lewis et al[47] 39 0.91 (0.63 L/m) inter: 6.8 ± 1.5 LV outflow 0.87 (0.59 L/m) inter: 16.4 ± Mitral 13.8 inflow Huntsman et al 45 0.94 (0.58 L/m) Aorta [45] Nicolosi et al[48] 30 — inter: 6.8 Six ‡ methods mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 15 intra: 5.9 methods 16.0 Inter, interobserver variability; intra, intraobserver variability; method, variability of the method; LV, left ventricular; SEE, standard error of estimate. * Correlation with stroke volume/cardiac output measured by roller pump and thermodilution cardiac output. † Canine studies. ‡ Healthy volunteers without thermodilution measurements. the setting of heart failure, however, the biplane "method of discs" is less dependent on geometric assumptions and provides a more accurate determination of ventricular volume.[43] The major limitation to this method is the requirement for apical four- |
and two-chamber views with endocardial definition of sufficient technical quality to permit manual tracing during freeze-frame analysis. Developments in automated border detection may resolve this problem (see Chapter 7) . Aside from these technical considerations, ejection fraction is largely dependent on the loading conditions of the left ventricle, and therefore may not serve as an accurate surrogate of myocardial contractility. For example, in the setting of mitral regurgitation, ejection fraction poorly reflects myocardial contractility. Determination of stroke volume and cardiac output provides more accurate assessment of ventricular performance. Stroke volume can be calculated from diastolic and systolic left ventricular volumes by echocardiography.[43] [44] However, as with calculation of ejection fraction, significant error may occur because of suboptimal visualization of endocardial borders during freeze-frame analysis. Studies by several investigators in different laboratories have demonstrated excellent correlation between cardiac outputs obtained by Doppler echocardiography and flow measured by invasive techniques[45] [46] [47] [48] [49] (Table 26-2) . Doppler echocardiographic assessment of stroke volume is based on the principle that flow (Q) across an orifice can be calculated as the product of the cross-sectional area of the orifice (CSA) and the time velocity integral (TVI) across the orifice: Q = CSA × TVI mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 15 Stroke volume = CSA × TVI Cardiac output = stroke volume × heart rate Theoretically, flow can be assessed across any vessel or cardiac valve. Thus, stroke volume has been calculated using Doppler sampling of left ventricular outflow, ascending aorta, and mitral, tricuspid, and pulmonic valves.[45] [46] [47] [48] [49] [50] Each method is limited by the ability to measure orifice size accurately. Calculation of stroke volume and cardiac output from the flow velocity in the left ventricular outflow tract (Fig. 26-5) utilizes cross-sectional area calculated from diameter measurement of the left ventricular outflow tract, assuming a circular geometry: Area = π(diameter / 2)2 As is apparent, small differences in diameter measurement result in relatively larger differences in calculation of cross-sectional area and stroke volume. Nonetheless, the overall correlation of cardiac output determined from the left ventricular outflow Doppler method and output measured by thermodilution is excellent, and reproducibility of this method is approximately 16%.[47] Use of ascending aortic flow velocity for calculation of stroke volume is technically more difficult and has been less commonly applied.[48] [49] Several approaches have been assessed for measurement of stroke volume from the mitral inflow velocity waveform.[46] [47] [48] [49] The simplest method employs Doppler sampling in the center of the mitral annulus and measurement of the mitral annulus, assuming a circular geometry for calculation of cross-sectional area (Fig. 26-6) . The mitral annular method for calculation of stroke volume and cardiac output also shows close correlation with thermodilution measurement but with larger interobserver variability than with the outflow method. Because of the noncircular geometry of the mitral annulus, alternative approaches to the calculation of mean mitral valve area during diastole utilize M-mode correction of two- dimensional measurements as well as biplane measurement of mitral annulus diameter, assuming an elliptical geometry. These approaches have also shown good correlation with thermodilution cardiac output but are more tedious and do not appear to offer significant advantage. Pulmonary artery flow calculation of stroke volume has been less widely used in adult patients because of limited visualization of the pulmonary mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 15 artery boundaries but has been extensively applied in pediatric patients.[50] The pulmonary artery dilation often observed in patients with dilated cardiomyopathy may improve visualization of the pulmonary boundaries and thus facilitate the use of this method in adults. Because of the difficulties encountered with calculation of cross-sectional area, use of the flow velocity integral alone to obtain a stroke distance has been proposed as a correlate of stroke volume.[51] Measurement of stroke distance 576 Figure 26-5 Calculation of cardiac output using the left ventricular outflow method. The diameter of the left ventricular outflow immediately proximal to the aortic cusp is measured from the parasternal long-axis view (A, upper and lower). Pulsed Doppler sample volume is placed proximal to the aortic valve in the apical view (B, upper) to obtain the left ventricular outflow flow velocity waveform (B, lower). LA, left atrium; LV, left ventricle. for serial evaluation of patients undergoing therapeutic intervention appears to be a reasonably accurate alternative to stroke volume measurement. Ejection phase indices derived from M-mode and Doppler echocardiographic measurements have also been used to assess left ventricular systolic function. These indices are significantly influenced by loading conditions of the ventricle. On the other hand, indices related to isovolumic contraction, such as the rate of pressure rise Figure 26-6 Calculation of cardiac output using the mitral inflow method. A, Diameter of the mitral annulus is measured from the apical four-chamber view during maximal excursion of the mitral valve. B, Doppler sample volume is placed in the center of the mitral annulus to obtain the mitral flow velocity waveform (lower). LA, left atrium; LV, left ventricle. during this period (dP/dt), appear to be less influenced by load and are especially useful for evaluating directional changes of myocardial contractility. The mitral regurgitant jet velocity is largely a consequence of temporal changes in the relationship between left ventricular and left atrial pressures. During isovolumic contraction, left atrial pressure does not change appreciably in patients with chronic mitral regurgitation and a mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 15 compliant left atrium. Thus, the rate of change in velocities (and derived pressures) in 577 Figure 26-7 (Figure Not Available) Drawing of a mitral regurgitant flow velocity jet illustrating the basis for determining rate of pressure rise (RPR) in the left ventricle. Two points are selected along the velocity curve (A, 1 m/sec = 4 mm Hg; B, 3 m/sec = 36 mm Hg), and the time interval (t) between them is measured. ECG, electrocardiogram. (From Bargiggia GS, Bertucci C, Recusani F, et al: Circulation 1989; 80:1287–1292, with permission.) this pre-ejection phase provides information about ventricular systolic performance. [52] [53] [54] [55] Bargiggia et al[52] used Doppler echocardiography to obtain dP/dt from mitral regurgitant jet velocities and found good correlation with peak dP/dt measured at cardiac catheterization (Fig. 26-7) (Figure Not Available) . Doppler-derived dP/dt is obtained by digitization of mitral regurgitant jet velocities at 1 msec intervals to obtain the rate of increase in velocity. This rate of velocity change is converted to rate of pressure increase using the modified Bernoulli equation (pressure gradient = 4[velocity]2 ). In the normal heart, the rate of pressure rise exceeds 1200 mm Hg per second. A pressure rise of less than 400 mm Hg per second is consistent with severe systolic dysfunction.[54] Assessment of Left Ventricular Diastolic Function and Estimation of Left Ventricular Filling Pressure Left ventricular diastolic function plays an important role in the pathophysiology of a variety of diseases.[17] [18] , [56] [57] [58] [59] In patients with systolic dysfunction, abnormalities of diastolic function may importantly contribute to clinical manifestations of disease. Indeed, diastolic function appears to be significantly related to the severity of cardiac symptoms and prognosis in patients with heart failure.[41] [42] [60] [61] [62] [63] [64] [65] [66] [67] Transmitral flow velocity obtained by pulsed Doppler echocardiography has been extensively used to assess left ventricular diastolic function[68] [69] [70] [71] [72] [73] [74] [75] (see Chapter 6) . The normal mitral waveform is characterized by an early peak flow velocity and a second, late peak with atrial systole (Fig. 26-8) . A number of diastolic indices have been used to assess left ventricular diastolic function, including peak velocity during early filling (E), peak velocity following atrial contraction (A), the time integrals of early and late filling velocities, the ratio of early and late peak mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 8 di 15 velocities (E/A), and deceleration time (measured as the time from peak early filling to descent of filling to the baseline). Mitral inflow waveform patterns have been correlated with hemodynamic findings and therefore provide important noninvasive hemodynamic information.[66] [67] [70] A pattern of impaired relaxation is characterized by reduced early peak flow velocity, prolonged deceleration time, and augmented late flow velocity [70] (see Fig. 26-8) . This pattern has been observed in a variety of conditions (e.g., systemic hypertension, coronary artery disease, and early amyloidosis) and is associated with abnormal left ventricular relaxation with relatively normal left ventricular diastolic pressure. In comparison, a "restrictive" pattern of filling has been observed with marked elevation of left atrial and left ventricular diastolic pressure and is most commonly observed in advanced congestive heart failure[41] [42] [66] , [67] [70] [76] (see Fig. 26-8) . Although the transmitral flow velocity waveform provides important information regarding left ventricular diastolic function, the appearance of the transmitral waveform is also influenced by a number of variables, including age, heart rate, and left atrial/left ventricular crossover pressure at the time Figure 26-8 Spectrum of mitral inflow patterns. A, Normal mitral velocity flow pattern. B, Pattern of impaired relaxation with decreased peak early velocity (E) and increased peak late velocity (A). C, Restrictive filling pattern showing increased E velocity, short deceleration time, and reduced A velocity. 578 Figure 26-9 Illustration of left ventricular and left atrial pressures with simultaneous mitral flow velocity waveforms in a normal ventricle, a ventricle with impaired relaxation, and a ventricle with increased preload. Note the relation of the atrioventricular gradient on the appearance of the mitral waveform. Hatched areas represent the atrial filling fraction; large arrows denote isovolumic relaxation time; small arrows indicate deceleration time (Dec Time). A, peak late velocity; E, peak early velocity; LA, left atrium; LV, left ventricle. (From Mulvagh S, Quinones MA, Kleiman NS, et al: J Am Coll Cardiol 1992;20:112– 119, with permission from the American College of Cardiology.) of mitral opening[70] [72] [77] [78] [79] (Fig. 26-9) . The latter accounts for the "pseudonormal" pattern observed in patients with impaired relaxation and mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 9 di 15 elevated left atrial pressure. The dependence of transmitral filling on factors other than left ventricular diastolic dysfunction presents an important consideration for the use of mitral indices of left ventricular filling for assessment of diastolic function. Assessment of pulmonary vein flow velocity waveforms provides information complementary to that obtained from the transmitral flow patterns.[80] [81] [82] [83] Pulmonary venous sampling is most readily obtained from a transesophageal study but with practice can be obtained with the transthoracic approach in most patients. The normal pulmonary vein flow pattern is characterized by antegrade systolic and diastolic waves and a retrograde diastolic wave following atrial systole (Fig. 26-10) . During forward systolic pulmonary vein flow, the left atrium functions as a reservoir. Systolic flow from the pulmonary vein into the left atrium is influenced by contractility of the left ventricle and descent of the mitral annulus, as well as left atrial pressure. Thus, impaired left ventricular systolic function and elevated left atrial (or pulmonary capillary wedge) pressure are associated with decreased systolic antegrade flow in the pulmonary veins[81] [83] (Fig. 26-11) (Figure Not Available) . A ratio of pulmonary vein systolic to diastolic velocity integrals of less than 0.40 correlates with left atrial pressures of greater than 15 mm Hg. During forward diastolic flow of the pulmonary vein, the left atrium functions as a conduit. Pulmonary venous diastolic flow is therefore largely influenced by left ventricular diastolic pressure, as well as factors that affect early transmitral filling: age, heart rate, and differences in left atrial/left ventricular crossover pressure at the time of mitral opening. Retrograde diastolic flow (atrial reversal) depends on the integrity of atrial systole and left atrial pressure. Elevated left atrial pressure is usually associated with a pulmonary vein retrograde diastolic flow velocity of greater than 40 cm per second.[81] An integrated approach to assessment of left ventricular diastolic function utilizes both transmitral and pulmonary venous flow velocities. In the presence of impaired relaxation with relatively normal left ventricular diastolic pressure, transmitral filling shows the classic pattern of E to A reversal (E/A ratio <1.0) and prolonged deceleration time (>150 msec). The pulmonary venous waveform shows a ratio of forward systolic to diastolic flow of 1.0 or greater and a retrograde diastolic flow velocity of less than 40 cm per second. In the presence of elevated left Figure 26-10 Pulmonary vein flow velocity waveforms obtained by mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... |
06/02/2005 Book Text Pagina 10 di 15 transesophageal study in a patient with normal flow pattern (A) and a patient with severe mitral regurgitation (B). There is marked systolic flow reversal in the presence of severe mitral regurgitation. 579 Figure 26-11 (Figure Not Available) Scatterplot of correlation of systolic fraction (pulmonary venous velocity time integral as fraction of the sum of systolic and early diastolic velocity time integral) with pulmonary capillary wedge pressure (PCWP). SEE, standard error of estimate. (From Kuecherer HF, Muhiudeen IA, Kusumoto FM, et al: Circulation 1990;82:1127–1139, with permission.) atrial pressure, early peak mitral flow velocity is increased, followed by shortened deceleration and reduced late peak velocity. Pulmonary venous flow in this situation shows reduced forward systolic flow, a systolic to diastolic ratio of less than 0.4, and increased retrograde diastolic (atrial systolic) flow velocity. The duration of transmitral late flow velocity (A) relative to the duration of pulmonary vein retrograde diastolic flow (Ar) is a useful indicator of left ventricular end-diastolic pressure. In a study by Rossvoll and Hatle, a duration of the pulmonary venous Ar wave exceeding the transmitral A wave duration predicted an end-diastolic pressure of greater than 15 mm Hg, with a sensitivity of 85% and specificity of 79%[84] (Fig. 26-12) . A number of formulas have been derived for estimation of pulmonary capillary wedge and left ventricular end-diastolic pressures (Table 26-3) .[84] [85] [86] [87] [88] [89] [90] The formulas vary considerably in complexity but provide reasonable assessment TABLE 26-3 -- Calculation of Left Ventricular Diastolic Pressure by Echocardiography Study Equation Pozzoli et al[50] PCWP = 1.85 × DR - 0.10 × SF + 10.9 Giannuzzi et al[87] PCWP = 32.16 - 0.104E + 0.1345A - 0.17DT + 4.95E/A Nagueh et al[89] PCWP = 45 - 0.16DT Nagueh et al[84] PCWP = 1.24 (E/Ea) + 1.9 Garcia et al[86] PCWP = 5.27 (E/Vp) + 4.66 Mulvagh et al[85] PWCP = 46 - 0.22IVRT - 0.10AFF - 0.03DT - 2E/A + 0.05MAR mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 11 di 15 Mulvagh et al[85] LVEDP = 46 - 0.22IVRT - 0.03DT - 0.01AFF - (2/E/A) + 0.05MAR Nagueh et al[88] mean PCWP = 17 + 5.3E/A - 0.11IVRT Pozzoli et al[90] PCWP = 0.93DR - 0.155F + 0.03 (dZ - dA) + 0.87E/A + 16.2 A, mitral inflow peak late diastolic velocity; AFF, mitral atrial filling fraction; DT, early mitral velocity deceleration time; DR, early mitral inflow velocity deceleration rate; dZ - dA, difference in duration of reverse pulmonary venous and mitral velocity at atrial contraction; E, mitral inflow peak early velocity; Ea, peak early velocity measured by tissue Doppler at mitral annulus; IVRT, isovolumic relaxation time; MAR, time from mitral closure by Doppler to R wave on ECG; PCWP, pulmonary capillary wedge pressure; SF, peak pulmonary venous flow velocity systolic fraction; Vp, early diastolic color flow propagation velocity. of pressures in patients with reduced left ventricular systolic function. Assessment of Pulmonary Artery Systolic Pressure Pulmonary artery pressure measured invasively has been commonly employed to assess left ventricular diastolic function. The relation of tricuspid regurgitant jet velocity to right ventricular pressure (and pulmonary artery pressure) as estimated by the modified Bernoulli equation (pressure gradient = 4[velocity]2 ), combined with the frequent finding of Doppler-detected tricuspid regurgitation, even in the absence of structural cardiac disease, affords the opportunity to noninvasively estimate pulmonary artery systolic pressure.[91] Thus, PASP = 4V2 + RAP where PASP is pulmonary artery systolic pressure, V is peak velocity of the tricuspid regurgitant jet, and RAP is estimated right atrial pressure. Figure 26-12 Bar charts showing the effect of different left ventricular (LV) pressures before atrial contraction (pre-a) (A) and of LV pressure (a- wave) increases at atrial systole (B) on the mean duration of pulmonary venous retrograde velocity (PV-a) and mitral A wave, and the difference in flow duration. The duration of flow on the vertical axis is in milliseconds. + P <.05 versus normal pressure. + + P < .01 versus mildly increased pressure. + P < .05 versus normal pressure. + + P < .05 versus mildly increased pressure. (From mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 12 di 15 Rossvoll O, Hatle LK: J Am Coll Cardiol 1993; 21:1687–1696, with permission from the American College of Cardiology.) 580 Several approaches have been taken to the estimation of right atrial pressure.[91] [92] [93] Clinical measurement of jugular venous pressure shows significant error. Assumption of a right atrial pressure of 10 mm Hg has been used but has obvious limitations. Right atrial pressure can be more accurately estimated on the basis of the size and respiratory changes of the inferior vena cava. The normal vena cava measures less than 20 mm and shows a 50% reduction in size with inspiration. As right atrial pressure rises, vena caval size increases and the inspiratory decrease in size is blunted, ultimately disappearing when right atrial pressure exceeds 20 mm Hg.[92] Assessment of hepatic vein flow also affords more quantitative determination of right atrial pressure.[93] Pulmonary artery end-diastolic pressure can be estimated from the pulmonary regurgitant jet velocity using the modified Bernoulli equation. This assessment appears to be less reproducible and is less commonly employed in clinical practice. Secondary Valvular Regurgitation Mitral and tricuspid regurgitation are commonly present in congestive heart failure, particularly in heart failure occurring as a consequence of dilated cardiomyopathy.[3] [9] [20] Mitral competence depends on the integrity of all the components of the mitral valve apparatus (including the mitral annulus, leaflets, chordae tendineae, and papillary muscles) as well as the function of the underlying left ventricular myocardium.[94] [95] Several mechanisms have been proposed for mitral regurgitation occurring in the presence of dilated cardiomyopathy. Mitral annular dilation occurring as a consequence of left ventricular dilation has been implicated as an important cause of mitral regurgitation,[96] whereas other reports have disputed the role of annular dilation as a significant factor in functional regurgitation. [97] Papillary muscle dysfunction is a well-accepted cause of mitral regurgitation in ischemic heart disease and is believed to contribute to the development of regurgitation in dilated cardiomyopathy. In support of this view, recent investigations suggest that mitral regurgitation in the presence of dilated cardiomyopathy is related largely to the abnormal shape of the left ventricle. In the presence of heart failure, the left ventricle not only dilates but also loses its normal elliptical shape and becomes more spherical. The presence and severity of mitral regurgitation have been mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 13 di 15 shown to be related to the sphericity of the left ventricular chamber during diastole and systole.[97] The mechanism by which this alteration in chamber shape causes mitral regurgitation may be explained by abnormal papillary muscle alignment and abnormal leaflet apposition during systole. Although the degree of regurgitation is usually mild to moderate in severity, severe regurgitation may be present and may contribute significantly to symptoms as well as prognosis. The importance of mitral regurgitation in dilated cardiomyopathy is underscored by reports demonstrating worse symptomatic status, poorer response to therapy, and reduced survival in patients with severe mitral regurgitation. [98] [99] [100] Doppler echocardiography is exquisitely sensitive for detection of atrioventricular valve regurgitation. However, quantitation of regurgitation is among the more difficult challenges in echocardiography. Experience with Doppler color flow imaging to quantitate the severity of mitral regurgitation has shown reasonable correlation between regurgitant jet size and angiographic grade of mitral regurgitation,[101] [102] but the significant overlap among patients with mild, moderate, or severe regurgitation limits the use of jet size alone for quantitation. Size of the color regurgitant jet is influenced by a number of factors other than regurgitant flow, including pressure difference between left ventricle and left atrium, left ventricular systolic function, size and compliance of the left atrium, entrainment of blood in the atrium, and direction of the jet (central versus eccentric jet)[103] [104] [105] [106] [107] (see Chapter 17) . Doppler echocardiographic quantitation of regurgitant stroke volume and regurgitant fraction has also been used to assess the severity of mitral regurgitation. [108] [109] Thus, the difference between stroke volume through the mitral annulus and stroke volume through the left ventricular outflow represents the regurgitant stroke volume (RSV). This method shows good correlation with angiographic grade of mitral regurgitation, but has shown a tendency toward overestimation of regurgitant stroke volume. This tendency appears to be overcome with experience.[109] Calculation of valve orifice size has conventionally been used to evaluate valvular stenosis but can also be applied to regurgitant lesions to obtain an effective regurgitant orifice area (ERO)[110] (see Chapter 17) : ERO = RSV/TVI where TVI is the time velocity integral of the mitral regurgitant jet recorded mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 14 di 15 with continuous wave Doppler ultrasonography. In the presence of severe mitral regurgitation, regurgitant orifice area generally exceeds 35 to 40 mm2 . Examination of the pulmonary veins is useful for evaluation of the severity of mitral regurgitation. Normal pulmonary vein flow demonstrates phasic forward systolic and diastolic flow and retrograde diastolic flow with atrial contraction. In the presence of mitral regurgitation, forward systolic flow shows an inverse relation to the severity of mitral regurgitation and flow reversal with severe disease [111] (see Fig. 26-10) . Importantly, discordance in pulmonary vein flow velocity may occur in up to 25% of patients with mitral regurgitation and in nearly 40% with severe regurgitation. This discordance occurs most commonly with eccentric regurgitant jets and less commonly with central jets typical of dilated cardiomyopathy. Observations of flow through a restricted orifice (such as that occurring in mitral regurgitation) show that flow converges toward the orifice in a series of proximal isovelocity hemispheric surfaces.[112] This flow convergence region can be demonstrated by Doppler echocardiography as a color mosaic on the ventricular side of the valve (Fig. 26-13) . The continuity principle dictates that regurgitant flow rate (Q) can be calculated as the product of the hemispheric surface area of the flow convergence region and the velocity at that hemispheric surface Q = 2πr2 V n 581 Figure 26-13 (See also color plate.) Apical four-chamber views from a patient with dilated cardiomyopathy and mitral regurgitation. Color flow imaging shows a region of flow convergence on the ventricular side of the mitral valve. LV, left ventricle; RA, right atrium; RV, right ventricle. where r is the radial distance between the color reversal at the first aliasing and the regurgitant orifice and V is the Nyquist velocity. Calculation of n regurgitant flow and regurgitant orifice size by the flow convergence method has shown excellent correlation with angiographic assessment.[112] , [113] Moreover, reduction in mitral regurgitant orifice size appears to be an mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 7 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Serial Two-Dimensional and Doppler Echocardiography in Guiding Treatment and Assessing Prognosis Several pharmacologic and nonpharmacologic treatments are available for treatment of congestive heart failure, including digoxin, diuretics, vasodilators, angiotensin converting enzyme inhibitors, beta-adrenergic blocking agents, and cardiac transplantation.[10] [11] [12] [13] [15] [16] , [115] Therapy can be tailored to the individual patient with the use of noninvasive hemodynamic information obtained by two-dimensional and Doppler echocardiography. For example, although most patients with heart failure and left ventricular systolic dysfunction benefit from positive inotropic agents, either oral digoxin administration or parenteral drugs such as dobutamine, appropriate additional therapy should be geared toward the hemodynamics of the individual patient. Thus, patients with elevated left ventricular filling pressure generally receive significant symptomatic benefit from diuretics and venodilators such as nitroglycerin. On the other hand, patients with normal or only mildly elevated filling may have further deterioration of cardiac output with the use of diuretics and preload reduction. In such patients, management should be directed at optimizing cardiac output with afterload reduction using angiotensin converting enzyme inhibitors or other vasodilators or both. Cardiac transplantation is generally reserved for severely symptomatic patients who do not respond to pharmacologic intervention.[14] [116] At present, the 5-year survival rate after transplantation is |
approximately 75%. Because of the limited resources and significant cost, however, this intervention is available to only a small minority of patients with heart failure. Thus, assessment of the prognosis, and therefore the urgency of transplantation, is of major importance. Doppler Echocardiography in Intensive Care Unit Monitoring Invasive cardiac monitoring in intensive care units allows objective and mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 7 serial hemodynamic assessment of critically ill patients. This information is often vital to the selection of an optimal therapeutic regimen as well as to determining the efficacy of treatment. However, invasive cardiac monitoring is not without considerable costs and finite risks attributable to complications from placement of intravenous or intra-arterial catheters, including pneumothorax, infection, and blood loss. In contrast, noninvasive hemodynamic assessment obtained by two-dimensional and Doppler echocardiography is not associated with these adverse events and presents an important alternative to invasive monitoring. However, effective use of these noninvasive techniques depends largely on the reliability and reproducibility as compared with invasive measurements. Table 26-2 summarizes the accuracy and reproducibility of these noninvasive measures in several major studies. The author's experience with two-dimensional and Doppler echocardiography suggests that there are few situations in which a careful noninvasive hemodynamic assessment yields clinically important differences from similar information obtained invasively. Thus, in most patients, determination of left ventricular volume, ejection fraction and cardiac output, pulmonary artery systolic pressure, and diastolic filling indices provides adequate data for assessment of overall hemodynamic status. 582 TABLE 26-4 -- Echocardiographic Parameters Correlated with Clinical Outcome in Dilated Cardiomyopathy Parameter References LV size [42] [67] [119] LA size [42] LV ejection fraction [8] [12] [64] [119] [126] PA pressure [117] RV size/function [9] [42] Mitral inflow pattern [41] [42] [66] [68] [126] [127] Mitral regurgitation [98] [99] LA, left atrial; LV, left ventricular; PA, pulmonary artery; RV, right ventricular. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 7 Prognostic Value of Echocardiography Determination of prognosis in patients with dilated cardiomyopathy (Table 26-4) remains a challenging clinical problem. A variety of clinical symptoms and signs and invasive hemodynamic and echocardiographic factors have been reported to be predictive of prognosis in patients with dilated cardiomyopathy and may be helpful in guiding therapy[4] [8] [14] , [35] [41] [42] , [65] [66] [86] , [117] [118] [119] [120] [121] [122] [123] [124] [125] [126] [127] [128] [129] [130] (Fig. 26-14 and Table 26-5) . Among the echocardiographic parameters, left ventricular ejection fraction, chamber size and shape, and wall thickness are strong independent predictors of prognosis. Marked reduction of ejection fraction, progressive left ventricular dilation, and increased sphericity of the left ventricle are associated with poor survival in patients with dilated cardiomyopathy. In populations with uniformly markedly depressed ejection fraction (<25%), there is weaker correlation with survival. Increased right TABLE 26-5 -- Univariate Analysis of Clinical, Doppler Echocardiographic, and Hemodynamic Variables Predicting Death or Transplantation in Dilated Cardiomyopathy Parameter Cut-off Points P value EDT <115 msec <.0001 Age <26 yr <.0001 mAoP <71 mm Hg <.0001 LVEDVI >179 mL/m2 <.0001 RVFSA 36% <.0001 NYHA III + IV .0001 LVESVI >150 mL/m2 .0001 LAAI >18 cm2 /m2 .0001 E/A ratio >1.9 .0003 E >0.6 m/sec .0005 mPAP >29 mm Hg .0007 LADI >23 mm/m2 .0008 CTR >57% .0018 B point Present .0041 mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 7 A <0.4 m/sec .0051 S Present .006 3 LVESDI >37 mm/m2 .01 mPAWP >17 mm Hg .02 A, peak velocity of A wave; CTR, cardiothoracic ratio; E, peak velocity of E wave; EDT, E deceleration time; LAAI, left atrial area index; LADI, left atrial diameter index; LVESDI, left ventricular end- systolic diameter index; LVEDVI, left ventricular end- diastolic volume index; LVESVI, left ventricular end- systolic volume index; mAoP, mean aortic pressure; mPAP, mean pulmonary artery pressure; mPAWP, mean pulmonary artery wedge pressure; NYHA, New York Heart Association functional class; S3 , third heart sound; RVFSA, right ventricular fractional shortening area. From Pinamonti B, DiLenarda A, Sinagra G, Camerii F: J Am mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 7 Coll Cardiol 1993;22:808–815. ventricular size and poor systolic function are also associated with poorer prognosis [9] [42] (Fig. 26-15) . A spectrum of transmitral flow velocity patterns have been observed in heart failure that reflect the hemodynamic milieu and severity of disease, as discussed previously.[41] [42] [66] [67] [68] [69] Transmitral filling in patients with dilated cardiomyopathy shows a strong correlation with functional status and survival.[41] [42] [66] , [68] A "restrictive" pattern of filling characterized by increased early transmitral flow velocity, shortened deceleration time, and reduced late velocity is more commonly observed in patients with severe cardiac symptoms and markedly depressed systolic function of the right and left ventricles[42] , [68] (see Fig. 26-8) . This pattern correlates with elevated left ventricular Figure 26-14 Survival curves in patients with congestive heart failure demonstrating the effect of New York Heart Association (NYHA) functional class (A) and gender (B) on cumulative cardiac mortality. (From Xie G-Y, Martin RB, Smith MD, et al: J Am Coll Cardiol 1994;24:132–139, with permission from the American College of Cardiology.) 583 Figure 26-15 Kaplan-Meier survival curves in two morphologic subsets of patients with dilated cardiomyopathy. The top curve (closed circles) depicts survival in patients with predominant and disproportionate dilation of the left ventricular chamber. The bottom curve (triangles) depicts survival in patients with a relatively equal degree of left and right ventricular chamber enlargement. (From Lewis JF, Webber JD, Sutton LL, et al: J Am Coll Cardiol 1993; 21:649–654, with permission from the American College of Cardiology.) diastolic and pulmonary capillary wedge pressure and more severe mitral regurgitation. As much as a 10-fold difference in the 1-year mortality rate has been identified in patients with dilated cardiomyopathy and a restrictive transmitral filling pattern compared with a nonrestrictive pattern[41] (Fig. 26- 16) . Pulmonary artery pressure assessed by Doppler echocardiography is also an mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 7 important predictor of survival in patients with congestive heart failure. In a series of 108 patients with both ischemic and nonischemic disease, tricuspid regurgitant jet velocity exceeding 2.5 m per second was associated with more frequent hospitalization and increased mortality due to heart failure over a follow-up period of 28 months.[117] Aside from these specific echocardiographic measurements, a recent report suggests that the use of echocardiography, in general, is associated with better outcome in patients with congestive heart failure. Patients with heart Figure 26-16 Survival curve in patients with congestive heart failure demonstrating the effect of transmitral flow velocity patterns on cumulative cardiac mortality. (From Xie G-Y, Martin RB, Smith MD, et al: J Am Coll Cardiol 1994;24:132–139, with permission from the American College of Cardiology.) failure who did not undergo echocardiography were less often treated with angiotensin converting enzyme inhibitors and experienced poorer overall survival.[131] Limitations of Echocardiography in Assessment of Heart Failure A significant limitation of echocardiography in the evaluation of congestive heart failure relates to the variability in echocardiographic measurements. This variability is a consequence of both technical factors and intraobserver and interobserver interpretation variability of the serial studies. These factors can be minimized by close adherence to standardized protocols in both performance and interpretation of studies. Despite the previously discussed inherent limitations, ejection fraction remains the most commonly used measure of left ventricular systolic function, with clinically acceptable variability. Ejection fraction can also be accurately obtained by radionuclide angiography, albeit with a small but finite radiation exposure. However, radionuclide angiography does not provide the information about chamber sizes, wall thickness, and valvular function afforded by echocardiography. Ejection fraction obtained by contrast ventriculography has several important limitations, including the use of geometric assumptions that may be less applicable in dilated cardiomyopathy, inherent risk of cardiac catheterization, and impracticality and costs of serial evaluations. Cardiac output measured by Doppler echocardiography also has important limitations for use in evaluation and serial follow-up of patients with heart mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 7 di 7 failure. Observer variability for this technique is substantial, ranging from about 6% to 16%. This variability is largely attributable to discrepancies in measurement of orifice cross-sectional area and is more marked in measurement of transmitral stroke volume. Some investigators have proposed the use of stroke distance to avoid the inherent error incurred by calculating stroke volume and cardiac output.[51] Stroke distance appears to be particularly applicable to serial evaluation after therapeutic intervention. [132] Several circumstances preclude the use of Doppler echocardiography for assessment of cardiac output. These include poor acoustic windows, suboptimal image quality, and valvular regurgitation or stenosis. Despite these limitations, noninvasive estimation of stroke volume and cardiac output is an important adjunct in the evaluation of patients with heart failure. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/222.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Research Applications Research applications of echocardiography in patients with dilated cardiomyopathy can be divided into two major categories: use of existing techniques to evaluate the effects of novel therapeutic interventions and application of newer echocardiographic techniques for improved diagnostic and prognostic information. The former use was discussed in the preceding sections. Several new and innovative echocardiographic developments have potential application to the diagnosis and management of congestive heart failure. The development of newer contrast agents allows better endocardial definition and may be 584 useful for quantitation of ventricular volume and ejection fraction in patients with technically suboptimal study results.[133] [134] In addition, the ability to more reproducibly assess ventricular volume and ejection fraction in general has important implications for assessment of pharmacologic management and therapeutic interventions. The use of contrast agents for measurement of regional coronary perfusion offers potential for noninvasive distinction between ischemic and nonischemic disease (see Chapter 8) .[135] [136] [137] [138] Myocardial characterization using ultrasonic backscatter has been used to distinguish normal from abnormal myocardial tissue[139] [140] [141] [142] (see Chapter 9) . This technique has been most widely applied in the evaluation of ischemic heart disease, but recent investigations have demonstrated distinctive ultrasonic tissue characterization in dilated cardiomyopathy, which may be useful for diagnosis, assessment of disease progression, and evaluation of response to therapy. [141] Three-dimensional echocardiography offers promise of more accurate assessment of ventricular volume and mass[143] [144] [145] (see Chapter 10) . Further developments of these techniques are expected to refine the echocardiographic assessment of individuals with dilated cardiomyopathy and provide important noninvasive data for diagnosis and management. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company 588 Chapter 27 - Echocardiography in the Evaluation and Management of Patients with Hypertrophic Cardiomyopathy Anna Woo MD E. Douglas Wigle MD Harry Rakowski MD Hypertrophic cardiomyopathy is a cardiac disorder characterized by a wide spectrum of clinical, echocardiographic, and hemodynamic findings.[1] [2] This condition is defined as unexplained ventricular hypertrophy that predominantly affects the left ventricle and is usually asymmetric (Fig. 27- 1) .[3] The histopathologic features of hypertrophic cardiomyopathy include myocyte hypertrophy, myocardial fiber disarray, and interstitial fibrosis. Since its modern description more than four decades ago,[4] [5] there have been significant advances in the diagnosis of hypertrophic cardiomyopathy, the understanding of its complex pathophysiology, and the evolution of its management. Echocardiography has played a crucial role in defining hypertrophic cardiomyopathy, determining its pathophysiology, quantitating its morphologic and hemodynamic severity, and assessing the acute and chronic responses to various therapies. [6] Echocardiographic studies have provided invaluable insight into the epidemiology,[7] inheritance,[8] and mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 prognosis[9] of this condition. The ability to perform serial safe, noninvasive, real-time studies makes |
echocardiography the diagnostic modality of choice in the screening,[10] [11] diagnosis,[12] and serial monitoring of patients with hypertrophic cardiomyopathy. In recent years, the role of echocardiography in this condition has extended to intraprocedural decision making, with the use of intraoperative transesophageal echocardiography during surgical myectomy[13] and the application of myocardial 589 Figure 27-1 Hypertrophic cardiomyopathy. Gross pathologic specimen of the heart from a patient with hypertrophic cardiomyopathy and left ventricular outflow tract obstruction who died suddenly. Note the asymmetric hypertrophy with a markedly thickened interventricular septum and the narrow outflow tract between the basal septum and anterior mitral leaflet, which is thickened and fibrosed from repeated mitral leaflet- septal contact (arrow). contrast echocardiography to the guidance of septal ethanol ablation.[14] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/225.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Epidemiology Hypertrophic cardiomyopathy was initially believed to be a rare disorder affecting young adults.[5] This concept was reinforced by studies that focused on highly selected patients with the obstructive form of hypertrophic cardiomyopathy.[15] However, modern studies using echocardiography in the evaluation of subjects suggest a much higher prevalence of this condition than previously anticipated. The Coronary Artery Risk Development in Adults (CARDIA) study, a prospective study of 4111 apparently healthy adults younger than 40 years of age from a general population, detected hypertrophic cardiomyopathy by echocardiographic examination in 0.17% of subjects.[7] There was a similar prevalence of hypertrophic cardiomyopathy in a large study of 33,735 young athletes undergoing preparticipation medical screening in Italy, with a total of 22 cases (0.07%) identified from this cohort.[16] Studies of more selected subjects have reported the prevalence of hypertrophic cardiomyopathy as 0.17% in a study of Japanese workers who underwent electrocardiographic screening and targeted echocardiography,[17] and as 0.5% in a study of 714 consecutive patients referred to an echocardiography laboratory.[18] The reported incidence of hypertrophic cardiomyopathy has ranged from an incidence rate of 0.4 per 100,000 person-years from 1980 to 1981 in Western Denmark[19] to a rate of 2.5 per 100,000 person-years between the years 1975 and 1984 in Olmsted County, Minnesota.[20] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/226.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Molecular Genetics Hypertrophic cardiomyopathy is a genetic disorder with an autosomal dominant pattern of inheritance. This condition is believed to arise from a genetic defect involving one of the proteins of the cardiac myofibrillar apparatus (Fig. 27-2) (Figure Not Available) [21] (1) β-myosin heavy chain (β-MHC), (2) myosin binding protein C, (3) troponin T, (4) α-tropomyosin, (5) troponin I, (6) ventricular myosin essential light chain, (7) ventricular myosin regulatory light chain, (8) α-cardiac actin, or (9) titin. The initial genetic defect was described more than a decade ago.[22] Since then, more than 100 different mutations have been associated with this condition. Various molecular diagnostic techniques have been used to detect these mutations. An abnormal genotype cannot be identified in approximately one third of patients with a definite family history of hypertrophic cardiomyopathy.[2] It remains controversial whether the underlying genotype contributes to the overall phenotypic expression of hypertrophic cardiomyopathy and whether it should be considered in the risk stratification and management of patients.[2] Previous studies have suggested that certain genetic defects, such as missense mutations of the β-MHC gene resulting in an amino acid charge change[23] or cardiac troponin T mutations, [24] are associated with a poor prognosis. A study of six different missense mutations of the β-MHC gene showed no significant relationship between the genetic defect and the degree or morphologic pattern of hypertrophy.[25] Other studies, however, have suggested that patients with troponin T[24] or cardiac myosin binding protein C defects[26] may have a milder degree of hypertrophy compared with patients with β-MHC mutations. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/227.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 4 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Diagnosis The diagnosis of hypertrophic cardiomyopathy is based on the demonstration of left ventricular hypertrophy in the absence of other causes, such as systemic hypertension or aortic stenosis.[3] M-mode echocardiography assumed an early role in the diagnosis of hypertrophic cardiomyopathy.[27] The echocardiographic finding of a septal-to-posterior Figure 27-2 (Figure Not Available) (See also color plate.) Schematic diagram of the cardiac myofibrillar apparatus. Hypertrophic cardiomyopathy is a genetic disorder involving one of the nine cardiac sarcomeric proteins. The percentages (in parentheses) represent the relative frequency of the mutations of the individual sarcomeric proteins reported from various studies. (From Spirito P, Seidman CE, McKenna WJ, Maron BJ: N Engl J Med 1997;336:775–785. Copyright © 1997 Massachusetts Medical Society.) 590 Figure 27-3 Cross-sectional, two-dimensional echocardiographic views obtained at the midpapillary level from a normal heart (A) and from two cases of hypertrophic cardiomyopathy (B and C). In B and C, there is an asymmetric increase in septal wall thickness without involvement of the posterior free wall. Hypertrophy is limited to the septum (arrows) in B, whereas there is anterolateral extension of the hypertrophy (arrows) in C. (From Wigle ED, Sasson Z, Henderson M, et al: Prog Cardiovasc Dis 1985;28:1–83.) wall thickness ratio of greater than 1.3 is strongly associated with hypertrophic cardiomyopathy (Fig. 27-3) . [28] The use of a septal-to- posterior wall thickness ratio of 1.5:1 increases the specificity of asymmetric septal hypertrophy for this condition.[6] Other M-mode findings associated with obstructive hypertrophic cardiomyopathy, such as systolic anterior motion and mid-systolic notching of the aortic valve, have been detected in other conditions and are no longer considered pathognomonic mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 4 for this condition. Family Screening The first-degree relatives of patients with hypertrophic cardiomyopathy should be screened for this condition.[29] Possible screening methods for family members include molecular genetic analysis,[12] [21] 12-lead electrocardiogram,[30] and echocardiography. M-mode and two-dimensional echocardiography have been used as investigational tools in the family screening of this condition for the past three decades,[8] and echocardiography is the most widely accepted diagnostic screening test for hypertrophic cardiomyopathy.[29] The diagnosis of this condition is made in children when left ventricular wall measurements are more than two standard deviations above the mean for weight and age.[31] New criteria for the diagnosis of hypertrophic cardiomyopathy in first-degree adult relatives of patients with hypertrophic cardiomyopathy have been proposed (Table 27-1) .[10] The diagnosis in first-degree relatives would be made in the presence of (1) one major echocardiographic or electrocardiographic criterion, (2) two minor echocardiographic criteria, or (3) one minor echocardiographic and two minor electrocardiographic criteria. These criteria were formulated on the premise that mild echocardiographic or electrocardiographic abnormalities will have a high probability of being the phenotypic expression of a genotypic abnormality in first-degree relatives. Screening throughout adulthood, usually at 5-year intervals, is currently recommended because hypertrophic cardiomyopathy may have delayed penetrance, particularly in those patients with underlying cardiac myosin binding protein C defects. [26] Preparticipation Screening in Athletes The screening of young athletes prior to involvement in competitive sports remains a contentious issue.[32] Previous studies of medical screening (a combination of history, physical examination, and 12-lead electrocardiogram or echocardiography alone) of a total of 766 American college athletes found no cases of hypertrophic cardiomyopathy.[33] [34] The investigators concluded that systematic medical screening was not beneficial, especially since there was confusion between possible physiologic versus pathologic ventricular hypertrophy (see "Differential Diagnosis"). However, a large Italian study of 33,735 young athletes undergoing preparticipation medical screening detected 22 individuals with hypertrophic cardiomyopathy. [16] All of these subjects were barred from competitive athletic activities and none of these subjects died during a mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 4 mean TABLE 27-1 -- Proposed Diagnostic Criteria for Hypertrophic Cardiomyopathy in Adult First-Degree Relatives Major Criteria Minor Criteria Echocardiographic Criteria Left ventricular wall thickness: Left ventricular wall thickness: • ≥13 mm in anterior septum or • 12 mm in anterior septum or posterior wall posterior wall • ≥15 mm the posterior septum or • 14 mm in posterior septum or free free wall wall Severe SAM (septal-leaflet Moderate SAM (no leaflet-septal contact) contact) Redundant mitral valve leaflets Electrocardiographic Criteria Left ventricular hypertrophy and Complete BBB or (minor) repolarization changes (Romhilt & interventricular conduction defect (in Estes criteria) left ventricular leads) T wave inversion in one of the Minor repolarization changes in left following sets of leads: ventricular leads • ≥3 mm in leads I and a VL (with QRS-T wave axis difference ≥30 degrees) • ≥3 mm in leads V3–V6 • ≥5 mm in leads II, III, aVF Abnormal Q (>40 msec or >25% R Deep S wave in lead V2 (>25 mm) wave) in at least two leads from following sets of leads: • Leads II, III, aVF (in absence of left anterior hemiblock) • Leads V1–V4 • Leads I, aVL, V5–V6 Unexplained chest pain, dyspnea or syncope SAM, systolic anterior motion. mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 4 Modified from McKenna WJ, Spirito P, Desnos M, et al: Heart 1997;77:130–132. 591 follow-up of 8 years. There was one case of sudden death due to hypertrophic cardiomyopathy in an athlete in whom the condition was not detected during life. The results of this study suggest that preparticipation screening may prevent sudden death in hypertrophic cardiomyopathy. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/228.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Differential Diagnosis The differential diagnosis of asymmetric or disproportionate septal hypertrophy includes such lesions as right ventricular hypertension secondary to valvular pulmonary stenosis, pulmonary hypertension, and d- transposition of the great arteries. Increased septal wall thickness has been described in such various conditions as amyloidosis,[35] septal sarcomas, glycogen and mucopolysaccharide storage diseases, Friedreich's ataxia, and myxedema (Fig. 27-4) .[36] Hypertrophy secondary to such known conditions as systemic hypertension or valvular aortic stenosis may commonly have a prominent degree of focal septal hypertrophy. Other Causes of Left Ventricular Hypertrophy: Common Clinical Dilemmas Athlete's Heart The clinical and echocardiographic differentiation between hypertrophic cardiomyopathy and athlete's heart may be difficult.[37] [38] [39] The left ventricular wall thickness may be 13 to 16 mm in 2% of elite athletes, raising the possibility of underlying hypertrophic cardiomyopathy.[37] Multivariate analyses have shown that the major determinants of cardiac morphologic adaptations to training include body size (body surface area or height) and participation in certain endurance sports. Therefore, alterations in left ventricular wall thickness may be more striking in athletes engaging in rowing or canoeing, cycling, and cross-country skiing.[38] The distinction between athlete's heart and pathologic hypertrophy may be less of an issue Figure 27-4 (See also color plate.) Two-dimensional echocardiographic parasternal long-axis (A) and short-axis (B) views from a 45-year-old woman with heart failure referred for evaluation of hypertrophic cardiomyopathy. Echocardiographic evaluation revealed asymmetric increased wall thickness of the septum, no systolic anterior motion, thickened mitral mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 |
Book Text Pagina 2 di 2 and aortic valve leaflets, central mitral regurgitation, and moderate aortic regurgitation. Subsequent investigations revealed underlying systemic amyloidosis. in women, since the left ventricular wall thickness of elite female athletes is in the range of 6 to 12 mm, which does not exceed normal age-adjusted limits for wall thickness. This suggests that athletic training may not be a stimulus for significant hypertrophy in females.[40] Septal Hypertrophy in the Elderly It may be difficult to distinguish between elderly patients with hypertrophic cardiomyopathy and those with hypertensive heart disease.[41] Elderly subjects may develop a sigmoid-shaped septum as an age-related phenomenon. [42] Terms that have been used to describe this finding are sigmoid septum, septal bulge,[43] or discrete upper septal hypertrophy. It is controversial whether this finding should be considered a subtype of hypertrophic cardiomyopathy or whether it represents a benign anatomic variant.[44] [45] Other findings on echocardiographic examination that are more compatible with a septal bulge rather than hypertrophic cardiomyopathy of the elderly include focal hypertrophy limited to less than 3 cm length of the basal anterior septum, protrusion of the focal hypertrophy into the left ventricular outflow tract, a normal left ventricular end-diastolic diameter, and the absence of other characteristic echocardiographic findings of hypertrophic cardiomyopathy.[44] Echocardiographic and clinical features of hypertrophic cardiomyopathy in the elderly are discussed later (see "Hypertrophic Cardiomyopathy of the Elderly"). MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/229.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 4 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Evaluation by Echocardiography Left Ventricular Hypertrophy: Severity, Distribution, and Patterns of Hypertrophy The advent of two-dimensional echocardiography greatly increased the ability to detect the full extent, distribution, and severity of myocardial hypertrophy. [46] [47] [48] Comprehensive echocardiographic assessment requires imaging of the left ventricle from several transthoracic 592 Figure 27-5 Optimal echocardiographic evaluation of the degree, extent, and distribution of hypertrophy in hypertrophic cardiomyopathy requires imaging from multiple transthoracic windows. Parasternal long-axis (A),, parasternal short-axis at the basal level (B), apical long- axis (C), and apical four-chamber (D) views in a 22-year-old woman with hypertrophic cardiomyopathy and left ventricular outflow tract obstruction. Massive hypertrophy was detected with a maximal septal thickness of 34 mm, anterolateral wall involvement, and extension of hypertrophy to the apical level. The patient had New York Heart Association class III symptoms, severe systolic anterior motion, and a resting outflow tract gradient of 70 mm Hg and was referred for surgical myectomy. windows, including the parasternal long-axis view, serial parasternal short- axis views, and the apical windows (Fig. 27-5) . Measurements of the anterior septum, posterior septum, posterior wall, and anterolateral wall obtained from cross-sectional parasternal short-axis views are made at three levels: basal (at the level of the mitral valve), midventricular (at the level of the papillary muscles), and apical.[6] A 10-point scoring system to quantify the extent of left ventricular hypertrophy in hypertrophic cardiomyopathy has been developed by Rakowski and Wigle (Table 27-2) .[47] [49] This score incorporates the degree of septal hypertrophy at the basal level, the length mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 4 of septal hypertrophy, and the extension of hypertrophy to the anterolateral free wall. The parasternal short-axis view of the left ventricle at the level of the mitral leaflet tips can be used to define anterolateral wall involvement. The apical four-chamber TABLE 27-2 -- Extent of Hypertrophy According to Echocardiographic Point Score Extent of Hypertrophy Points Septal thickness, mm (basal third of septum) 15–19 1 20–24 2 25–29 3 >30 4 Extension to papillary muscles (basal two thirds of septum) 2 Extension to apex (total septal involvement) 2 Anterolateral wall extension 2 Maximum total 10 From Wigle ED, Sasson Z, Henderson M, et al: Prog Cardiovasc Dis 1985;28:1–83. and long-axis views can determine the length of septal involvement. In a study of 100 consecutive patients with hypertrophic cardiomyopathy presenting to our echocardiography laboratory, 25% of cases had localized subaortic hypertrophy, 27% had septal hypertrophy extending to the midpapillary level, and 48% had hypertrophy extending to the apex. There was a significant relationship between the hemodynamic subtype of hypertrophic cardiomyopathy (resting left ventricular outflow tract obstruction, latent or provocable outflow tract obstruction, or the nonobstructive form) and the extent of hypertrophy (Table 27-3) .[47] [49] Maron et al[48] classified asymmetric septal hypertrophy into four types (Table 27-4) . A minority of patients had involvement of the anterior septum alone (type I). Panseptal hypertrophy, with involvement of both the anterior and posterior septum, was detected in 20% of patients (type II). More than half of the patients with hypertrophic cardiomyopathy had extension of hypertrophy to the anterolateral wall (type III). All other patterns of hypertrophy (type IV), such as isolated posteroseptal, apical septal, or lone anterolateral wall involvement (Fig. 27-6) , constituted 18% mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 4 of the study cohort. Technical Factors and Echocardiographic Pitfalls Echocardiographic studies have demonstrated changes in the acoustic texture of the myocardium in patients with hypertrophic cardiomyopathy.[46] [50] There may be increased ultrasonic reflectivity of the left ventricular walls, especially the interventricular septum. Diffuse bright echoes 593 TABLE 27-3 -- Extent of Hypertrophy Related to Hemodynamic Subg Hypertrophic Cardiomyopathy Basal Basal No. One Two Whole Hemodynamic of Interventricular Third, Third, Septum, Anterola Subgroup Cases Septum (mm) % % % Extensio Resting 39 2.45 ± 0.55 8% 20% 72% 83% obstruction Latent 34 1.89 ± 0.35 53% * 35% 12% * 13% obstruction No obstruction 27 2.09 ± 0.57 14% † 26% 59% † 63% † From Rakowski H, Fulop J, Wigle ED: Postgrad Med J 1986;62:557–561 *P < 0.001 latent vs both resting and no obstruction †P < 0.05 no obstruction vs resting obstruction may be seen throughout the myocardium and may give a ground-glass appearance. One study demonstrated significantly greater reflectivity of the septal and posterior walls in patients with hypertrophic cardiomyopathy compared with age-matched control subjects. There are important technical considerations in the echocardiographic assessment of hypertrophic cardiomyopathy. Oblique cuts of the left ventricle can spuriously produce the appearance of asymmetric septal hypertrophy and overestimate wall thickness.[36] [51] Two-dimensional echocardiographic studies have demonstrated that hypertrophy can be quite mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 4 localized or eccentric in distribution.[6] [52] More atypical forms of hypertrophic cardiomyopathy, such as isolated lateral wall hypertrophy or asymmetric apical hypertrophy, may be missed from standard parasternal long-axis views, since the septum and anterior wall appear normal in thickness and there is no systolic anterior motion of the mitral valve. The diagnosis of apical hypertrophy by echocardiography may be missed in patients with difficult or suboptimal apical windows or if the apical segments are foreshortened. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/230.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 7 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Left Ventricular Outflow Tract Obstruction Pathophysiology M-mode echocardiographic studies demonstrated narrowing of the left ventricular outflow tract,[53] systolic anterior motion of the mitral valve,[54] and mid-systolic notching of the aortic valve,[55] and established the important role of echocardiography in the assessment of left ventricular outflow tract obstruction in patients with hypertrophic cardiomyopathy.[56] Advances in two-dimensional echocardiography and Doppler techniques would provide additional insights into the mechanisms responsible TABLE 27-4 -- Morphologic Classification of Hypertrophic Cardiomyopathy Percentage of Maron Type Distribution of Hypertrophy Cases I Isolated anterior septum 10 II Panseptal (anterior and posterior septum) 20 without free wall involvement III Septum and anterolateral free wall 52 IV Regions other than basal anterior septum 18 From Maron BJ, Gottdiener JS, Epstein SE: Am J Cardiol 1981;48:418–428, with permission from Excerpta Medica Inc. for dynamic outflow tract obstruction,[6] summarized in Table 27-5 . Morphologic features of hypertrophic cardiomyopathy that contribute to left ventricular outflow tract obstruction include narrowing of the outflow tract by ventricular septal hypertrophy, [57] intrinsic abnormalities of the mitral leaflets, [58] [59] [60] anterior displacement of the mitral apparatus,[46] [56] [58] and anterior malposition of the papillary muscles.[61] There is a close relationship between the extent of left ventricular mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 7 hypertrophy and the presence of left ventricular outflow tract obstruction. The presence of resting left ventricular outflow tract obstruction is associated with a higher hypertrophy point score (see Table 27-3) .[49] The mitral leaflets in hypertrophic cardiomyopathy are typically elongated.[59] These mitral leaflets coapt abnormally in the body of the leaflets, rather than at the tip.[58] [59] The degree of anterior displacement of the mitral apparatus has been related to the degree of obstruction.[46] [56] [58] Furthermore, in hypertrophic cardiomyopathy, the papillary muscle tips are displaced anteriorly and toward one another. This results in a decrease in the relative tension on the chordae tendineae to the body of the anterior mitral leaflet, producing relative chordal slack in the central and anterior leaflet portions.[59] [62] Reduced chordal tension is more likely when the distance from the papillary muscle tips to the mitral leaflets is decreased by a combination of hypertrophy at the base of the papillary muscles and increased leaflet length. Mitral Leaflet Systolic Anterior Motion Although the nature of the hydrodynamic forces on the anterior mitral leaflet remains controversial, it is believed that the anterior leaflet distal to the site of coaptation is subjected to Venturi[1] or drag forces, or both.[62] [63] Therefore, systolic anterior motion occurs, and the tip of the anterior mitral valve leaflet typically develops a sharp TABLE 27-5 -- Factors Contributing to Dynamic Left Ventricular Outflow Tract Obstruction Narrowing of left ventricular outflow tract Septal hypertrophy Anterior displacement of mitral apparatus Anterior displacement of papillary muscles Hydrodynamic forces (Venturi and drag forces) causing systolic anterior motion Rapid early left ventricular ejection Elongated mitral leaflets 594 Figure 27-6 Atypical pattern of hypertrophy with predominant mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 7 anterolateral wall hypertrophy in a 36-year-old woman with a strong family history of hypertrophic cardiomyopathy. Two-dimensional end-diastolic frames from parasternal long-axis (A) and short-axis (B) views show an anterior septal thickness of 13 mm and maximal hypertrophy involving the basal anterolateral wall, with a wall thickness of 19 mm. anterior and superior angulation, leading to mitral leaflet-septal contact in early to mid-systole (Fig. 27-7) . There is a significant relationship between systolic anterior motion (SAM) and the onset of the obstructive pressure gradient, which was demonstrated in patients undergoing simultaneous cardiac catheterization and M-mode echocardiographic studies (Fig. 27-8) . [64] The presence of mitral leaflet–septal contact occurs almost simultaneously with the onset of the pressure gradient. M-mode, two-dimensional, and Doppler echocardiography are established noninvasive techniques in the assessment of the degree of left ventricular outflow tract obstruction in patients with hypertrophic cardiomyopathy. An M-mode echocardiographic study classified the degree Figure 27-7 (See also color plate.) Schematic diagram of a transesophageal echocardiogram (frontal long-axis plane) demonstrating the anterior and basal motion of the anterior mitral leaflet leading to leaflet-septal contact and failure of leaflet coaptation in mid- systole. At the onset of systole (A), the coaptation point (thick arrow) is in the body of the mitral leaflets. During early systole (B) and mid-systole (C), there is anterior and basal movement of the residual length of the anterior mitral leaflet (thick arrow) with septal contact and failure of leaflet coaptation (thin arrow). The interleaflet gap (arrow) results in a posteriorly directed jet of mitral regurgitation into the left atrial cavity (stippled area). Corresponding two-dimensional transesophageal views (D and E) with color flow imaging in a patient with obstructive hypertrophic cardiomyopathy show septal hypertrophy, anterior motion of the anterior mitral leaflet, and color turbulence in the outflow tract with the posteriorly directed mitral |
regurgitation. (A to C, From Grigg LE, Wigle ED, Williams WG, et al: J Am Coll Cardiol 1992;20:42–52. Reprinted with permission from the American College of Cardiology.) of SAM into three categories: (1) mild (SAM-septal distance > 10 mm) (2) moderate (SAM-septal distance ≤10 mm or brief mitral leaflet–septal contact), and (3) severe (prolonged SAM-septal contact, lasting at least 30% of echocardiographic systole).[54] A subsequent study documented severe SAM in all patients with resting obstruction. There was a linear relationship between the time of onset of SAM and the severity of left ventricular outflow tract obstruction (Fig. 27-9) (Figure Not Available) .[65] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 7 Color M-mode echocardiography is a valuable technique for demonstrating SAM-septal contact as the site of left ventricular outflow tract obstruction. [6] Blood flow toward the site of mitral leaflet-septal contact is seen as a blue jet while the signal aliases to red as flow velocity 595 Figure 27-8 Simultaneous hemodynamic and M-mode echocardiographic recordings in a patient with obstructive hypertrophic cardiomyopathy and a gradient of 86 mm Hg. Arrow indicates simultaneous onset of systolic anterior motion-septal contact and onset of pressure gradient (defined as peak of aortic percussion wave). AO, central aortic pressure; ECG, echocardiogram; IVS, interventricular septum; LV, left ventricular pressure; MV, mitral valve; PW, posterior wall. (From Pollick C, Morgan CD, Gilbert BW, et al: Circulation 1982;66:1087–1094.) increases during rapid early ejection into the aorta. At the site of mitral leaflet-septal contact, the site of left ventricular outflow tract obstruction, two turbulent mosaic jets develop: one is directed into the posterior portion of the Figure 27-9 (Figure Not Available) Method of quantitating pressure gradient (PG) from degree of systolic anterior motion (SAM)-septal contact is shown in M-mode echocardiogram (ECG). The two time periods used to calculate PG are as follows: X = duration of SAM-septal contact and Y = period from onset of SAM to onset of SAM- septal contact. IVS, interventricular septum; MV, mitral valve; PW, posterior wall. (From Pollick C, Rakowski H, Wigle ED: Circulation 1984;69:47.) obstructed left ventricular outflow tract and the second is an eccentric, posteriorly directed jet of mitral regurgitation into the left atrium. Two-dimensional echocardiography further defines the structures involved in causing systolic anterior motion. The distal anterior mitral leaflet and chordae tendineae move anteriorly to contact the septum in the presence of severe systolic anterior motion. The parasternal short-axis views demonstrate that mitral leaflet-septal contact may be extensive, involving much of the circumference of the anterior leaflet, which leads to significant narrowing of the left ventricular outflow tract.[46] [49] Finally, left ventricular outflow tract obstruction may develop secondary to posterior leaflet SAM and posterior leaflet-septal contact (Fig. 27-10) .[66] [67] Doppler Assessment mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 7 Pulsed wave and continuous wave Doppler have been used to determine the pressure gradient across the left ventricular outflow tract in patients with hypertrophic cardiomyopathy. Pulsed wave Doppler signals can be recorded sequentially from the left ventricular apex to the outflow tract. The peak velocity increases as the sample volume approaches the site of mitral leaflet-septal contact.[6] Continuous wave Doppler assessment from an apical approach with the beam directed across the left ventricular outflow tract can be used to determine the peak velocity (V) at the site of obstruction. Patients with outflow tract obstruction have a characteristic spectral profile with an asymmetric leftward concave shape (Fig. 27-11) .[68] This results from a relatively rapid initial rise in velocity followed by a more gradual increase in the outflow tract velocity to cause a peak in late systole, resulting in a dagger-shaped configuration. [69] There may be some variability in the waveform contour, and some spectral profiles will demonstrate lesser degrees of asymmetry with the outflow tract jet peaking earlier in systole. The peak gradient (∆P) can be estimated using the modified Bernoulli equation2 : ∆P = 4V2 There is an excellent correlation between the pressure gradient determined by continuous wave Doppler measurements and that determined by high- fidelity micromanometer recordings during cardiac catheterization.[68] [70] Color flow mapping has been used to characterize the level of obstruction, either in the left ventricular outflow tract or in the midventricle.[71] Serial Doppler studies have shown that there is significant spontaneous variability in the left ventricular outflow tract gradient in hypertrophic cardiomyopathy.[72] Technical Aspects of Doppler Evaluation There are important technical considerations in the performance and interpretation of Doppler studies in patients with hypertrophic cardiomyopathy. It was not possible 596 Figure 27-10 (color plate.) Two-dimensional frames from a transesophageal echocardiogram illustrating posterior leaflet-septal contact. A, During diastole, the mitral leaflets open. Note the unusually mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 6 di 7 elongated posterior leaflet. The mitral annulus is tilted so that the posterior leaflet extends into the left ventricular cavity farther than normal. B, In early systole, the anterior leaflet coapts behind the posterior leaflet. C through E, In mid- to late systole, anterior motion of the posterior leaflet occurs (C), and posterior leaflet- septal contact develops (D), resulting in left ventricular outflow tract obstruction (E). F, Color flow imaging demonstrates the development of a turbulent mosaic jet in the left ventricular outflow tract and a jet of mitral regurgitation. to obtain a discernible signal from the left ventricular outflow tract in 16% of patients in one study comparing continuous wave Doppler echocardiography to cardiac catheterization.[68] This inability to acquire a clear spectral display from the outflow tract may be secondary to inadequate transthoracic windows or distortion of left ventricular geometry. In addition, it is imperative to distinguish the high-velocity systolic signal coming from the outflow Figure 27-11 Continuous wave Doppler recordings of the left ventricular outflow tract in a young patient with hypertrophic cardiomyopathy and severe systolic anterior motion and severe mitral regurgitation. The spectral profile has a characteristic dagger-shaped configuration. The peak velocity in the outflow tract is 4.4 m per second, which corresponds to a peak outflow tract gradient of 77 mm Hg, based on the modified Bernoulli equation. tract from the signal of mitral regurgitation. The spectral profile of mitral regurgitation is characterized by an earlier onset, a more abrupt initial increase in velocity, and a higher peak velocity than that of an outflow tract signal. Systolic jets with a peak velocity of greater than 5.5 m per second (gradient >120 mm Hg) are most likely secondary to mitral regurgitation rather than left ventricular outflow tract obstruction.[68] Further differentiation of these two jets can be accomplished by orienting the transducer more medially and anteriorly and away from the mitral regurgitant jet. Nevertheless, there may still be contamination of the high- velocity signal of outflow tract obstruction from the jet of mitral regurgitation (Fig. 27-12) . This pitfall is particularly more common in patients with concomitant intrinsic mitral valve disease and a more centrally directed jet of mitral regurgitation. Despite optimal imaging, adjustments in instrument settings, and consideration of the differences in the timing and contour of these systolic jets, the distinction between these different Doppler signals may occasionally still be difficult.[73] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 3 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Mitral Regurgitation in Hypertrophic Cardiomyopathy Anterior mitral leaflet-septal contact results in failure of coaptation with the posterior mitral leaflet, creating a funnel-shaped gap through which mitral regurgitation can develop, predominantly in mid-systole to late systole.[13] Studies of patients undergoing myectomy for obstructive 597 Figure 27-12 In a patient with obstructive hypertrophic cardiomyopathy, continuous wave Doppler signals from the left ventricular outflow tract at the site of obstruction (A), from the intermediate position (B), and at the site of mitral regurgitation in posterior left atrium (C). Obstructive outflow tract jet starts after the QRS wave, is preceded by low velocity presystolic flow, and has characteristic change in acceleration velocity (arrow, A). Mitral regurgitation is typically of higher velocity and starts earlier in systole. Care must be taken to avoid contamination of left ventricular outflow tract jet with mitral regurgitation. (From Rakowski H, Sasson Z, Wigle ED: J Am Soc Echocardiogr 1988;1:31–47.) hypertrophic cardiomyopathy have demonstrated a predominant posteriorly directed jet in the majority of patients without independent mitral valve disease (Fig. 27-13) .[13] , [74] Mitral valve leaflet size contributes to the development of systolic anterior motion. A study combining echocardiographic features and pathologic findings in hypertrophic cardiomyopathy detected enlarged mitral valves in 44% of patients.[60] Patients with enlarged mitral valves had echocardiographic evidence for "typical" systolic anterior motion, characterized by the presence of a sharp, right-angled bend of the distal half of the anterior mitral valve leaflet and contact of the distal and central portions of the anterior mitral leaflet with the ventricular septum. In contrast, in patients with normal-sized mitral valves, systolic anterior motion was "atypical," involving greater portions of the body of the anterior mitral leaflet body and related chordae mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 3 tendineae, and with little bending of the anterior mitral valve leaflet. Mitral regurgitation associated with obstructive hypertrophic Figure 27-13 (color plate.) Patient with severe obstructive hypertrophic cardiomyopathy and severe mitral regurgitation. A, Parasternal long- axis view showing turbulent left ventricular outflow tract and severe mitral regurgitation directed toward the posterior left atrial (LA) wall. B, Color M- mode study from the apical four-chamber view. C, Color M-mode line highlighted by arrow. Systolic flow at the midventricular level is homogeneously blue and then laminar. As the flow approaches the area of obstruction at the site of anterior leaflet septal contact, aliasing to red occurs over a depth of about 1 cm. The obstructed area of the outflow tract then has a mosaic pattern indicative of turbulent flow. In early systole, there is a narrow band of blue flow with brief duration of aliasing to red, followed by turbulent flow, indicating early development of turbulent flow and of outflow tract obstruction, which was timed with the onset of systolic anterior motion. LV, left ventricle; AO, aortic root. (From Rakowski H, Sasson Z, Wigle ED: J Am Soc Echocardiogr 1988;1:31–47.) cardiomyopathy has been shown to be related to the degree of anterior leaflet systolic anterior motion and to the length and mobility of the posterior leaflet, which determine the size of the interleaflet gap and the degree of mid-systolic coaptation of the mitral leaflets.[75] These findings were corroborated by an intraoperative transesophageal echocardiographic study of 104 patients that demonstrated a significant correlation between the degree of mitral regurgitation, as assessed by color jet area and pulmonary venous flow pattern, and the degree of left ventricular outflow tract obstruction.[74] The presence of a nonposterior jet of mitral regurgitation suggests intrinsic mitral valve leaflet disease independent of SAM. Independent mitral valve lesions can be identified by echocardiography and are usually related to mitral valve prolapse, [76] ruptured chordae,[77] mitral annular calcification,[78] anomalous insertion of a papillary muscle into the anterior mitral leaflet,[79] or leaflet trauma (Fig. 27-14) . Repeated mitral leaflet-septal contact is associated with fibrosis and thickening 598 Figure 27-14 (color plate.) Transesophageal echocardiographic images from the long-axis view in three patients with obstructive hypertrophic cardiomyopathy. A, Posteriorly directed jet of mitral regurgitation (arrow) in a patient without independent mitral valve disease. B, Anteriorly directed mitral regurgitant jet mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 3 (arrow) in a patient with posterior mitral valve leaflet prolapse. C, Centrally directed jet of mitral regurgitation (arrow) in a patient with rheumatic mitral stenosis. Ao, aorta; LV, left ventricle; MR, mitral regurgitation. (From Yu E, Omran AS, Wigle ED, et al: J Am Coll Cardiol 2000;36:2219–2225.) of the anterior mitral leaflet and with subaortic septal endocardial fibrosis and thickening, previously described as a septal "callus."[46] Myectomy alone is generally successful in relieving mitral regurgitation, without the requirement for associated mitral valve replacement.[74] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/232.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any |
medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Atypical Forms of Hypertrophic Cardiomyopathy Asymmetric Apical Hypertrophy Asymmetric apical hypertrophic cardiomyopathy was initially reported by Japanese investigators in the 1970s.[80] [81] This unusual variant of hypertrophic cardiomyopathy has Figure 27-15 Two-dimensional echocardiographic and pulsed-wave Doppler recordings in a patient with asymmetric apical hypertrophic cardiomyopathy. A and B, Parasternal long-axis and short-axis views demonstrating normal septal wall thickness and no systolic anterior motion. C, Apical four-chamber view shows increased thickness of the apicolateral wall and spade-shaped configuration of the left ventricle at end-diastole. D, Pulmonary venous inflow pattern with sampling of right upper pulmonary vein demonstrates increased velocity of PV(a) (arrow), reflecting increased left ventricular end-diastolic pressure. subsequently been described in non-Asian populations.[82] The striking features of patients with apical hypertrophy include the presence of giant negative T waves (≥10 mm) in the precordial electrocardiographic leads and an "ace of spades" configuration to the left ventricle (Fig. 27-15) . The diagnosis may be missed if acoustic windows are suboptimal and endocardial definition is poor. Contrast echocardiography may be useful in enhancing endocardial definition for identification of apical hypertrophy.[83] Echocardiography plays an important role in the assessment of the degree of hypertrophy at the apex, the extent of hypertrophy, and the development of such complications as impaired diastolic filling, apical aneurysm formation, apical infarction and subsequent midventricular obstruction, 599 and left atrial enlargement. Magnetic resonance imaging studies have mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 identified a non-spade-shaped type of apical hypertrophy.[84] Serial magnetic resonance imaging of patients with this condition has suggested that apical hypertrophy can begin with the involvement of a single apical segment, which may produce a non-spade-shaped configuration. Circumferential hypertrophy of all four apical segments may subsequently develop and lead to the classic spade-shaped configuration.[85] Midventricular Obstruction The midventricular form of obstructive hypertrophic cardiomyopathy, initially described in 1976,[86] is an uncommon variant of this condition. Invasive angiographic and hemodynamic features of this condition include an hourglass-shaped left ventricular cavity, systolic midcavity obliteration, a distinct apical chamber, and a systolic pressure gradient at the midventricular level. Echocardiographic and Doppler findings include septal hypertrophy with hypertrophy extending to the midpapillary level, midcavity obliteration in systole, a persistent residual apical cavity in systole, and color turbulence at the midventricular level (Fig. 27-16) .[47] [71] [87] Subtypes of midventricular obstruction include lone midcavity obstruction, combined left ventricular outflow tract and midventricular obstruction, or midventricular obstruction associated with apical infarction or apical aneurysm formation. The combination of color flow mapping, pulsed wave, and continuous wave Doppler techniques is useful in localizing the site or sites and severity of obstruction.[71] Figure 27-16 (color plate.) A, Diastolic two-dimensional echocardiographic apical long-axis view of a patient with midventricular obstruction, apical infarction, and apical aneurysm formation. B, Note the poorly contractile and partially dyskinetic apical chamber in early systole. Flow away from the transducer is depicted in blue. C, Continuous wave Doppler recording through the area of midventricular obstruction shows a peak gradient of approximately 60 mm Hg. D, Midventricular obstruction develops in mid-systole and a mosaic color jet is seen at the level of the obstruction. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/233.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Hypertrophic Cardiomyopathy of the Elderly Hypertrophic cardiomyopathy of the elderly is a subset of this condition with some distinguishing clinical and echocardiographic features (Fig. 27- 17) .[88] [89] [90] Hypertrophic cardiomyopathy of the elderly is more commonly identified in women. The pattern of hypertrophy tends to be focal and localized to the anterior or posterior interventricular septum.[91] Elderly patients with hypertrophic cardiomyopathy tend to have a milder degree of hypertrophy. The shape of the left ventricular cavity in elderly patients is typically ovoid with normal septal curvature. In contrast, younger patients tend to have a crescent-shaped left ventricular cavity and an abnormal convexity to the septum, characterized as a reversal of septal curvature.[43] Concomitant mitral annular calcification was detected in 30% of patients older than 40 years with hypertrophic cardiomyopathy in one autopsy series.[92] The mechanisms leading to left ventricular outflow tract obstruction in hypertrophic cardiomyopathy of the elderly are different from those seen in younger patients. Elderly patients have a relatively small heart and distorted geometry of the left ventricular outflow tract.[78] Mitral annular calcification results in anterior displacement of the mitral apparatus, narrowing of the outflow tract, and less angulation of the mitral leaflets. In contrast to younger patients, there is restricted systolic anterior motion of the anterior leaflet, with leaflet-septal contact occurring in the body of the leaflet rather than at the tip. Outflow tract obstruction, either at rest or with provocation, is associated with the majority of patients with hypertrophic cardiomyopathy of the elderly.[93] Furthermore, 600 Figure 27-17 (color plate.) Transesophageal echocardiographic images in the long-axis view obtained from a patient with hypertrophic mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 cardiomyopathy of the elderly. A, There is narrowing of the left ventricular outflow tract secondary to septal hypertrophy and anterior displacement of the mitral apparatus from mitral annular calcification. Outflow tract obstruction results from systolic anterior motion and anterior leaflet septal contact. B, Color flow imaging demonstrates a mosaic jet of color turbulence in the outflow tract and a large jet of mitral regurgitation, which is more central in origin, unlike in younger patients who have a predominant eccentric posterior mitral regurgitant jet. Ao, aorta; IVS, interventricular septum; LA, left atrium; LV, left ventricle; MR, mitral regurgitation; SAM, systolic anterior motion. (From Rakowski H, Freedman D, Wigle ED: Cardiol Elderly 1995;3:415–422.) the presence of mitral annular calcification distorts the mitral annulus and may lead to an independent jet of mitral regurgitation, which is often centrally directed and distinct from the posteriorly directed mitral regurgitant jet caused by systolic anterior motion. In one study of patients with hypertrophic cardiomyopathy of the elderly, the significant risk factors associated with an adverse prognosis were class III dyspnea and left atrial size.[94] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/234.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Stress Echocardiography in Hypertrophic Cardiomyopathy The application of stress echocardiography is important in the management of patients with hypertrophic cardiomyopathy, since the outflow tract gradients obtained after exercise may be very different from those measured after amyl nitrite inhalation and more accurately reflect patients' symptoms.[95] There may be a 50% increase in the left ventricular outflow tract gradient during supine exercise.[96] The magnitude of the pressure gradient has been shown to increase almost twofold with upright bicycle exercise. [97] Exercise echocardiography is beneficial in assessing the results of such interventions as septal ethanol ablation or surgical myectomy.[98] In addition, exercise testing has important prognostic implications.[99] [100] Exercise-induced hypotension may occur in one third of patients with hypertrophic cardiomyopathy and has been associated with a family history of hypertrophic cardiomyopathy or sudden death and with a smaller left ventricular cavity size.[99] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/235.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 4 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Evaluation of Diastolic Function Factors Contributing to Impaired Diastolic Function In the past two decades, the application of Doppler techniques has been extremely beneficial in the evaluation of diastolic function in hypertrophic cardiomyopathy (Fig. 27-18) . [101] Diastolic filling of the left ventricle is impaired in hypertrophic cardiomyopathy and may result in dyspnea on exertion, elevated filling pressures, and progressive left atrial enlargement. Table 27-6 outlines the factors that contribute to diastolic filling in hypertrophic cardiomyopathy.[6] , [47] [102] Impaired relaxation of the left ventricle is secondary to increased contraction load, decreased relaxation loads, decreased inactivation, and increased nonuniformity. The early contraction load of outflow tract obstruction impairs and delays the onset of relaxation. The major relaxation loads, coronary and ventricular filling, are decreased. Calcium overload secondary to hypertrophy or ischemia leads to myofibril inactivation of actinmyosin cross-bridges. Relaxation is further impaired by the nonuniformity of load and inactivation in different segments of the left ventricle. Chamber stiffness is directly proportional to the myocardial mass and the degree of TABLE 27-6 -- Factors Affecting Diastolic Function in Hypertrophic Cardiomyopathy Relaxation Loads Contraction load Subaortic stenosis Relaxation loads Late systolic loading End-systolic deformation (restoring forces) Coronary filling mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 4 Ventricular filling Inactivation Myocardial calcium overload Nonuniformity of load and inactivation (nonuniformity of contraction and relaxation) Chamber Stiffness Myocardial mass Left ventricular volume Myocardial stiffness (fibrosis) Adapted from Wigle ED, Sasson Z. Henderson M, et al: Prog Cardiovasc Dis 1985;28:1–83; and Rakowski H, Sasson Z, Wigle ED: J Am Soc Echocardiogr 1988;1:31–47. 601 Figure 27-18 (color plate.) Patient with hypertrophic cardiomyopathy and midventricular obstruction. Diastolic function is evaluated by pulsed-wave Doppler recording from the right upper pulmonary vein (A), tissue Doppler imaging of the mitral annulus (B), and pulsed-wave Doppler recording of the mitral leaflet tip (C). The mitral inflow velocities appear normal. The pulmonary venous inflow pattern shows blunting of the systolic wave and an increased PV(a) velocity, compatible with increased left ventricular filling pressures, suggesting pseudonormalization of the diastolic mitral inflow pattern. myocardial fibrosis and is inversely proportional to the left ventricular chamber volume. Pulsed Wave Doppler Assessment Pulsed wave Doppler assessment of mitral inflow velocities at the level of the mitral leaflet tips is the most commonly used method to assess diastolic left ventricular filling. Impaired relaxation is the predominant diastolic abnormality identified in patients with hypertrophic cardiomyopathy.[103] The mitral inflow pattern typically demonstrates a prolonged isovolumic relaxation time (IVRT), reduced early rapid filling (E), a prolonged deceleration time (DT), and increased atrial filling (A). The early diastolic velocity gradually increases and the deceleration time decreases with mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 4 worsened left ventricular compliance and increased left atrial pressure. However, unlike in patients with ischemic or dilated cardiomyopathy, a study of simultaneous Doppler and invasive hemodynamic assessments showed that there was no significant correlation between the mean left atrial pressure and the deceleration time in patients with hypertrophic cardiomyopathy.[104] These findings are supported by other Doppler studies that showed no significant relationship between diastolic filling abnormalities and exercise capacity[105] or the magnitude of left ventricular hypertrophy.[106] Asynchronous Relaxation The inhomogeneity of relaxation seen in patients with hypertrophic cardiomyopathy may result in left ventricular intracavitary flow during isovolumic relaxation. Asynchronous relaxation in patients with asymmetric septal hypertrophy leads to earlier relaxation of the apex. Blood flow from the left ventricular base to apex is detected during isovolumic relaxation and has been termed intracavitary IVRT flow.[107] In contrast, patients with asymmetric apical hypertrophic cardiomyopathy may have intracavitary apex-to-base flow, previously described as a paradoxic jet flow, with earlier relaxation of proximal left ventricular segments.[108] Tissue Doppler Imaging Tissue Doppler imaging is an emerging modality for the evaluation of diastolic function in patients with hypertrophic cardiomyopathy.[109] A study of |
simultaneous cardiac catheterization, Doppler echocardiography, and tissue Doppler imaging showed that the ratio of E velocity to flow propagation velocity and the ratio of E velocity to early diastolic annular velocity (Ea) correlated reasonably well with left ventricular filling pressures. Left atrial pressure (LAP) is determined by the following equation[110] LAP = E/Ea × 1.25 + 1.9 Improvements in left ventricular relaxation and compliance, left atrial size reduction, and decreased symptoms were demonstrated following the relief of left ventricular outflow tract obstruction by septal ethanol ablation (see "Septal Ablation").[111] [112] In addition, tissue Doppler imaging has identified left ventricular regional relaxation mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 4 602 abnormalities and asynchrony in patients with hypertrophic cardiomyopathy.[113] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/236.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Prognostication by Echocardiography Multiple risk factors for sudden cardiac death have been associated with hypertrophic cardiomyopathy.[2] Clinical risk factors that have been implicated as risk factors include younger age of presentation, a malignant family history of hypertrophic cardiomyopathy, a history of syncope, and a history of ventricular tachycardia. The overall extent of left ventricular hypertrophy, as determined by a left ventricular wall thickness index, was significantly greater in one study of patients with sudden death.[114] Patients with marked and diffuse hypertrophy, defined as a maximal wall thickness of 30 mm or greater or a wall thickness of 25 mm or greater in two or more segments, had an eightfold increase in sudden death compared with control patients, who had lesser degrees of hypertrophy. One recent study stratified patients according to five subgroups of maximal left ventricular wall thickness (≤15 mm, 16 to 19 mm, 20 to 24 mm, 25 to 29 mm, and ≥30 mm) and demonstrated a significant increasing risk for sudden death based on maximal wall thickness.[9] The cumulative 20-year risk of sudden death for patients with a maximal wall thickness of 15 mm or less was minimal, whereas the risk was nearly 40% for patients with a maximal wall thickness of 30 mm or greater at initial presentation. Atrial fibrillation is a significant complication of hypertrophic cardiomyopathy. Left atrial enlargement is a common finding in this condition, secondary to the presence of mitral regurgitation, left ventricular outflow tract obstruction, impaired diastolic function, and elevation of left ventricular end-diastolic pressure. Early studies have correlated the development of atrial fibrillation with the severity of left atrial enlargement. [115] [116] The onset of atrial fibrillation is frequently associated with rapid clinical deterioration. The incidence of systemic embolism and stroke increases significantly with left atrial enlargement and atrial fibrillation.[117] MD Consult L.L.C. http://www.mdconsult.com mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Medical Therapy Medical management in hypertrophic cardiomyopathy is optimized by monitoring the response to therapy with serial echocardiographic and Doppler studies (Table 27-7) .[6] The three different classes of pharmacologic agents used for the treatment of obstructive hypertrophic cardiomyopathy are beta blockers, disopyramide, and calcium channel blockers. The mechanism of benefit of these agents is felt to be a decrease in myocardial contractility, which results in decreased left ventricular ejection velocity, the delayed onset of mitral leaflet systolic anterior motion and, consequently, decreased outflow tract obstruction and mitral regurgitation. Beta-adrenergic blocking agents are beneficial in the management of symptomatic obstruction, particularly in patients with latent or provocable outflow tract obstruction.[1] They may indirectly improve left ventricular diastolic filling by reducing the heart rate and increasing passive ventricular filling.[118] Disopyramide TABLE 27-7 -- Echocardiographic and Doppler Assessment of Effects of Therapy Decreased/Abolished Obstruction • Decrease in or abolition of SAM • Decreased LVOT velocity • Disappearance of systolic aortic valve narrowing • Decrease in or abolition of mitral regurgitation Improved Diastolic Function • More rapid time to peak filling • Longer diastasis • Increased LV filling during early diastole • Lower atrial LV filling velocity LV, left ventricular; LVOT, left ventricular outflow tract; SAM, systolic mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 2 anterior motion. Adapted from Rakowski H, Sasson Z, Wigle ED: J Am Soc Echocardiogr 1988;1:31–47. is a type Ia antiarrhythmic agent with significant negative inotropic properties. [119] Cardiac symptoms and exercise capacity are generally improved in patients with obstructive hypertrophic cardiomyopathy following the institution of disopyramide. Calcium channel blockers may enhance ventricular filling and decrease myocardial ischemia in patients with hypertrophic cardiomyopathy. Multiple studies have demonstrated improvement in diastolic filling parameters with such calcium channel blockers as verapamil,[120] [121] nifedipine,[122] and diltiazem.[123] However, verapamil should be used with caution in patients with hypertrophic cardiomyopathy because it can lead to vasodilation and worsening outflow tract obstruction.[124] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/238.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 2 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Dual-Chamber Pacing Dual-chamber (DDD) atrioventricular pacing reduces left ventricular outflow tract obstruction by inducing both acute and chronic changes.[125] [126] Pacing from the right ventricular apex may cause paradoxic or diminished inward movement of the ventricular septum and asynchronous and late activation at the base of the septum, which may contribute to widening of the left ventricular outflow tract during systole, and decreased myocardial contractility. The atrioventricular delay must be optimized to achieve complete ventricular capture. Initial studies had suggested significant symptomatic improvement and left ventricular mass regression with DDD pacing.[127] However, the results of multiple subsequent studies have been less encouraging. DDD pacing may result in impairment of both systolic and diastolic function, possibly related to asynchronous contraction and relaxation.[128] Randomized crossover studies of DDD pacing (treatment arm) versus AAI pacing (control arm) have been completed by Nishimura et al,[129] the PIC study investigators,[130] and the MPATHY study investigators.[131] These studies have shown an incomplete reduction in the left ventricular outflow tract gradient, no significant decrease in left ventricular wall thickness, and no significant increase in peak myocardial oxygen consumption (VO ) during follow-up.[132] The perceived decline in 2 symptoms following pacemaker implantation may be due to a placebo effect.[129] [132] These findings were corroborated by a nonrandomized study comparing DDD pacing and septal myectomy, which showed a significantly greater improvement in the functional 603 class, peak VO2 , and left ventricular outflow tract gradient in the patients who underwent surgery.[133] The patients who seem to benefit from DDD pacing are the subset of older patients with lower baseline peak VO levels. 2 [130] [131] mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 5 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Septal Ablation Septal ethanol ablation is an innovative interventional technique that consists of the selective injection of ethanol into the septal perforator branch of the left anterior descending artery. This leads to occlusion of the septal branch and localized infarction of the hypertrophied interventricular septum. Synonymous terms for this technique include nonsurgical septal reduction therapy, percutaneous transluminal septal myocardial ablation, and transmyocardial ablation of septal hypertrophy. The targeted infarction results in acute myocardial stunning, decreased SAM, and relief of the left ventricular outflow tract obstruction.[134] [135] The initial clinical experience with septal ethanol ablation was reported in 1995.[136] The selection of the appropriate septal branch to be injected was determined by the reduction in the left ventricular outflow tract gradient following transient occlusion of the targeted vessel by a balloon catheter. However, a key development in this technique was the use of intraprocedural echocardiography. Transesophageal echocardiography is infrequently required.[134] [137] Myocardial contrast echocardiography with transthoracic imaging[138] [139] has become essential for the guidance and monitoring of septal ethanol ablation. Myocardial Contrast Echocardiography During Septal Ethanol Ablation The intra-arterial injection of an echo-enhancing agent allows for the specific localization of the vascular beds perfused by individual septal perforator branches of the left anterior descending artery. Contrast agents that have Figure 27-19 (color plate.) Intraprocedural myocardial contrast echocardiography during septal ethanol ablation. A, Following injection of Levovist into the first septal perforator of the left anterior descending artery, a contrast depot is identified in the region of the basal septum by transthoracic two- mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 5 dimensional apical imaging. This opacified area overlies the region of anterior mitral leaflet–septal contact, is adjacent to the site of left ventricular outflow tract turbulence, and is the targeted region of interest. B, Following alcohol injection into the first septal branch, an alcohol depot is identified in the same region as the area of contrast depot. Alcohol injection results in further increased echogenicity of the basal septum. C, Repeat transthoracic apical view with color flow imaging in a patient 3 months following septal ethanol ablation. There is now laminar flow in the left ventricular outflow tract. D, Continuous wave Doppler recording showing a nonsignificant resting gradient of 6 mm Hg across the left ventricular outflow tract. (From Faber L, Ziemssen P, Seggewiss H: J Am Soc Echocardiogr 2000;13:1074–1079.) been used during septal ethanol ablation are sonicated human albumin (Albunex, Mallinckrodt Inc, St. Louis, Mo[138] ) Optison (Mallinckrodt Inc), and Levovist (Schering AG, Berlin, Germany[139] ). Sonicated albumin is administered as a bolus injection of 1.0 to 1.5 mL of sonicated albumin diluted with normal saline (range of dilution 1:3 to 1:1). Levovist is a galactose-based agent, and 1 to 2 mL in a concentration of 350 ng/mL is injected through the inflated intra-arterial balloon catheter. High gain settings are required to visualize rapidly the effects of Levovist injection. [140] Following the injection of the contrast agent, the segments of the interventricular septum supplied by the septal branch become opacified. The spatial extent of myocardial opacification can be determined from multiple transthoracic windows. The vascular territory targeted by contrast echocardiography is the region of anterior mitral leaflet–septal contact, adjacent to the zone of flow acceleration and color turbulence in the left ventricular outflow tract (Fig. 27-19) .[139] In addition, contrast echocardiography is invaluable in detecting contrast opacification in regions remote from the site of mitral leaflet–septal contact.[14] [140] The demonstration of contrast enhancement in nonseptal sites necessitates the selection of another vessel to be targeted. The opacifying effects of intra- arterial Levovist usually disappear within 10 minutes, thus allowing for reinjection of this contrast agent into subsequent vessels. The contrast effect of ethanol has the same distribution as that of the contrast agent, and intra-arterial ethanol injection frequently results in increased echogenicity and reflectivity. The area of contrast enhancement with human sonicated albumin has been correlated with infarct size, as determined by the peak creatine kinase level and by the size of the perfusion defect on single- photon emission computed tomography thallium imaging (Table 27-8) .[138] Improved Outcomes with Contrast Echocardiography Two groups with extensive experience with intraprocedural contrast echocardiography during septal ethanol mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 5 604 TABLE 27-8 -- Myocardial Contrast Echocardiography During Septal Ethanol Ablation With |
MCE (n = No MCE (n = Variable 131/132) 28/30) P Value Maximum creatine 65 (32) 96 (62) <0.001 kinase-MB rise (U/L) DDD-Pacemaker 5 17 0.05 implantation rate, % Follow-up success rate 94 64% <0.001 (LVOT gradient reduction >50%) LVOT gradient (rest) at 3 9 (17) 27 (34) <0.01 months (mm Hg) LVOT, left ventricular outflow tract; MCE, intraprocedural myocardial contrast echocardiography. From Faber L, Ziemssen P, Seggewiss H: J Am Soc Echocardiogr 2000;13:1074–1079. ablation have demonstrated that this echocardiographic approach results in improved outcomes.[14] [139] [141] The use of intra-arterial sonicated albumin limited the number of vessels injected and the volume of ethanol used and resulted in fewer cases of atrioventricular block requiring permanent pacemaker implantation, one of the significant complications associated with septal ethanol ablation.[141] Faber et al[14] have reported on the largest experience with intraprocedural myocardial contrast echocardiography during septal ethanol ablation. They showed improved outcomes with contrast echocardiography using Levovist as compared with the strategy of target vessel selection by probatory balloon occlusion (see Table 27-8) . Contrast-guided septal ethanol ablation resulted in smaller infarcts, a 5% versus 17% pacemaker implantation Figure 27-20 A to H, Two-dimensional transthoracic echocardiographic still frames obtained during septal ethanol ablation in various patients. The opacification of such left ventricular regions as the posteromedial mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 5 papillary muscle (A, arrow), basal lateral wall (B, arrow), posterolateral wall (C and G, arrows), inferior wall (F, arrows) have been reported. Opacification of such right- sided structures as the right ventricular papillary muscles may also occur, in association with small (E) and large (D and H) contrast depots seen in the septum. LA, left atrium; RA, right atrium; RV, right ventricle. (From Faber L, Ziemssen P, Seggewiss H: J Am Soc Echocardiogr 2000;13:1074–1079.) rate, and greater reductions in the left ventricular outflow tract gradient. The opacification of myocardial segments distal to the target region of mitral leaflet–septal contact resulted in a change in the target vessel in 7% of cases (Fig. 27-20) . Therefore, myocardial contrast echocardiography optimizes septal ethanol ablation by permitting the targeted delivery of ethanol, limiting the induced infarction to the culprit region of mitral leaflet–septal contact, and by minimizing procedural complications. Clinical Results Following Septal Ethanol Ablation The major early outcomes of septal ethanol ablation from three recognized international centers are summarized in Table 27-9 (Table Not Available) . [137] [141] [142] [143] Subsequent studies beyond 1 year following this procedure have shown ongoing symptomatic improvement. [144] [145] The immediate relief in left ventricular outflow tract obstruction seen following ethanol injection is secondary to acute myocardial stunning following the controlled infarction. [135] There is a gradual and continued decrease in the degree of left ventricular outflow tract obstruction with healing and replacement fibrosis[137] and thinning of the infarcted septal segment and enlargement of the outflow tract.[146] The long-term risk of late ventricular arrhythmias following induced infarction in patients with hypertrophic cardiomyopathy remains unclear, although early studies have not demonstrated an increased risk.[137] Echocardiographic and Doppler studies are beneficial in the serial noninvasive follow-up of patients following septal ethanol ablation. Multiple studies have documented 605 TABLE 27-9 -- Summary of Results of Septal Ethanol Ablation (Not Available) LVOTG, left ventricular outflow tract gradient; PPM, Permanent mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 5 Pacemaker. significant progressive reductions in basal septal thickness and in the resting and provocable left ventricular outflow tract gradients over the first 2 years of follow-up (Fig. 27-21) .[147] These developments have been associated with favorable changes in the geometry of the left ventricular outflow tract[135] and with improvements in left ventricular diastolic function.[111] [112] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/240.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 5 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Surgical Myectomy Ventricular myotomy or myectomy has been performed for the past four decades for the management of severe obstructive hypertrophic cardiomyopathy refractory to maximally tolerated medical therapy. Septal myectomy relieves outflow tract obstruction by widening of the left ventricular outflow tract, which leads to decreased systolic anterior motion of the mitral valve and decreased dynamic outflow tract obstruction. Echocardiography is useful in the identification of patients suitable for surgical myectomy. The preoperative echocardiographic characteristics predictive of symptomatic benefit from surgical myectomy include asymmetric hypertrophy, severe SAM of the mitral leaflets, and a prolonged isovolumic relaxation time.[148] In addition, echocardiography plays an important role in Figure 27-21 Serial transthoracic echocardiograms in a 25-year-old patient prior to and 2 years following septal ethanol ablation for drug- refractory symptomatic obstructive hypertrophic cardiomyopathy. A, Parasternal long-axis view obtained prior to the procedure demonstrates prominent septal hypertrophy (arrow) and resting systolic anterior motion. B, During follow-up 2 years after septal ethanol ablation, there is striking localized thinning of the anterior septum (arrow), resolution of systolic anterior motion, and a resting outflow tract gradient of 6 mm Hg. detecting additional lesions requiring surgical management. Comprehensive preoperative echocardiographic imaging in patients referred for surgical myectomy includes the evaluation of independent mitral valve disease, concomitant aortic valve disease, and the assessment of additional levels of obstruction (midventricular or right ventricular outflow tract).[13] Intraoperative Echocardiography Surgical myectomy is performed from the transaortic approach and is technically challenging given the limited exposure and visualization of the mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 2 di 5 hypertrophied septum. Prior to the introduction of intraoperative echocardiography, the extent and degree of septal hypertrophy was estimated by surgical palpation[149] and by preoperative transthoracic echocardiographic studies. A key development in the surgical management of obstructive hypertrophic cardiomyopathy has been the use of intraoperative echocardiography with epicardial or transesophageal imaging (Fig. 27-22) . Intraoperative echocardiography guides the surgical interventions, assesses immediate results, and excludes important complications.[13] [150] Intraoperative transesophageal echocardiography allows for detailed 606 Figure 27-22 (color plate.) Intraoperative echocardiography in a patient with obstructive hypertrophic cardiomyopathy. A to D, Transesophageal study. A, Two-dimensional systolic frame obtained prior to myectomy, demonstrating marked anterior and basal motion of the anterior mitral leaflet with leaflet-septal contact (arrow). B, Same frame with Doppler color flow imaging demonstrating turbulence in the left ventricular outflow tract (arrowheads) arising at the site of leaflet-septal contact and a jet of posteriorly directed mitral regurgitation (arrow). C, Two-dimensional frame obtained after myectomy. Note the widened left ventricular outflow tract and absence of systolic anterior motion despite persistence of abnormal coaptation point (arrow). D, Same frame with Doppler color flow imaging demonstrating lack of turbulence in the outflow tract (arrowheads) and only a small centrally directed jet of mitral regurgitation (arrow). E and F, Intraoperative epicardial study of the same patient after myectomy. E, Parasternal long-axis frame demonstrating the absence of systolic anterior motion despite persistence of an abnormal coaptation point between the mitral leaflets. F, Parasternal short-axis frame demonstrating the site of myectomy (arrow). (From Grigg LE, Wigle ED, Williams WG, et al: J Am Coll Cardiol 1992;20:42–52.) delineation of the depth, width, and length of the required myectomy, the degree of systolic anterior motion and left ventricular outflow tract obstruction, and the quantitation and mechanisms of mitral regurgitation.[13] [74] Imaging from multiple transesophageal and transgastric views using a multiplane transducer allows for the careful Figure 27-23 A, Intraoperative transesophageal echocardiogram in the long-axis plane in a patient referred for myectomy. The depth, width, and length of the hypertrophied septum (measured from the base of the right coronary cusp of the aortic valve) and the point of anterior leaflet-septal contact are obtained to guide the resection. B, Transgastric views of the mitral valve and left mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 3 di 5 ventricular outflow tract permit detailed examination of the morphology of the mitral leaflets, the point of leaflet-septal contact (arrow) and the assessment of systolic anterior motion. LA, left atrium; Ao, aorta. assessment of the thickness of the anterior and posterior portions of the interventricular septum. The length of septal hypertrophy is measured from the base of the right coronary cusp of the aortic valve (Fig. 27-23) . The targeted length of resection is 1 cm below the point of anterior mitral leaflet–septal contact. The left ventricular 607 Figure 27-24 (color plate.) Intraoperative transesophageal echocardiogram (frontal long-axis plane) before (upper panels) and after (lower panels) myectomy in a patient with no independent mitral valve disease (A) and in a patient with thickened mitral leaflets (B). A, Upper left panel, Two-dimensional systolic frame demonstrating anterior leaflet-septal contact with failure of mitral leaflet coaptation. Upper right panel, Same frame with Doppler color flow imaging demonstrating turbulent left ventricular outflow and a large jet of posteriorly directed mitral regurgitation arising from the gap between the two mitral leaflets. Lower left panel, Two-dimensional systolic frame now showing a widened left ventricular outflow tract and abolition of systolic anterior motion. Lower right panel, Same frame with Doppler color flow imaging demonstrating nonturbulent left ventricular outflow with a marked reduction in the severity of mitral regurgitation and the presence of only a small residual central jet. B, Upper left panel, Two-dimensional systolic frame demonstrating thickened mitral leaflets and septal hypertrophy. Upper right panel, Same frame with color flow imaging demonstrating a posteriorly directed jet of mitral regurgitation. Lower panels, Following myectomy, two-dimensional and Doppler color flow imaging now show widening of the outflow tract, no significant turbulence in the outflow tract and the resolution of mitral regurgitation. (A, from Grigg LE, Wigle ED, Williams WG, et al: J Am Coll Cardiol 1992;20:42–52. Reprinted with permission from the American College of Cardiology.) outflow tract gradient can be measured by transgastric imaging in the long- axis view with the continuous wave Doppler beam aligned parallel to the left ventricular outflow tract. Following surgical excision of the basal septum, repeat echocardiographic imaging permits the instantaneous evaluation of the adequacy of the myectomy (Fig. 27-24) .[13] [150] Intraoperative echocardiography can determine whether there is significant residual outflow tract obstruction or hemodynamically important residual mitral regurgitation (Fig. 27-25) . In addition, intraoperative echocardiography allows for the immediate mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 4 di 5 detection of such operative complications as a ventricular septal defect[151] Figure 27-25 (color plate.) Transesophageal echocardiogram demonstrating an unsatisfactory result after myectomy. A, Before myectomy. Turbulence is shown in the left ventricular outflow tract and a jet of mitral regurgitation is seen in the left atrium (arrow). B through D, After myectomy. B, Two-dimensional frame in the frontal long-axis plane demonstrating the persistence of systolic anterior motion. C, Doppler color flow imaging shows persistence of turbulence in the outflow tract and severe mitral regurgitation (arrow). D, Two-dimensional frame demonstrating a very small myectomy site (arrowheads). (From Grigg LE, Wigle ED, Williams WG, et al: J Am Coll Cardiol 1992;20:42–52. Reprinted with permission from the American College of Cardiology.) and left ventricular dysfunction.[13] Three-dimensional transesophageal echocardiographic imaging with three-dimensional reconstruction has been used to assess the geometry of the hypertrophied septum and the cross- sectional area of the left ventricular outflow tract prior to and following extended myectomy. [152] Outcomes Following Myectomy Studies of the results of surgical myectomy from experienced tertiary referral centers have shown excellent early and long-term postoperative outcomes. [153] [154] [155] Potential 608 Figure 27-26 (color plate.) Echocardiographic imaging obtained following surgical myectomy. A and B, Two-dimensional and color flow imaging in the parasternal long-axis view (A) and short-axis view (B) demonstrate a widened outflow tract, a small jet of aortic regurgitation, and a separate jet of color flow turbulence secondary to septal perforator flow. Aortic regurgitation following myectomy is most commonly due to the postoperative loss of aortic annular support. C, Continuous wave Doppler imaging across the outflow tract confirms the presence of mild aortic regurgitation. D, Gross pathologic specimen of excised basal septum in a patient who underwent myectomy. Note the lumen of the septal perforator vessel within the excised septum (arrow). complications following myectomy include heart block, ventricular septal defect, aortic regurgitation, and arrhythmias. Aortic regurgitation is felt to be secondary to trauma of the aortic valve or secondary |
to the loss of aortic mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 5 di 5 annular support following myectomy (Fig. 27-26) . [156] Echocardiographic studies performed at rest and with provocative maneuvers are important in the serial monitoring of patients following myectomy.[98] Many studies have documented a significant reduction or abolition of the resting outflow tract gradient in the majority of patients following myectomy, resulting in substantial and lasting symptomatic improvement.[153] [154] [155] [157] , [158] Nonrandomized studies of medical therapy versus myectomy[159] and pacing versus myectomy[133] have suggested more favorable overall outcomes with myectomy. MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/241.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 1 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company Summary of Treatment Strategies Many therapeutic options are currently available in the management of symptoms attributable to outflow tract obstruction in hypertrophic cardiomyopathy. Pharmacologic agents such as beta blockers, disopyramide, and calcium channel blockers have variable effects in reducing the outflow tract gradient and in improving diastolic function. Patients with drug-refractory symptoms are candidates for DDD pacing, septal ethanol ablation, or surgical myectomy. There is a lesser magnitude of gradient reduction with pacing and septal ethanol ablation. Many studies from experienced centers suggest that the resting outflow tract gradient declines approximately 50% with pacing and more than 70% following septal ethanol ablation.[132] The subgroup of older, severely limited patients who are not candidates for surgical myectomy may benefit most from dual chamber pacing. The decreased outflow tract obstruction following septal ethanol ablation has been accompanied by significant improvements in symptomatic status, exercise tolerance, and left ventricular mass. The left ventricular outflow tract gradient may be completely abolished with surgical myectomy, which results in long-term symptomatic benefit. Trials are currently ongoing that compare the relative merits and outcomes of these different treatment modalities. [143] MD Consult L.L.C. http://www.mdconsult.com Bookmark URL: /das/book/view/26074653/1031/242.html/top mhtml:file://D:\Documents%20and%20Settings\Administrator\Desktop\Otto\ECOCA... 06/02/2005 Book Text Pagina 1 di 15 MD Consult information may not be reproduced, retransmitted, stored, distributed, disseminated, sold, published, broadcast or circulated in any medium to anyone, including but not limited to others in the same company or organization, without the express prior written permission of MD Consult, except as otherwise expressly permitted under fair use provisions of U.S. Copyright Law. Subscriber Agreement Otto: The Practice of Clinical Echocardiography, 2nd ed., Copyright © 2002 W. B. Saunders Company References 1. Wigle ED, Rakowski H, Kimball BP, Williams WG: Hypertrophic cardiomyopathy: Clinical spectrum and treatment. Circulation 1995;92:1680–1692. 2. Spirito P, Seidman CE, McKenna WJ, Maron BJ: The management of hypertrophic cardiomyopathy. N Engl J Med 1997;336:775–785. 3. Richardson P, McKenna W, Bristow M, et al: Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of Cardiomyopathies. Circulation 1996;93:841–842. 4. Brock RC: Functional obstruction of the left ventricle. Guys Hosp Rep 1957;106:221–238. 5. Teare RD: Asymmetrical hypertrophy of the heart in young adults. Br Heart J 1958;20:1–8. 6. Rakowski H, Sasson Z, Wigle ED: Echocardiographic and Doppler assessment of hypertrophic cardiomyopathy. J Am Soc Echocardiogr 1988;1:31–47. 7. 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