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Fication of Sports) or possible trauma.MITRAL REGURGITATION Mitral regurgitation, unlike MS, has a variety of etiologies, the most common of which is mitral valve prolapse (myxomatous mitral valve). Other common causes are rheumatic heart disease, infective endocarditis, CAD, connective tissue diseases (such as Marfan syndrome), and dilated cardiomyopathy. The recommendations outlined in this section are for patients with primary valvular MR rather than MR secondary to CAD or other conditions causing LV dilation (see Task Force 4: HCM and Other Cardiomyopathies, Mitral Valve Prolapse, Myocarditis, and Marfan Syndrome, and Task Force 6: Coronary Artery Disease). Evaluation.Mitral regurgitation can be detected by the characteristic physical findings and confirmed by Doppler echocardiography. The severity of the MR is related to the magnitude of the regurgitant volume, which results in LV dilation and increased left atrial pressure. The increased LV diastolic volume enhances total LV stroke volume enough to accommodate the regurgitant volume and to maintain the forward stroke volume within normal limits. The low impedance presented by regurgitation into the left atrium unloads the left ventricle during ventricular systole, such that measures of LV pump function (e.g., ejection fraction) tend to overestimate true myocardial performance (10). The severity of chronic MR can be adequately judged by noninvasive techniques, principally two-dimensional and Doppler echocardiography. The larger the jet area, and the wider the jet at its origin above the valve, the more severe the regurgitation. The entry of the jet into the atrial appendage or pulmonary vein or systolic reversal of the flow in pulmonary veins are all indicators of severity. Various measures of the severity of MR have been described (1,11). In some patients with eccentric jets or those impinging on the atrial wall, the assessment may be difficult (1). Generally, the LV diastolic volume reflects the severity of chronic MR. However, it should be noted that the upper limit of normal LV size is increased in the healthy, highly trained athlete. In a series of elite athletes, echocardiographic LV end-diastolic dimensions as high as 66 mm were recorded in women (mean, 48 mm) and up to 70 mm in men (mean, 55 mm) (12). LV end-diastolic dimensions greater than or equal to 55 mm were observed in 45% of participants and greater than 60 mm in 14% of participants. Therefore, assessment of LV enlargement in a highly trained athlete with known or suspected valvular heart disease must take this issue into consideration. Hence, for purposes of this discussion, an LV end-diastolic dimension greater than 60 mm is considered likely to represent the effects of LV volume overload due to valvular disease and not per se to physiologically based exercise training. Patients with chronic MR should be followed longitudinally with serial echocardiograms (5). A decrease in ejection fraction and/or increase in end-systolic volume with time is a helpful marker of declining LV function and an indication of having reached the limits of cardiac compensation. 1335 JACC Vol. 45, No. 8, 2005 Bonow et al. April 19, 2005:1334–40 Task Force 3: Valvular Heart Disease Effects of exercise.In general, exercise produces no signifi- cant change or a mild decrease in the regurgitant fraction because of reduced systemic vascular resistance. However, patients with elevation of heart rate (increased systolic ejection time per min) or blood pressure with exercise may manifest marked increases in regurgitant volume and pulmonary capillary pressures. Hence, static exercise that increases arterial pressure is potentially deleterious. Ejection fraction usually does not change or decreases slightly with exercise, although the ejection fraction response may be completely normal in young, asymptomatic subjects. The etiology of MR may be important in making recommendations concerning heavy physical activity. In patients with MR secondary to previous infective endocarditis or ruptured chordae, the valve tissues theoretically could be further damaged or torn by marked sustained increases in LV systolic pressure. Recommendations: Date: 2016-03-03; view: 860
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