Timing of surgical intervention in chronic mitral regurgitation.
1986
: Determination of the optimal time for surgical intervention in chronic mitral regurgitation has remained controversial. There are similarly important factors in favor of temporizing with medical treatment alone as there are in support of relatively early surgery (Table 1). Since rheumatic valvulitis may play a subordinate role, in contrast to etiologies such as myxomatous degeneration of the mitral valve, rupture of chordae tendineae, papillary muscle dysfunction due to coronary artery disease and other causes, left ventricular function is generally determined by the adaptations of the myocardium to the volume overload, or to ischemia or infarction from coronary artery disease rather than to a concomitant myocarditis. Based on actuarial survival curves in symptomatic patients with combined mitral regurgitation and stenosis or mitral regurgitation alone, it can be assumed that surgery can result in improved survival, in particular if a reconstructive mitral valve procedure rather than prosthetic valve replacement is performed. Medical treatment is carried out with digitalis to enhance myocardial contractility, diuretics and vasodilators to reduce pre- and afterload with resultant diminished effective mitral orifice area and regurgitant volume, lowering of pulmonary artery and pulmonary venous pressures and an increase in systemic cardiac output. Presently, however, there is no convincing evidence that symptom-status is improved or the natural history favorably affected over a number of years. For assessment of left ventricular myocardial function the end-systolic pressure/volume or the end-systolic stress/volume index appear preferable. Values of the latter less than or equal to 2.2 are associated with increased postoperative mortality and improbable improvement in functional status. Additionally, patients with an ejection fraction less than 40% or end-diastolic volume greater than 140 ml/m2 as well as those with end-diastolic dimension greater than 8 cm or end-systolic dimension greater than 5.5 cm have less favorable postoperative survival or further deterioration in ventricular function. Impaired right ventricular function secondary to the increased afterload imposed by pulmonary hypertension generally can be normalized postoperatively. Depression of right ventricular myocardial contractility is not, however, a common pathophysiologic feature in chronic mitral regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)
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