Vasoactive drugs in chronic regurgitant lesions of the mitral and aortic valves.

This review examines the results of vasodilator therapy in patients with chronic regurgitant lesions of the aortic and mitral valves. The analysis includes those studies which provide data on hemodynamic measurements, left ventricular systolic function, ventricular volumes and regurgitant flow. In patients with chronic aortic or mitral regurgitation, the short-term administration of nitroprusside, hydralazine, nifedipine or an angiotensin-converting enzyme (ACE) inhibitor produces salutary hemodynamic effects. The major difference in the response to combined preload and afterload reduction (i.e., nitroprusside) in patients with aortic versus mitral regurgitation was that forward stroke volume generally increased and ejection fraction remained unchanged in mitral regurgitation, whereas ejection fraction generally increased and forward stroke volume remained unchanged in aortic regurgitation. These observations suggest that a reciprocal relation between regurgitant and forward flow characterizes the response to preload and afterload reduction in mitral regurgitation (through a preload-dependent dynamic regurgitant orifice), whereas correction of afterload mismatch dominates the response in aortic regurgitation. In studies of long-term vasodilator therapy in patients with chronic aortic regurgitation, a reduction in left ventricular volumes and regurgitant fraction, with or without an increase in ejection fraction, has been observed during treatment with hydralazine, nifedipine and ACE inhibitors. Patients with the largest, sickest hearts generally benefit the most from treatment with vasoactive drugs. Nonetheless, favorable ventricular remodeling has been reported in asymptomatic patients, and long-term nifedipine use has delayed the need for operation in asymptomatic patients with chronic aortic regurgitation. For patients with chronic mitral regurgitation, definition of the etiology of the lesion is a prerequisite for choosing appropriate therapy. Excluding patients with obstructive hypertrophic cardiomyopathy and mitral valve prolapse, and some with fixed-orifice (i.e., rheumatic) mitral regurgitation, the signal importance of preload reduction suggests that the preferred long-term therapy for symptomatic chronic mitral regurgitation is an ACE inhibitor. There are no long-term studies that support the use of vasodilator therapy in asymptomatic patients with chronic mitral regurgitation.