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.