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

Abstract

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.

Valvular Heart Disease

“…74 Medical therapy is not able to significantly reduce regurgitant volume in chronic severe AR because the regurgitant orifice area is relatively fixed and the diastolic blood pressure is already low. 74 Further reducing diastolic blood pressure might adversely affect coronary perfusion and should be avoided. Moreover, the square root function dictates that a 25% reduction in diastolic pressure gradient would only achieve a 13% reduction in regurgitant volume.…”

“…Moreover, the square root function dictates that a 25% reduction in diastolic pressure gradient would only achieve a 13% reduction in regurgitant volume. 74 Therefore, the main goal of medical therapy is to reduce the systolic hypertension associated with chronic severe AR and thereby reduce wall stress and improve LV function. 74,75 A number of small studies have investigated the effects of various vasodilators on hemodynamics and LV function in chronic AR.…”

“…74 Therefore, the main goal of medical therapy is to reduce the systolic hypertension associated with chronic severe AR and thereby reduce wall stress and improve LV function. 74,75 A number of small studies have investigated the effects of various vasodilators on hemodynamics and LV function in chronic AR. 76 -82 Only 2 randomized, placebocontrolled studies have demonstrated significant reductions in LV end-diastolic diameter and an increase in LVEF with vasodilator therapy using hydralazine in 45 patients 77 and nifedipine in 72 patients.…”

Primary mitral valve regurgitation: Update and review

“…These studies failed to provide evidence of clinical or hemodynamic benefit. [67][68][69][70][71] Hypertension needs to be treated, because the increased left ventricular systolic pressure increases the trans-mitral gradients and worsens the severity of mitral regurgitation. 6…”

Quantitation of Mitral Regurgitation

“…As described by Levine and Gaasch, 13 the Gorlin hydraulic orifice equation can be rearranged to derive the hemodynamic determinants of regurgitant volume (RgV) in MR.…”