Vasodilator therapy of severe congestive heart failure: the special importance of angiotensin-converting enzyme inhibition with captopril.

Successful ambulatory afterload reduction therapy of severe chronic congestive heart failure (CHF) required the extensive evaluation of hemodynamic effects of vasodilator agents, precise characterization of differential cardiocirculatory actions, and objective confirmation of extended salutary improvements of the heart failure state. This article describes results of a series of investigations with the angiotensin-converting enzyme (ACE) inhibitor captopril (CPT) in several patients with severe CHF. CPT causes predominant peripheral venodilation, resulting in marked decline in elevated left ventricular preload and modest augmentation of the depressed cardiac output. These hemodymanic effects of oral CPT are similar to the effects of nitroprusside and prazosin on increased ventricular preload, but the latter vasodilators cause greater rise in low cardiac pump output. Importantly, the beneficial cardiocirculatory action of oral CPT provided prolonged cardiac benefits with symptomatic improvements confirmed by objective enhancement in left ventricular function documented by cardiac catheterization, echocardiography, nuclear scintigraphy, and treadmill exercise. Thus, ACE inhibition with oral CPT successfully provides marked long-term augmentation of cardiac performance and clinical status in refractory CHF.