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European Heart Journal 1984 5(1):47-54;
Copyright © 1984 by the European Society of Cardiology.
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© 1984 The European Society of Cardiology

Captopril in congestive heart failure resistant to other vasodilators*

F. M. FOUAD, S. EL-TOBGI, R.C. TARAZI, E.L. BRAVO, N.J. HART{dagger}, E.K. SHIREY{dagger} and J. LIM{dagger}

{dagger}Research Division and Department of Cardiology Cleveland, Ohio 44106
The Cleveland Clinic Foundation Cleveland, Ohio 44106

Received 22 March 1983; accepted 1 June 1983.

Requests for reprints to: M. Fouad, M.D., Research Division, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44106.

Abstract

In an attempt to study the possible mechanism(s) by which captopril controls resistant heart failure, sequential haemodynamic studies (radioisotope technique) and humoral measurements (plasma renin activity, plasma aldosterone and plasma catecholamines) were obtained in 11 such patients. The studies were made at the time patients became unresponsive to other vasodilators (hydralazine orprazosin); the vasodilator drug was then discontinued and five days later, the ‘no-vasodilator’ studies were obtained. Captopril therapy was then started. Optimum daily maintenance dose of captopril varied from 75 to 200 mg in different patients. Studies were again repeated aftera period of time equal to the duration of the previous vasodilator therapy. Digitalis and diureticdoses were kept constant throughout.Captopril improved effort tolerance in ten patients. Haemodynamically, mean blood pressure and peripheral resistance were lower than during vasodilator therapy (85±3-l v. 92±3-3 mmHgand 47±4-4 v. 59±4-4 U.M2, respectively; p<0-05 for both). Cardiacindex was higher during captopril treatment (l-95±0-15 v. l-63±0-10l/m1, p<0-01) and pulmonary mean transit was normalized by captopril (14-6±l-7 v. 18-4±l-3s, p<0-05).Humoral indices revealed a significant (p<0-05) reduction in plasma aldosterone during captopril therapy (25-9±5-6 ng/dl during captopril, v. 62±22 ng/dl with novasodilators and 50-9±6-l ng/dl with other vasodilators). Moreover, there was a decrease in circulating plasma catecholamines during captopril treatment, but differences between the three treatment periods were not statistically significant.Data suggest that the effectiveness of captopril in controlling congestive heart failure that became resistant to other forms of vasodilator therapy might be related to more than one factor including persistent haemodynamic unloading, decrease of plasma aldosterone, and possibly reduction of sympathetic activity.

Key Words: Captopril • vasodilators • heart failure


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