Abstract

The effects of captopril (CPT), an oral angiotensin-converting enzyme (ACE) inhibitor, on systemic renal and coronary hemodynamics were studied in 22 patients with severe congestive heart failure (CHF). In 15 patients, CPT decreased mean arterial pressure from 75 ± 3 to 60 ± 3 mm Hg associated with a 16% increase in cardiac output, a 24% reduction in systemic vascular resistance, and a 36% decrease in pulmonary capillary wedge pressure (all p < 0.01). Despite the improved cardiac output, renal blood flow, creatinine clearance, and sodium excretion did not rise during the first 2 days of CPT therapy. In eight patients, coronary sinus blood flow diminished from 98 ± 11 to 82 ± 9 ml/min ( p < 0.01) following drug administration in association with a fall in arterial pressure and heart rate but no change in coronary sinus oxygen saturation. Thus, despite improved systemic hemodynamics, short-term therapy with this ACE inhibitor failed to improve renal hemodynamics. In addition, initial CPT administration produced a decrease in coronary blood flow that was related to a decrease in myocardial oxygen requirements.

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