The renin-angiotensin system is thought to maintain elevated systemic vascular resistance in heart failure. The hemodynamic effects of captopril (SQ 14225), an oral inhibitor of angiotensin-converting enzyme, were measured in 10 patients with stable congestive heart failure poorly controlled by digitalis and diuretics. At single daily doses of 25 to 150 mg, the cardiac index rose from 1.75 +/- 0.18 to 2.27 +/- 0.39 (mean +/- S.D.) liters per minute per square meter (P less than 0.001), and pulmonary-wedge pressure fell from 26.5 +/- 7.5 to 17.3 +/- 6.1 mm Hg (P less than 0.01). Systemic vascular resistance decreased from 2006 +/- 300 to 1393 +/- 238 dyne seconds per centimeter (P less than 0.001), and mean arterial pressure fell from 83.7 +/- 7.0 to 70.3 +/- 9.9 mm Hg (P less than 0.001) (mean +/- S.D.). Heart rate did not change appreciably. Hemodynamic alterations peaked at 90 minutes and persisted for three to four hours. Control plasma renin activity ranged from 1.1 to 7.3 ng per milliliter per hour and did not correlate with changes in hemodynamic values. Three patients on long-term treatment maintained clinical improvement. Although its mechanism of action has not been completely elucidated, captopril may prove useful in the treatment of chronic congestive heart failure.

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Chronic congestive heart failure not controlled by conventional therapy was treated with intravenous amrinone, a new non-glycosidic, non-catecholamine cardiotonic agent. Eight patients with New York Heart Association functional class III-IV symptoms were hemodynamically monitored. At peak effect, cardiac index (CI) increased from 1.84 +/- 0.32 to 2.74 +/- 0.44 l/min/m2 (mean +/- SD) (p less than 0.001) and left ventricular filling pressure (LVFP) decreased from 25.8 +/- 6.2 to 19.5 +/- 6.8 mm Hg (p less than 0.05), while heart rate and mean aortic blood pressure did not change significantly. Mean endocardial circumferential fiber shortening (mean Vcf), determined by echocardiography, increased from 0.61 +/- 0.27 to 0.89 +/- 0.34 cir/sec (p less than 0.05). The duration of action after bolus infusion varied from 60--90 minutes. During continuous infusion of amrinone, sustained increases in CI and reductions in LVFP, similar to those at the time of peak effect after bolus administration, were maintained for 180 minutes. These marked cardiotonic effects of amrinone in patients already taking digitalis for severe heart failure occurred without side effects of arrhythmias or altered arterial pressures. The fact that the drug is orally active makes amrinone a v:ry promising inotropic agent for the treatment of chronic heart failure in man.

No abstract