Clinical improvement and hormonal changes in severe cardiac failure after captopril treatment.

Abstract

Abstract: The effects of oral captopril, an angiotensin converting enzyme inhibitor, on cardiac function and on the renin‐angiotensinaldosterone system were examined in nine male patients with severe congestive cardiac failure (New York Heart Association Class III or IV). All had been refractory to conventional therapy with bed rest and high dose frusemide and seven had failed to respond adequately to vasodilator therapy.One hour after the first dose of captopril (25 mg p.o.) there were significant falls in mean blood pressure (98±5 to 78±8 mmHg, P < 0.01), heart rate (88±5 to 79±4 beats/min, P < 0.01) and plasma angiotensin II (77±38 to 16±5pg/ml, P < 0.01); plasma renin concentration, initially very high (9.0±2.5 ng/ml/hour), increased further (11.9±2.7 ng/ml/hour).These changes were observed to persist during the first week of treatment. Urinary aldosterone excretion fell from 65±29 to 30±11 nmol/day on day 1 and further to 17±8 nmol/day after one week (P< 0.01). This was accompanied by both a natriuresis and a fall in potassium excretion. Creatinine clearance did not change. Rapid clinical improvement occurred in all but one patient who had severe aortic stenosis. Body weight fell (71.7±4.5 to 68.8±4.3 kg, P< 0.05), diuretic drugs were able to be reduced and, in the five patients in sinus rhythm, cardiac ejection fraction increased (13±2 to 17±2%, P<0.05) after one week's treatment. Three patients continued on longterm treatment have returned to work.Low dose oral captopril therapy blocks angiotensin converting enzyme, suppresses secondary hyperaldosteronism, prevents hypokalaemia and produces sustained improvement in cardiac performance in patients with severe refractory congestive cardiac failure. Orally‐active inhibitors of angiotensin converting enzyme, of which captopril is the forerunner, appear to offer considerable therapeutic advantages in the treatment of cardiac failure.