Captopril in refractory heart failure: clinical and hemodynamic observations

10 patients suffering from refractory heart failure were treated with an oral angiotensin converting enzyme inhibitor captopril. The etiology of heart failure in 9 patients was related to ischemic heart disease, and to valvular heart disease in 1 patient. All patients experienced subjective improvement and feeling of well-being. The functional capacity improved to class II-IIB. Serial chest X-ray films showed improvement in pulmonary congestion. The time course of the hemodynamic effect appeared to 0.5-1.5 h after intake, and tended to disappear about 6 h later. The optimal dose of the drug achieving maximal hemodynamic benefit without excessive hypotension was 50 mg. Some of the patients exhibited a triphasic response. The cardiac index increased from 1.99 +/- 0.1 to 2.69 +/- 0.151/min/m (p less than 0.001), while pulmonary capillary wedge pressure decreased from 25.3 +/- 5.86 to 13.67 +/- 4.14 mm Hg (p less than 0.001). Mean peripheral arterial blood pressure decreased from 90.06 +/- 3.7 to 71.4 +/- 2.7 mm Hg. The total peripheral resistance decreased from 1,942 +/- 169 to 1,170 +/- 109 dyn X s X cm-5. The total pulmonary resistance decreased from 272.6 +/- 42.9 to 142.34 +/- 13.76 dyn X s X cm-5. Heart rate decreased from 83.4 +/- 10.9 to 70.8 +/- 10.14 bpm (p less than 0.01). During a 6-month follow-up period the beneficial clinical effects of captopril were sustained, without late vasodilator tolerance. 1 death, unrelated to captopril, occurred. 2 patients developed transient rash, and 1 experienced transient dysgeusia.