[Long-term therapy with oral prazosin in chronic congestive heart failure: a clinical and echocardiographic evaluation (author's transl)].

Eight patients, ranging in age from 20 to 61 years (48 +/- 11 years, mean +/- 1 SD), with chronic heart failure due to idiopathic congestive cardiomyopathy (5 cases), ischemic heart disease with healed anterior myocardial infarction (2 cases), and rheumatic heart disease with a Björk-Shiley mitral valve prosthesis (1 case), received longterm therapy with oral prazosin in increasing doses (mean final dose: 26 +/- 6 mg/day). Administration of digoxin and diuretics were continued throught the study period (range: 21-228 days). All but one patient showed no functional improvement during the period of prazosin therapy (2 patients in New York Heart Association functional class IV, 5 patients in III class). One patient, the youngest of the group, who initially had class IV heart failure, showed improvement to III class after a 26 days administration of this vasodilator. Prazosin caused no consistent change in systemic arterial pressure, heart rate, cardio-thoracic ratio, and radiologic pulmonary venous stasis. Occasionally, on chest X-ray, a patient showed a transitory decrease of cardiomegaly and/or pulmonary venous congestion. P and QRS waves of ECG showed no evident change, as did serum creatinine and billirubin levels. On serial M-mode echocardiographic analyses, left ventricular minor axis dimension, ejection, and left atrial size showed no statistically significant change from pre-treatment averages of: 7.5 +/- 0.9 cm, 0.36 +/- 0.14, 4.9 +/- 1.3 cm, respectively. At late follow-up some indices of left ventricular performance showed a definite tendency to decrease: fractional shortening of the minor axis from 18.9 +/- 9.1 to 17.0 +/- 7.0, mean velocity of circumferential fiber shortening from 0.79 +/- 0.28 sec-1 to 0.69 +/- 0.28 sec-1, mean normalized systolic ejection velocity from 1.58 +/- 0.44 sec-1 to 1.47 +/- 0.39 sec-1, and mean normalized posterior wall velocity from 0.55 +/- 0.3 sec-1 to 0.49 +/- 0.18 sec-1. Prazosin in patients with chronic congestive failure due to cardiomyopathies, does not elict a persistent improvement of resting hemodynamics because of the development of pharmacodynamic tolerance in the majority of the patients. Prazosin, furthermore, does not improve the depressed myocardial contractility that necessarily affects the long-term prognosis of these patients.