[Effect of fosinopril on the rate of neurohumoral and proinflammatory activation in patients with heart failure].

The purpose of the study was to examine the effect of fosinopril on the magnitude of neurohumoral and proinflammatory activation in patients with severe heart failure (HF). Twenty-eight patients aged 52-68 years who had Functional Class (FC) III-IV HF that had developed due to coronary heart disease were examined. All the patients were divided into 2 groups (with 14 patients in each group) and they received routine therapy including an angiotensin-converting enzyme inhibitor (ACEI) and a beta-adrenoblocker. Group 1 patients were given the ACEI fosinopril in a dose of 10-20 mg/day, Group 2 patients took captopril in a dose of 50-75 mg/day. The course of therapy was 12 weeks. All the patients underwent echocardiography by the routine procedure. The plasma levels of angiotensin-II, aldosterone, and brain natriuretic peptide (BNUP) were determined by radioimmunoassay. The plasma contents of tumor necrosis factor-alpha (TNF-alpha) and C-reactive protein (C-RP) were verified by enzyme immunoassay. An analysis of the findings indicated that during therapy the FC of HF decreased on the average by 10.9% in Group 1 and by 11. 7% in Group 2 (p = 0.14). With this, fosinopril was superior to captopril not only in its capacity of improving overall left ventricular contractile function, but it was characterized by a more pronounced effect on regression of the plasma pool of C-RP and TNF-alpha. The marked depressive action of the ACEI fosinopril on the plasma pool of products of the renin-angiotensin system, BNUP, and proinflammatory cytokines may be considered to be as a basis for preferably prescribing the agent to patients with severe HF.