Cilazapril Treatment in a Cohort of Seven Patients with Congestive Heart Failure: A Seven-Year Follow-Up Study

Abstract

Background: Although angiotensin-converting enzyme inhibitors (ACEIs) have been shown to prolong life in patients with congestive heart failure (CHF), the prognosis of these patients remains poor. Objective: The purpose of the study was to reevaluate a cohort of patients with CHF after 7 years of follow-up with cilazapril therapy to assess the renin-angiotensin system (RAS), anatomic and functional capacity of the heart, and aldosterone escape. Methods: Surviving patients from a cohort hospitalized for CHF between January 1994 and December 1994 who were treated with cilazapril in our center were included in this study. Exercise testing was carried out using the Kattus protocol, and breath-by-breath oxygen analysis, echocardiography, and hormonal analysis were done. Results: Seven patients (5 men, 2 women; mean [SD] age, 70.6 [4.4]) were included in the study. Compared with the early effects (at 15 days) of cilazapril therapy, only mean (SD) peak exercise time decreased significantly at the 7-year follow-up (8.9 [2.4] minutes vs 5.1 [1.9] minutes; P = 0.02). Mean (SD) anaerobic threshold (AT) oxygen consumption and AT ratio increased slightly from 15 days, although these changes were not statistically significant (12.86 [3.5] mL/kg·min vs 13.57 [2.6] mL/kg·min; 70.3% [7.7%] vs 78.9% [9.8%], respectively). Compared with the early effect of therapy, patients had slightly lower mean (SD) ejection fractions (EFs), but the decrease did not reach statistical significance (52% [4%] vs 48% [4%]). Aldosterone levels were within normal limits in all patients, and 2 patients had increased RAS activity. Conclusions: In this study, the observed lack of aldosterone escape, as well as patient survival during ACEI therapy, may be due to selection bias of the surviving patients, who had better EFs and lack of aldosterone escape. Therefore, the remaining issue seems to be the selection of patients who will not show aldosterone escape during chronic ACEI treatment.