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Myocardial ischaemia: new evidence for angiotensin-converting enzyme inhibition

R. Ferrari1, G. Guardigli, D. Mele, M. Valgimigli and C. Ceconi

University of Ferrara and Cardiovascular Research Center, ‘Salvatore Maugeri’ Foundation, Gussago, Brescia, Italy

1 Prof. Roberto Ferrari, Chair of Cardiology, University of Ferrara, Via Savonarola, 9, 44100 Ferrara, Italy.

Abstract

Angiotensin-converting enzyme (ACE) inhibitors undoubtedly represent a milestone in cardiovascular therapy. They are known to halt the progression of coronary artery disease by interrupting the series of events that lead to end-stage ischaemic heart disease. Moreover, in patients with severe heart failure, ACE inhibitors, quite surprisingly, reduce the recurrence of angina pectoris and myocardial infarction, hospitalization for ischaemic heart disease, and the rate of coronary artery bypass surgery or angioplasty. More recently ACE inhibitors have been postulated to reduce vascular hypertrophy, attenuate atherosclerosis and influence mortality and hospitalization when used in patients with left ventricular dysfunction without overt heart failure. The results of the Heart Outcomes Prevention Evaluation (HOPE) study confirm that this is the case, and that these agents can reduce the incidence of coronary events. Two other major trials, on the same subject but substantially different from HOPE, namely the European trial on Reduction Of cardiac events with Perindopril in stable coronary Artery disease (EUROPA) and the Prevention of Events with ACE inhibitors (PEACE) study, are underway. The clinical hypothesis to be tested is that prolonged ACE inhibition reduces the progression of coronary atherosclerosis; the biological hypothesis is that prolonged ACE inhibition reduces or even reverses endothelial dysfunction to normal—a mechanism in which bradykinin might be significantly involved. This is the main topic of the present article.

Key Words: Acute coronary syndromes • Angina • Atherosclerosis • Myocardial infarction • Perindopril


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