Copyright © 1995 by the European Society of Cardiology.
© 1995 The European Society of Cardiology
Role of angiotensin converting enzyme inhibitors in preventing left ventricular remodelling following myocardial infarction
Department of Medicine, Tufts University, New England Medical Center Boston, U.S.A.
Correspondence: Marvin A. Konstam, MD, Box 108, New England Medical Center, 750 Washington St., Boston, MA 02111, U.S.A.
Progressive changes typically occur in left ventricular (LV) architecture following moderate- to large-sized myocardial infarction (MI). These changes include early expansion and thinning of the infarct zone and subsequent increase in myocardial mass within the non-infarcted zone, with LV dilatation and loss of the normal elliptical configuration of the LV cavity. These changes are accompanied by impaired myocyte function and advancing clinical expression of heart failure. Numerous animal and human studies have documented inhibition of LV remodelling post-MI by angiotensin converting enzyme (ACE) inhibitors. Although the ideal timing for initiating treatment remains uncertain, evidence exists that benefit persists long after the time of initial injury. Mechanisms for the effects of ACE inhibitors on LV remodelling may be dependent on changes in myocardial load may be load independent, or both. These effects are likely to be mediated by reductions in circulating and local tissue concentrations of angiotensin II and in bradykinin degradation. Regardless of the exact mechanism or mechanisms by which ACE inhibitors exert their favourable influence on LV remodelling, it is likely that this effect is a key mediator of the documented clinical benefits afforded by treatment with this class of agents.
Key Words: Angiotensin converting enzyme inhibitors • collagen deposition • fibroblast proliferation • heart failure • left ventricular remodelling • myocardial infarction • myocyte growth