Role of angiotensin converting enzyme inhibitors in preventing left ventricular remodelling following myocardial infarction.

Abstract

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 remodeling 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.