The role of angiotensin-converting enzyme inhibitors in reducing ventricular remodeling after myocardial infarction.

Ventricular remodeling is a pathologic change in the size and shape of the heart after myocardial infarction. Human and animal studies have described the mechanisms responsible for the thinning and enlargement that progresses for years beyond the initial infarction. As a result of elevations in preload and afterload, ventricular pressures increase, and changes occur in both the infarcted and uninfarcted regions of the ventricle, increasing overall heart size. Recent investigation has demonstrated that the initiation of angiotensin-converting enzyme (ACE) inhibitor drugs after myocardial infarction reduces both systolic and diastolic wall stresses, thereby averting changes in heart size. These findings are significant, as increases in heart size and ventricular volumes have proved to be powerful predictors of early mortality after myocardial infarction.

Ventricular remodeling following myocardial infarction: a description of the pathologic process, current investigation, and suggested therapy.

The pathophysiologic process of ventricular remodeling after AMI involves an alteration in myocardial cell contraction. The stretching and redistribution of myocardial cells in the ischemic area promote dyssynergic contraction and an overall reduction in ventricular function. Expansion of the infarcted area and volume-overload hypertrophy of the uninfarcted area remodel the shape of the ventricle. Ventricular enlargement and dilation are associated with early mortality and morbidity. This has prompted further study to identify measures that can attenuate the process. Limited investigation on human subjects suggests that ACE inhibition reduces ventricular wall stress and preserves ventricular shape and function. A multicenter trial, SAVE, is under way to study the effects of long-term captopril therapy for patients suffering from AMI. This study and future investigations will focus on inhibition of ventricular remodeling following AMI in the hope of reducing symptomatic CHF and mortality.