Prevention of ventricular remodeling after myocardial infarction and in congestive heart failure

Abstract

Myocardial infarction is associated with remodeling of infarcted and noninfarcted myocardium over weeks to months, resulting in progressive ventricular dilation, hypertrophy, and dysfunction. Major determinants of infarct remodeling are infarct size and transmurality, the efficacy of infarct healing, and magnitude of mechanical deformation forces such as the degree of ventricular loading and the magnitude of ventricular wall stress. These factors also influence remodeling of noninfarcted myocardium. In addition, two other factors that play major roles in the remodeling of non-infarcted myocardium are the patency of the non-infarct-related coronary artery and the integrity of the supporting collagen matrix. Prevention of remodeling involves efforts to decrease infarct size and transmurality, to reduce ventricular loading and wall stress, to promote healing, to preserve the supporting collagen matrix, and to restore patency of the infarct and non-infarct-related coronary arteries. Outcome depends critically on the timing and duration of therapy, and attention to the pathophysiologic stage of the remodeling process. Thrombolytic therapy is of proven value and should be available to all. Maximum benefit from ventricular un-loading therapy is achieved when it is begun very early, spans the infarct-healing process, and extends beyond. Early un-loading therapy should avoid hypotension and the paradoxical J-curve effect. Several large clinical trials favor the long-term use of angiotensin-converting enzyme (ACE) inhibitors to prevent progressive ventricular remodeling, to improve function, to prevent congestive heart failure, and to improve survival. Optimal strategies targeted at restoring ventricular funetion in viable but stunned or hibernating myocardium and preserving collagen matrix are lacking and need to be developed.