Ventricular remodeling following myocardial infarction

Abstract

Ventricular remodeling denotes structural changes that occur in ventricular chamber size, wall thickness, and composition following myocardial damage. Following acute coronary occlusion, there are various factors to consider at different times that may contribute to subsequent ventricular dilation. Early infarct expansion and later healing may be accompanied by compensatory hypertrophy in the noninfarcted region and progressive global dilation, that may progress long term, the major stimulus being increased wall stress. The 2 major factors influencing ventricular remodeling following myocardial infarction are infarct artery patency and the ventricular loading conditions. Thrombolytic therapy may produce coronary reperfusion and limit infarct size. Patency of the infarct-related artery may also provide later benefits for ventricular remodeling. Following infarct evolution, pharmacologic intervention provides the potential to minimize the sequelae of infarct expansion and ventricular dilation. Clinical studies indicate that treatment of symptomless left ventricular dysfunction with angiotensin-converting enzyme inhibition at greater than or equal to 1 week following myocardial infarction may prevent further ventricular dilation and reduce the probability of progression to heart failure. Earlier intervention, at 24-48 hours following Q-wave myocardial infarction, is also practicable and effective. Even earlier intervention, in combination with or immediately following thrombolysis, is being assessed in other studies. The timing of treatment is of considerable importance because blockade of compensatory mechanisms activated at the time of infarction may not be desirable immediately, even though these mechanisms may be deleterious later. The results of large-scale mortality studies are awaited to indicate the benefit of this type of treatment in terms of heart failure prevention and survival long term.