LV enlargement is an important determinant of survival after AMI. Pathophysiologic mechanisms leading to LV dilatation after an AMI include early thinning and stretching of the infarcted segment (e.g., infarct expansion) and hypertrophy of the noninfarcted myocardium. Such LV dilatation may adversely affect subsequent cardiac function, leading to heart failure and death. Experimental data in animals and preliminary studies in humans have demonstrated that early administration of captopril, an angiotensin-converting enzyme inhibitor, may limit infarct expansion and will attenuate progressive LV dilatation. This article discussed the clinical importance of the dilated left ventricle and reviewed advances and ongoing research in the use of angiotensin-converting enzyme inhibitors in the chronic phase after AMI.