Left ventricular (LV) remodeling, which can result from myocardial damage or ventricular pressure or volume overload, has genomic, cellular, and interstitial components with associated changes in ventricular size, shape, wall thickness, and function. It is a process that is detectable and measurable clinically, generally progressive, and associated with adverse outcomes. However, it is amenable to intervention, prevention, or reversal. Following myocardial infarction (MI), LV remodeling is particularly likely in patients with transmural or anterior infarction and in those with failed reperfusion or LV failure. Infarct artery patency and neurohormonal blockade are key management considerations for prevention or reversal of LV remodeling. Combination treatment with angiotensin-converting enzyme inhibition and beta-blockade is of proven benefit following MI, improving LV remodeling and long-term outcomes.