MI is one of the most common causes of CHF (2). The way in which MI leads to heart failure is a complex multifactorial process known as LV remodeling. MI, caused by occlusion of an epicardial coronary artery, leads within hours to irreversible death of the cardiomyocytes in the distribution supplied by that artery. MI also initiates a cascade of neurohormonal changes that attempt to compensate for the lack of contractile function caused by the MI. This initially maintains cardiac output and perfusion to the vital organs, but with time, these compensatory mechanisms fail, and there is progressive deterioration of cardiac function. The end result is a dilated, poorly functioning ventricle, and the clinical syndrome of heart failure ensues (3). At the organ level, important pathological features of post-infarction LV remodeling include infarct expansion, myocardial hypertrophy, cardiac fibrosis, and global ventricular dilation (3). However, at the cellular level, the precise pathophysiological changes associated with LV remodeling remain incompletely characterized. Several molecular and cellular processes appear to be particularly important, including ongoing apoptosis of cardiac myocytes, particularly at the border zone of the MI, dysfunctional cardiomyocyte autophagy, and reduction in the proliferative capacity of new cardiomyocytes. This ongoing cell loss and inability to replace lost cells may contribute to the deterioration in cardiac function (Figure 1). These cardiac changes are particularly pronounced in the elderly. As our population ages (4), the burden of heart failure is likely to increase. Developing targeted therapies for post-infarction heart failure in the elderly will require investigation into the specific pathophysiological changes of LV remodeling in this age group.