Abstract: 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 functions. These cardiac changes are particularly pronounced in the elderly. With increasing age, the burden of heart failure is likely to increase. Developing targeted therapies for post-infarction heart failure in the elderly requires investigation into the specific pathophysiological changes of LV remodeling in this age group.