Autophagy is an important process in the heart which is responsible for the normal turnover of long lived proteins and organelles. Inhibition of autophagy leads to the accumulation of protein aggregates and dysfunctional organelles which can cause cell death. Autophagy occurs at low basal levels under normal conditions in the heart, but is rapidly upregulated in response to stress such as nutrient deprivation, hypoxia, and pressure overload. Autophagy is a prominent feature of myocardial ischemia and reperfusion. Although enhanced autophagy is often seen in dying cardiac myocytes, the functional significance of autophagy under these conditions is not clear. Upregulation of autophagy has been reported to protect cardiac cells against death as well as be the cause of it. Here, we review the evidence that autophagy can have both beneficial and detrimental roles in the myocardium, and discuss potential mechanisms by which autophagy provides protection in cells.