Although myocardial ischemia was once thought to result in irreversible cellular damage, it is now demonstrated that in cardiac tissue, submitted to the stress of oxygen and substrate deprivation, endogenous mechanisms of cell survival may be activated. These molecular mechanisms result in physiological conditions of adaptation to ischemia, known as myocardial stunning and hibernation. These conditions result from a switch in gene and protein expression, which sustains cardiac cell survival in a context of oxygen deprivation and during the stress of reperfusion. The pattern of cell survival elicited by ischemia in myocardial stunning or hibernation results in the activation of cytoprotective mechanisms that will protect the heart against further ischemic damage, a condition referred to as ischemic preconditioning. The basic mechanisms underlying stunning and hibernation are still a matter of intense research, which includes the discovery and characterization of novel survival genes not described in the heart before, or the unraveling of new cellular processes, such as autophagy. Understanding how the molecular adaptation of the cardiac myocyte during stress sustains its survival in these conditions therefore might help defining novel mechanisms of endogenous myocardial salvage, in order to expand the conditions of maintained cellular viability and functional salvage of the ischemic myocardium.