PATHOPHYSIOLOGY, CLINICAL SIGNIFICANCE AND POSSIBILITIES OF CARDIOPROTECTION IN MYOCARDIAL STUNNING, HIBERNATION AND PRECONDITIONING

The prolonged acute myocardial ischemia was once thought to result in irreversible cellular damage. Nevertheless, it is now demonstrated that in cardiac tissue under the stress of oxygen and substrate deprivation endogenous mechanisms of cell survival may be activated. Hibernating myocardium is a state of persistently impaired myocardial function at rest due to reduced coronary blood flow owing to residual stenosis that can be restored toward normal by revascularization. The success of revascularization procedures depends on the presence of dysfunctional but viable myocardium. The pattern of cell survival elicited by ischemia in myocardial stunning, hibernation and preconditioning results in the activation of cytoprotective mechanisms that will protect the heart against further ischemic damage. The basic mechanisms underlying stunning and hibernation are still a matter of intense research, which includes the discovery and characterization of new survival genes not revealed in the heart before, the unraveling of new cellular processes, such as autophagy, and study of metabolic biochemical disturbances. Therefore, understanding pathways of molecular adaptation of the cardiac myocyte during stress maintains its survival in these states and might help defining novel mechanisms of endogenous myocardial salvage in order to expand the conditions of preserved cellular viability and function of ischemic myocardium. Basic, clinical aspects and opportunities of therapeutic approaches in these types of cardiac dysfunctions are reviewed in this paper.