According to estimates, up to 50% of patients with coronary artery disease and impaired left ventricular function have areas of viable myocardium. This dysfunctional, yet viable myocardial tissue, which can improve functionally after myocardial oxygen supply is reestablished, has been called hibernating myocardium. The possible pathophysiological mechanism that leads to hibernating myocardium is controversial: is the phenomenon due to persistent ischemia or is it the result of repetitive episodes of ischemia and reperfusion, such as myocardial stunning? Regardless of the mechanism, the presence of viable myocardial tissue indicates that structural and biochemical cellular changes occur, and the recovery of left ventricular function after revascularization depends on the severity and extent of these changes. Whether these changes reflect a long-lasting state of cellular dedifferentiation, an adaptive process that is reversible, or eventually lead to cellular degeneration has not been determined. Perhaps early detection of hibernating myocardial tissue via noninvasive imaging techniques used to assess contractile response, integrity of the cellular membrane, myocardial metabolism, and myocardial blood flow and subsequent early coronary revascularization may prevent infarction and deterioration in left ventricular function. Knowledge that reversible changes and areas of viable myocardium can occur in patients with left ventricular dysfunction will assist healthcare providers in the care and management of patients with hibernating myocardium.
P448Dietary protein restriction throughout intrauterine development and postnatal life alters myocardial tissue composition but not left ventricular function in the adult mouse heart
