Myocardial hibernation: Clinical and pathological perspectives

Myocardial hibernation refers to a state of persistent regional contractile ventricular dysfunction, in patients with coronary artery disease that is reversible with revascularization. Identification of hibernating myocardial segments is critical for selecting patients who are most likely to benefit from revascularization procedures. Positron emission tomography, thallium scintigraphy, dobutamine stress echocardiography, myocardial contrast echocardiography and magnetic resonance imaging have been extensively used for detection of viable dysfunctional myocardial segments. Although chronic hypoperfusion and repetitive episodes of brief ischemia may play a role in mediating the changes associated with myocardial hibernation the exact pathogenetic mechanisms are not well understood. The structural alterations found in hibernating myocardial segments involve both the cardiomyocytes and the cardiac interstitium. Depletion of contractile elements, loss of myofilaments, disorganization of myocyte cytoskeletal proteins and alterations in adrenergic receptor density have been reported in segments with reversible systolic dysfunction and may cause segmental hypocontractility. In addition, activation of the inflammatory cascade is noted, leading to cytokine and chemokine induction, leukocyte recruitment, interstitial remodeling and fibrosis. Myocardial hibernation represents a part of the spectrum of ischemic cardiomyopathy, which in the absence of a completed myocardial infarction is a dynamic continuous process ultimately leading to irreversible injury and dysfunction. Understanding of the specific molecular signals involved in the pathogenesis of myocardial hibernation is crucial in order to design strategies preventing irreversible dysfunction.