Myocardial hibernation as a cause of heart failure in acute myocardial infarction

There are clinical observations and morphological data indicating that acute myocardial infarction (AMI) causes myocardial hibernation (MH) of hypoperfused cardiomyocytes (CMC) of the left ventricle (LV). This process leads to cardiac dysfunction and heart failure which could be partly reversible within a few weeks or months after appropriate pharmacotherapy or revascularization. Long-term. hibernation leads to severe myocyte degeneration of near-necrotic zones of the myocardium and their apoptosis. Cardiogenic shock and pulmonary edema induce acute CMC hibernation of LV intact zones, causing their damage and death via apoptosis within several hours. A better understanding of morphology of MH will provide rationale for developing new therapeutic strategies designed to prevent LV systolic dysfunction and heart failure.