The pathophysiology of myocardial hibernation: current controversies and future directions.

ABSTRACT

It is now widely accepted that patients with chronic coronary artery disease can experience prolonged regional ischemic dysfunction that does not necessarily arise from irreversible tissue damage and, to some extent, can be reversed by restoration of blood flow. Recent clinical and experimental data suggest that this form of chronic but reversible left ventricular dysfunction represents a complex, progressive, and dynamic phenomenon. The initial stages of dysfunction are probably caused by chronic stunning. They are characterized by normal resting perfusion but reduced flow reserve, mild myocyte alterations, maintained membrane integrity (allowing the transport of both thallium and glucose), preserved capacity to respond to an inotropic stimulus, and no or little tissue fibrosis. After revascularization, functional recovery will probably be rapid and complete. On the other hand, the more advanced stages of dysfunction likely correspond to chronic hibernation. They usually are associated with reduced rest perfusion; increased tissue fibrosis; more severe myocyte alterations (degeneration[?], apoptosis); and a decreased ability to respond to inotropic stimuli. Nonetheless, membrane function and glucose metabolism may long remain preserved. After revascularization, functional recovery, if any, will probably be quite delayed and mostly incomplete.