Chronic hibernation and chronic stunning: A continuum

Identification of myocardial viability is of increasing clinical importance in managing patients with coronary artery disease and advanced left ventri cular dysfunction, Although viable chronically dysfunctional myocardium is always the result of repetitive episodes of reversible ischemia, there may be multiple mechanisms responsible for the contractile dysfunction. Many pa tients have contractile dysfunction with normal resting perfusion, as deter mined by imaging, that is related to chronic myocardial stunning. Viability studies are generally unnecessary because normal resting perfusion would p reclude significant fibrosis, The clinical problem arises in evaluating pat ients with depressed resting flow that can be due to hibernating myocardium or nontransmural infarction, In this circumstance viability studies are re quired to assess the likelihood of functional recovery after revascularizat ion, Although hibernating myocardium was originally posited to develop in r esponse to prolonged episodes of myocardial ischemia (experimentally termed "short-term hibernation"), subsequent studies have shown that this tenuous balance can only be maintained for a period of several hours before result ing in some degree of subendocardial infarction. More recent experimental s tudies have demonstrated that there is a progression from chronic stunning with normal flow to hibernating myocardium with reduced resting flow. This presumably arises from repetitive episodes of spontaneous ischemia that inc rease in frequency as the physiologic significance of a coronary stenosis p rogresses. Thus in this new paradigm reduced flow is a result, rather than the cause, of the contractile, dysfunction. This review summarizes basic an d clinical pathophysiologic studies supporting the claim that chronic stunn ing and hibernation are distinct entities that may represent opposite ends of a continuum of mechanisms in viable chronically dysfunctional myocardium .