Key result
Contractile dysfunction of viable myocytes in the absence of myocardial infarction may be accounted for by two phenomena: hibernating myocardium or stunned myocardium.
Discusses the concepts of hibernating and stunned myocardium as causes of reversible contractile dysfunction in patients with coronary artery disease.
Less than 20 years ago, contractile dysfunction of the myocardium in patients with coronary-artery narrowing was thought to be caused by either irreversible damage to myocytes (that is, myocardial infarction or scarring) or reversible ischemia (such as would occur during an attack of angina). During the past decade, however, both clinical and laboratory studies have demonstrated that contractile dysfunction in the heart may also occur in the absence of a myocardial infarction or after an acute ischemic event is over.1 Specifically, two phenomena may account for this contractile dysfunction of viable myocytes: hibernating myocardium or stunned myocardium. The report by . . .
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Kloner et al. (1991) conducted an editorial in Contractile dysfunction of the myocardium. Contractile dysfunction of viable myocytes in the absence of myocardial infarction may be accounted for by two phenomena: hibernating myocardium or stunned myocardium.
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