'Myocardial hibernation'--questions and controversies.

Abstract

Time for primary review 44 days. The term ‘hibernation’ has been borrowed from zoology and implies an adaptive reduction of energy expenditure through reduced activity in a situation of reduced energy supply. In the context of coronary artery disease, myocardial hibernation was originally seen as a chronic , adaptive reduction of myocardial contractile function in response to a reduction of myocardial blood flow. It was also viewed as a condition where there would be a complete recovery of contractile function upon restoration of flow. Thus, in the concept of myocardial hibernation, the observed chronic reduction of myocardial contractile function was not regarded as the result of a persistent energetic deficit, but instead as a regulatory event which acted to avoid an ongoing energy deficit and thereby maintain myocardial integrity and viability. The concept of myocardial hibernation did not originate in the laboratory, instead it was entirely founded on clinical grounds when, in the early eighties, Rahimtoola reviewed the results of coronary bypass surgery trials and identified a subset of patients with coronary artery disease and chronic left ventricular dysfunction that improved upon revascularization [1, 2]. Rahimtoola then popularized the term ‘hibernation’ previously coined by Diamond et al. [3]. Whereas originally the idea of an adaptive reduction of contractile function in response to a reduction in blood flow was straightforward and simple, the situation of chronic, yet reversible contractile dysfunction in the setting of coronary artery disease is now recognized to be enormously complex and controversial. The aim of this article is not to give definite answers to any questions, but rather to identify the most pressing questions and controversies in the field of hibernation. The introduction of the concept of hibernation has challenged the traditional view that the extent of chronic contractile dysfunction reflects the amount of infarcted … * Corresponding author. Abteilung fur Pathophysiologie, Zentrum fur Innere Medizin, Universitatsklinikum Essen, Hufelandstrase 55, 45122 Essen, Germany. Tel.: +49 (201) 7234480; fax: +49 (201) 7234481.