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(Circulation. 2002;105:1517.)
© 2002 American Heart Association, Inc.

Editorials

Myocardial Hibernation

Restorative or Preterminal Sleep?

Douglas B. Sawyer, MD, PhD; Joseph Loscalzo, MD, PhD

From the Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass.

Correspondence to Joseph Loscalzo, MD, PhD, Boston University School of Medicine, Boston, Mass 02118-2394. E-mail jloscalz@bu.edu

Key Words: Editorials • hibernation • myocardial contraction • nitric oxide synthase • ventricles

Oppressed nature sleeps.

—Shakespeare, King Lear, Act III, Scene VI

The term hibernating myocardium was first proposed by S. Rahimtoola in 1985 to describe a state of left ventricular dysfunction at rest caused by reduced coronary blood flow, which can be reversed by restoring myocardial oxygen supply or reducing myocardial oxygen demand.¹ The clinical context in which it was first recognized, viz, impaired left ventricular function at rest that recovers after revascularization, was refined further when it was recognized that "fixed" defects on [²⁰¹Tl] perfusion images could improve after revascularization² or with rest-redistribution³ or reinjection.⁴ To date, the molecular mechanisms underlying myocardial hibernation have remained elusive.

See p 1537

Hibernation defines one form of pathophysiological response to myocardial ischemia, the other two being stunning and ischemic preconditioning. Myocardial stunning is defined as ventricular dysfunction that recovers gradually after a brief period of severe ischemia, and ischemic preconditioning is defined as the ability of the myocardium to tolerate an acute ischemic episode with limited ventricular dysfunction as a result of prior brief episodes of ischemia. As one might imagine, these three myocardial responses to ischemia are not mutually exclusive of one another: For example, repetitive stunning superimposed on reduced basal blood flow may contribute to the development of hibernation, and repetitive stunning likely promotes ischemic preconditioning.

Hibernation currently is viewed not as a simple consequence of an oxygen deficit, but as an adaptive response to maintain cardiomyocyte viability in the setting of reduced blood flow.⁵ Characterization of the . . . [Full Text of this Article]

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