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(Circulation Research. 2004;94:1005.)
© 2004 American Heart Association, Inc.

Editorials

Myocardial Hibernation

A Double-Edged Sword

Gerd Heusch, Karin R. Sipido

From the Institut für Pathophysiologie (G.H.), Zentrum für Innere Medizin, Universitätsklinikum Essen, Germany and the Laboratory of Experimental Cardiology (K.R.S.), University of Leuven, Belgium.

Correspondence to Gerd Heusch, MD, PhD, Institut für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Essen, Germany, E-mail gerd.heusch@uni-essen.de; or Karin R. Sipido, MD, PhD, Laboratory of Experimental Cardiology, University of Leuven Campus Gasthuisberg O/N 7th floor, Herestraat 49, B-3000 Leuven, Belgium. E-mail Karin.Sipido@med.kuleuven.ac.be

See related article, pages 1142–1149

Key Words: ischemic heart disease • hibernating myocardium • arrhythmias • sudden cardiac death • remodeling

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Ischemic heart disease remains a leading cause of morbidity and mortality. The survival after acute ischemic events has improved substantially in recent years, but new syndromes have emerged. Cardiac remodeling following a large myocardial infarction, with dilatation of the left ventricle, has deleterious hemodynamic consequences and is a major cause of chronic heart failure.¹ The increased incidence of potentially lethal arrhythmias² is related to the presence of scar tissue but also to altered properties of the surviving myocardium, as characterized in experimental studies. Myocytes in the remote myocardium are hypertrophied, and the contraction of isolated cells is reduced.^3–5 This is related to a reduction in Ca²⁺ transient amplitude and slower Ca²⁺ removal. The changes in electrogenic Ca²⁺ transport via the Na/Ca exchanger also contribute to the electrical remodeling. Indeed, the action potential profile is altered and its duration is increased because of reduced density of K⁺ currents and the changes in Ca²⁺-dependent ionic currents, and these changes are variable throughout the remaining myocardium.^5–8 This remodeling process results in an increased susceptibility for arrhythmias with the myocardium as the substrate on which specific events trigger arrhythmias.²

In contrast to the extensive characterization of cellular remodeling following myocardial infarction, much less information is available on the changes in hibernating myocardium, ie, myocardium with reduced baseline blood flow and contractile dysfunction, which retains viability and recovers on revascularization.⁹ (This is the classical definition of hibernation,¹⁰ but others have viewed hibernation as a manifestation of repetitive stunning.¹¹) Nevertheless, the importance of this . . . [Full Text of this Article]

This article has been cited by other articles:

				G. Heusch, R. Schulz, and S. H. Rahimtoola Myocardial hibernation: a delicate balance Am J Physiol Heart Circ Physiol, March 1, 2005; 288(3): H984 - H999. [Abstract] [Full Text] [PDF]