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(Circulation. 1997;95:1961-1971.)
© 1997 American Heart Association, Inc.

Articles

Chronic Myocardial Hibernation in Humans

From Bedside to Bench

Jean-Louis J. Vanoverschelde, MD; William Wijns, MD; Marcel Borgers, PhD; Guy Heyndrickx, MD; Christophe Depré, MD; Willem Flameng, MD; Jacques A. Melin, MD

the Division of Cardiology, University of Louvain, Brussels (J.-L.J.V., C.D., J.A.M.); the Cardiovascular Center, Aalst (W.W., G.H.); the Janssen Research Foundation, Beerse (M.B.); and the Department of Cardiovascular Surgery, Katholieke Universiteit Leuven (W.F.), Belgium.

Correspondence to Jean-Louis Vanoverschelde, MD, Divisionof Cardiology, Cliniques Universitaires St Luc, Ave Hippocrate10 (2881), B-1200 Brussels, Belgium. E-mail vanoverschelde@card.ucl.ac.be

Key Words: myocardium • stunning, myocardial • blood flow • tomography • metabolism

	Introduction

 
Since the pioneering work of Tennant and Wiggers,¹ it has been known that total ischemia leads to a prompt cessation of contraction and eventually results in the appearance of cell damage and irreversible myocardial necrosis. Accordingly, in the minds of many cardiologists, the discovery of an abnormal regional contraction in a patient with coronary artery disease has long been equated with the presence of irreversible myocardial necrosis. With the advent of recanalization therapy, however, evidence progressively accumulated that prolonged regional "ischemic" dysfunction did not always arise from irreversible tissue damage and, to some extent, could be reversed by restoration of blood flow.^{2 3 4 5} These observations have led to the speculation that chronically hypoperfused myocardium, which is often referred to as "hibernating,"^{2 3 4 5 6} could maintain viability by simply reducing its metabolic demand to match the decreased supply for as long as myocardial perfusion was inadequate. The chronic impairment of contractile function in this setting has been regarded as a protective mechanism by which the heart spontaneously downgrades its myocardial function, minimizes its energy requirements, and prevents the appearance of irreversible tissue damage.^{2 4 5} The concept of chronic hibernation thus consists of two parts: a unique clinical observation that bears important implications for the management of patients with chronic coronary artery disease^{2 3 4 5 6} and a pathophysiological hypothesis, yet to be demonstrated, implying that the chronic dysfunction is due to a chronic reduction of resting MBF.^{4 5} Other aspects that were not included in the original description, ie, the rapidity of mechanical recovery after successful revascularization⁷ and the . . . [Full Text of this Article]