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Circulation Research. 2008;102:3-5
doi: 10.1161/CIRCRESAHA.107.168278
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(Circulation Research. 2008;102:3.)
© 2008 American Heart Association, Inc.


Editorials

Hibernating Myocardium

Is the Program to Survive a Pathway to Failure?

Rosemary F. Kelly, Wim Sluiter, Edward O. McFalls

From Cardiac Surgery (R.F.K.) and Cardiology (E.O.M.), Veterans Affairs Medical Center, University of Minnesota, Minneapolis; and the Mitochondrial Research Unit (W.S.), Erasmus Medical Center, Rotterdam, The Netherlands.

Correspondence to Edward O. McFalls, MD, PhD, Cardiology (111C), Veterans Affairs Medical Center, 1 Veterans Dr, Minneapolis, MN 55417. E-mail mcfal001@umn.edu



See related article, pages 103–112


Key Words: myocardial hibernation • mitochondria • preconditioning • superoxide • heart failure


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


*    Introduction
 
Winter hibernation carries the promise of rejuvenation in the spring. In a similar fashion, myocardial "hibernation" describes a clinical phenomenon in which patients with ischemic left ventricular dysfunction demonstrate improved cardiac function following bypass surgery.1 The signature of myocardial hibernation is decreased blood flow with preserved glucose uptake, as demonstrated by positron emission tomography imaging, and identifies individuals with ischemic cardiomyopathy who may benefit from revascularization.2 In experimental models of hibernating myocardium, oxygen consumption is reduced in the absence of active ischemia.3,4 This implies that hibernation is a coordinated response to balance myocardial energy utilization with energy production capacity.5 However, within hibernating myocardium, several morphological and functional changes have been observed that can identify regions in which complete revascularization may not result in normalization of contraction.6–10 In fact, those myocardial regions with the greatest metabolic abnormalities in the hibernating tissue demonstrate the longest delay in recovery.11

In the current issue, Page et al12 demonstrate that the process of hibernation is associated with altered expression of mitochondrial proteins. Using 2D differential-in-gel electrophoresis and matrix-assisted laser desorption ionization time-of-flight mass spectrometry in a swine model of hibernation, they have found that key mitochondrial proteins associated with the electron transport chain are reduced. The functional importance of the decreased protein expression is documented by reduced activity measurements of the pyruvate dehydrogenase complex, cytochrome c oxidase, and citrate synthase. The parallel reductions in mitochondrial proteins and contractile function 5 months after placement of the coronary artery constrictor suggest that the "downregulation" of electron transport . . . [Full Text of this Article]


Related Article:

Persistent Regional Downregulation in Mitochondrial Enzymes and Upregulation of Stress Proteins in Swine With Chronic Hibernating Myocardium
Brian Page, Rebeccah Young, Vijay Iyer, Gen Suzuki, Maciej Lis, Lioubov Korotchkina, Mulchand S. Patel, Kenneth M. Blumenthal, James A. Fallavollita, and John M. Canty, Jr
Circ. Res. 2008 102: 103-112. [Abstract] [Full Text] [PDF]