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Cardiovascular Research 2000 45(4):805-806; doi:10.1016/S0008-6363(99)00419-8
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Mitochondrial dysfunction in heart failure: potential for therapeutic interventions?

William C Stanleya,* and Charles L Hoppelb,c

aDepartment of Physiology and Biophysics, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106-4970, USA
bDepartments of Pharmacology and Medicine, Case Western Reserve University, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106-4970, USA
cVeterans Affairs Medical Center, Cleveland, OH, USA

* Corresponding author. Tel.: +1-216-368-5585; fax: +1-216-368-3952 wcs4@po.cwru.edu

Received 7 December 1999; accepted 7 December 1999

KEYWORDS Cardiomyopathy; Heart failure; Mitochondria

The first 10% of the full text of this article appears below.

See article by Jarreta et al. [4] (pages 860–865) in this issue.

Cardiac work is supported by a high rate of ATP hydrolysis, matched by ATP production through mitochondrial oxidative phosphorylation (Fig. 1). Low ATP content in cardiac tissue was observed in patients with chronic heart failure despite the absence of myocardial ischaemia [1]. Mitochondrial function in cardiac tissue from the failing heart demonstrated that the capacity of the mitochondria for oxygen consumption and oxidative phosphorylation are significantly reduced compared to the normal heart [2]. Furthermore, morphological examination of the failing heart . . . [Full Text of this Article]


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