PURPOSE OF REVIEW: Energetic abnormalities in cardiac and skeletal muscle occur in heart failure and correlate with clinical symptoms and mortality. It is likely that the cellular mechanism leading to energetic failure involves mitochondrial dysfunction. Therefore, it is crucial to elucidate the causes of mitochondrial myopathy, in order to improve cardiac and skeletal muscle function, and hence quality of life, in heart failure patients. RECENT FINDINGS: Recent studies identified several potential stresses that lead to mitochondrial dysfunction in heart failure. Chronically elevated plasma free fatty acid levels in heart failure are associated with decreased metabolic efficiency and cellular insulin resistance. Tissue hypoxia, resulting from low cardiac output and endothelial impairment, can lead to oxidative stress and mitochondrial DNA damage, which in turn causes dysfunction and loss of mitochondrial mass. Therapies aimed at protecting mitochondrial function have shown promise in patients and animal models with heart failure. SUMMARY: Despite current therapies, which provide substantial benefit to patients, heart failure remains a relentlessly progressive disease, and new approaches to treatment are necessary. Novel pharmacological agents are needed that optimize substrate metabolism and maintain mitochondrial integrity, improve oxidative capacity in heart and skeletal muscle, and alleviate many of the clinical symptoms associated with heart failure. © 2007 Lippincott Williams & Wilkins, Inc.

Item Type:	Refereed Article
Research Division:	Biomedical and Clinical Sciences
Research Group:	Cardiovascular medicine and haematology
Research Field:	Cardiology (incl. cardiovascular diseases)
Objective Division:	Health
Objective Group:	Clinical health
Objective Field:	Clinical health not elsewhere classified
UTAS Author:	Edwards, LM (Dr Lindsay Edwards)
ID Code:	64375
Year Published:	2007
Web of Science® Times Cited:	55
Deposited By:	Medicine
Deposited On:	2010-07-21
Last Modified:	2012-02-27
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