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Acquired skeletal muscle metabolic myopathy in atherosclerotic peripheral arterial disease

Department of Medicine, Harbor-UCLA Medical Center, Torrance, CA, USA

William R Hiatt

Colorado Prevention Center and the Section of Vascular Medicine, University of Colorado Health Sciences Center, Denver, CO, USA

Peripheral arterial disease (PAD) is associated with an increased risk of overall cardiovascular mortality, and substantial morbidity resulting from claudication. While the initial disease process is clearly the result of atherosclerosis in the arterial circulation of the limb, altered hemodynamics do not completely explain the pathophysiology of claudication. Work from several laboratories has demonstrated secondary changes in the skeletal muscle of patients with PAD which are consistent with the presence of an acquired metabolic myopathy in these patients. Key findings include an alteration in the expression of mitochondrial enzymes, the accumulation of metabolic intermediates, altered regulation of mitochondrial respiration, increased oxidative stress, and the presence of somatic mutations in the mitochondrial genome. Understanding the metabolic changes associated with PAD is important in understanding the pathophysiology of claudication and in the development of novel therapeutic strategies.

Key Words: carnitine • mitochondria • mitochondrial DNA • peripheral arterial disease

Vascular Medicine, Vol. 5, No. 1, 55-59 (2000)
DOI: 10.1177/1358836X0000500109


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