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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:2441.)
© 2005 American Heart Association, Inc.

Editorials

Mechanisms of Statin-Induced Myopathy

A Role for the Ubiquitin–Proteasome Pathway?

M. John Chapman; Alain Carrie

From the Dyslipidemia and Atherosclerosis Research Unit (M.J.C., A.C.), National Institute for Health and Medical Research (INSERM); University Pierre et Marie Curie (M.J.C., A.C.); and Molecular Endocrinology Unit, Department of Medical Biochemistry, APHP (A.C.), Hopital de la Pitié, Paris, France.

Correspondence to M. John Chapman, PhD, DSc, Dyslipidemia and Atherosclerosis Research Unit, INSERM U.551, Hôpital de la Pitié, 83, Blvd de l’Hôpital, 75651 Paris Cedex 13, France. E-mail chapman@chups.jussieu.fr

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

The advent of the HMG-CoA reductase inhibitors, or statins, in the 1980’s as highly efficacious agents for the lowering of low-density lipoprotein-cholesterol (LDL-C) revolutionized treatment of hypercholesterolemia, a long established risk factor for premature coronary heart disease. Indeed, a recent prospective meta-analysis of data from more than 90 000 participants in 14 randomized clinical trials revealed that a statin-mediated reduction of 1 mmol/L (40 mg/dL) in LDL-C that is sustained for 5 years may produce a proportional reduction in major vascular events of some 23%.¹ Greater reductions in LDL-C, which may be attained with intensive statin therapy as exemplified in the recent Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22), Treating to New Targets (TNT), and Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trials involving use of atorvastatin (80 mg/d), produce larger reductions in vascular disease risk.^2–4 Importantly, risk reductions are proportional to the absolute reduction in LDL-C¹, and moreover clinical benefit may be apparent with intensive statin treatment as early as 30 days after initiation in acute coronary syndrome patients, with significant decrement in cardiovascular morbi-mortality.⁵

See page 2560

Statins not only exhibit a remarkably high benefit to risk ratio, but are equally characterized by a safety profile with excellent tolerance.^6,7 Nonetheless, statins may exert toxic effects on skeletal muscle which are generally referred to as myopathy, and whose overall incidence is typically <0.1% of patients receiving statin monotherapy.⁶ Although myopathy can refer to any muscular disease, the recent clinical advisory . . . [Full Text of this Article]

Related Article:

Changes in Ubiquitin Proteasome Pathway Gene Expression in Skeletal Muscle With Exercise and Statins

Maria L. Urso, Priscilla M. Clarkson, Dustin Hittel, Eric P. Hoffman, and Paul D. Thompson
Arterioscler Thromb Vasc Biol 2005 25: 2560-2566. [Abstract] [Full Text] [PDF]