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β-Hydroxy-β-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) are highly efficacious in the prevention of coronary artery disease. Although statins are generally considered safe, their use may be associated with musculoskeletal complaints that limit tolerance to treatment and, in the most extreme case, can lead to rhabdomyolysis. Both candidate gene and genome-wide association studies are being used to assess possible genetic susceptibility to statin-induced myopathy, with the recognition that this phenotype represents a broad spectrum of syndromes influenced by other drugs and disease states. In addition to potentially guiding statin therapy, the results of such studies may provide mechanistic insight into the critical cellular events linking statin use to muscle pathology in patients at risk.
Clinical Background
Multiple large clinical trials have demonstrated that statins (HMG-CoA reductase inhibitors) reduce the incidence of both primary and secondary coronary artery disease in patients at risk (1–4). Primary prevention trials have demonstrated that statin use can reduce the risk of a first major coronary event by more than 30 percent (3, 5). Secondary prevention trials reveal a risk reduction of similar magnitude (2). Aggressive intervention trials suggest that greater lipid lowering is associated with further reduction in risk (6).
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