Statin-Induced Myopathy

Abstract

Statins (3-hydroxy-3-methylglutaryl-coezyme A [HMG-CoA] reductase inhibitors) are a highly effective group of cholesterol-lowering drugs. Although generally well tolerated, they may exert a toxic effect on skeletal muscle. In considering the myotoxicity of the statins, it is helpful to make a distinction between minimally or asymptomatic elevations in serum creatine kinase (CK) concentrations on the one hand, and the presentation with myositis or rhabdomyolysis on the other. In the relevant literature, significant elevations of serum CK concentration are taken to be those that are at least 9–10 times the upper limit of normal. Asymptomatic or minimally symptomatic patients with such elevations of CK have been distinguished from those with myositis (muscle pain and/or weakness) that is accompanied by a marked (greater than 10 times the upper limit of normal) elevation of serum CK concentration. The term “rhabdomyolysis” has variably been used to describe this latter syndrome, especially when accompanied by renal failure. In some studies, the term rhabdomyolysis is reserved for those in whom the CK concentration is at least 40 times the upper limit of normal. The potential for such severe statininduced myotoxicity achieved particular prominence following the voluntary withdrawal of cerivastatin from the US market in 2001 because of the apparently high risk of rhabdomyolysis. Notwithstanding this adverse publicity, the statins remain a frequently prescribed class of dugs given their efficacy in reducing the risk of coronary heart disease.