AbbreviationsAFatrial fibrillationAICAR5‐aminoimidazole‐4‐carboxamide ribonucleotideCCDcentral core diseaseFDBflexor digitorum brevisHMG‐CoA3‐hydroxy‐3‐methylglutaryl CoALog Dpartition coefficientMHmalignant hyperthermiaPoopen probabilityRyRryanodine receptorSim‐Hsimvastatin hydroxy acidSim‐Lsimvastatin lactoneSRsarcoplasmic reticulumTransluminalIntroductionStatins are competitive inhibitors of 3‐hydroxy‐3‐methylglutaryl‐CoA (HMG‐CoA) reductase, the rate‐limiting enzyme in the synthesis of cholesterol. They are the most widely prescribed medication for the treatment of hypercholesterolaemia and prevention of cardiovascular disease. Furthermore, statin use is increasing with recent reductions in the cardiovascular risk threshold for statin prescription (NICE, ). The efficacy of statin drugs has been demonstrated in many large clinical trials (Collins et al., ), and while their success has been unrivalled, they are also associated with causing a variety of muscle‐related complaints (Bruckert et al., ; Buettner et al., ; Stroes et al., ). Patients prescribed statin treatment often report muscle pain and weakness, and in serious cases, fatal rhabdomyolysis can occur (Hodel, ). Observational studies have suggested that between 10 and 15% of patients undergoing statin therapy experience these side effects, and this has restricted their use in certain contexts. As a result many patients have so far been unable to benefit from statins protection against cardiovascular disease, as well as their pleiotropic cardioprotective effects (Thompson et al., ).All statins are reported to cause muscle‐related side effects; however,
British Journal of Pharmacology – Wiley
Published: Jan 1, 2018
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