Statins and Myalgia: Fact or Fiction?

Peter Sever

Disclosures

Br J Cardiol. 2015;22(4):127-129. 

In This Article

Introduction

Contemporary guidelines have lowered the threshold for statin use in primary prevention (7.5% risk of a cardiovascular event over 10 years in the USA,[1] 10% risk according to National Institute for Health and Care Excellence [NICE] guidelines in the UK).[2] Applying these thresholds, the majority of men over 50 years and more than half of women over 60 years will qualify for statin use. Countering the more widespread uptake of statin use in primary prevention advocated by these guidelines are claims, popularised by the lay press and uncritically published in some medical journals,[3,4] that statin use is accompanied by an unacceptable incidence of side effects that adversely compromise lifestyle and which challenge whether the small absolute benefits in some lower risk groups are worth the intolerance of the statin.

So what are the facts? Before discussing the data, it is important to distinguish between severe muscle-related events (myopathy and rhabdomyolysis) and less severe muscle aches and pains (myalgia) – the former being associated with marked elevation in creatine kinase levels, in contrast with the latter, which is not. All statins can cause myopathy, but the incidence is low – about 0.1%. This compares with an incidence of about 0.04% on placebo. Rhabdomyolysis is much rarer.[5] Preclinical studies show that statins decrease mitochondrial function, attenuate energy production and alter muscle protein degradation, thereby providing a mechanistic explanation for a potential link between statin use and muscle symptoms. Moreover, an increased frequency of rare pathogenic variants in muscle disease-associated genes has been reported to be associated with a substantial increase (up to 20-fold) in subjects with severe myopathy.[6,7] Pharmacokinetic interactions of statins with inhibitors of cytochrome P450 isoenzymes will also increase the risk of myopathy.

There is, however, no evidence that these molecular mechanisms are responsible for the more generalised aches and pains, without evidence of creatine kinase elevation, reported in clinical practice.

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