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Randomized Controlled Trial
. 2013 Jan 1;127(1):96-103.
doi: 10.1161/CIRCULATIONAHA.112.136101. Epub 2012 Nov 26.

Effect of statins on skeletal muscle function

Affiliations
Randomized Controlled Trial

Effect of statins on skeletal muscle function

Beth A Parker et al. Circulation. .

Abstract

Background: Many clinicians believe that statins cause muscle pain, but this has not been observed in clinical trials, and the effect of statins on muscle performance has not been carefully studied.

Methods and results: The Effect of Statins on Skeletal Muscle Function and Performance (STOMP) study assessed symptoms and measured creatine kinase, exercise capacity, and muscle strength before and after atorvastatin 80 mg or placebo was administered for 6 months to 420 healthy, statin-naive subjects. No individual creatine kinase value exceeded 10 times normal, but average creatine kinase increased 20.8±141.1 U/L (P<0.0001) with atorvastatin. There were no significant changes in several measures of muscle strength or exercise capacity with atorvastatin, but more atorvastatin than placebo subjects developed myalgia (19 versus 10; P=0.05). Myalgic subjects on atorvastatin or placebo had decreased muscle strength in 5 of 14 and 4 of 14 variables, respectively (P=0.69).

Conclusions: These results indicate that high-dose atorvastatin for 6 months does not decrease average muscle strength or exercise performance in healthy, previously untreated subjects. Nevertheless, this blinded, controlled trial confirms the undocumented impression that statins increase muscle complaints. Atorvastatin also increased average creatine kinase, suggesting that statins produce mild muscle injury even among asymptomatic subjects. This increase in creatine kinase should prompt studies examining the effects of more prolonged, high-dose statin treatment on muscular performance.

Clinical trial registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00609063.

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Conflict of interest statement

Conflict of Interest Disclosures: Paul D. Thompson reports receiving research grants from the National Institutes of Health, GlaxoSmithKline, Anthera, B. Braun, Genomas, Roche, Aventis, Novartis, and Furiex; serving as a consultant for Astra Zenica, Furiex, Regeneron, Merck, Roche, Genomas, Abbott, Lupin, Runners World, Genzyme, Sanolfi, Pfizer, and GlaxoSmithKline; receiving speaker honoraria from Merck, Pfizer, Abbott, Astra Zenica, GlaxoSmithKline, and Kowa: owing stock in General Electric, JA Wiley Publishing, J&J, Sanolfi-Aventis and Abbott; and serving as a medical legal consultant on cardiac complications of exercise, statin myopathy, tobacco, ezetimibe and non-steroidals. No other authors have any financial disclosures.

Figures

Figure 1
Figure 1
Study flow diagram detailing numbers (n) of participants who were screened, randomized, completed and analyzed in the study.
Figure 2
Figure 2
Group mean ± SD of creatine kinase (CK; top) and alanine aminotransferase (ALT; bottom) before (Pre) and after (Post) 6 months of atorvastatin (ATOR) or placebo (PL) treatment with brackets indicating the p value for group-by-time interaction. *Significant difference between groups within a timepoint at p <0.05.
Figure 3
Figure 3
Group mean ± SD of changes in physical activity (average counts/day) by age group after 6 months of atorvastatin (ATOR) or placebo (PL) treatment with brackets indicating the p value for treatment-by-age interaction.

Comment in

References

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