Abstract 11708: Increased CK Levels on High Dose Atorvastatin are Related to Decreases In Muscle Strength but do not Predict Myalgia

Abstract

Introduction Recent results from the randomized, double-blind Effect of Statins on Skeletal Muscle Performance (STOMP) study indicated that subjects treated with 80 mg atorvastatin for six months exhibited an average 20 U/L increase in creatine kinase (CK) not observed with placebo (p < 0.01). The objective of this analysis was to further characterize CK changes in STOMP and the relationship between CK changes and skeletal muscle side effects and function.

Methods The STOMP study enrolled 419 healthy, statin-naïve subjects ages 20-79. Myalgia was defined as the onset of new muscle pain following statin treatment that ceased upon cessation of treatment and recurred upon drug rechallenge. CK levels and muscle strength were measured before and after treatment. Univariate analyses were used to compare CK levels between the atorvastatin and placebo groups. Repeated measures were performed to evaluate the relationship between change in CK and measurements of muscle strength.

Results More subjects on high dose atorvastatin treatment increased their CK greater than twice their baseline CK value (p= 0.020) and increased their CK > 20 U/L (p <0.001), Figure 1. The increase in CK was related to a decrease in handgrip strength (p= 0.030) and isometric knee extension (p=0.022). Greater increases in CK, however, were not observed in patients with statin-induced myalgia (p >0.05).

Conclusions Doubling of CK or an increase > 20 U/L are associated with high dose statin use, and greater increases in CK with atorvastatin are also related to decreases in muscle strength. Changes in CK do not predict the development of statin myalgia, however, confirming reports that statin-associated myalgia can occur in the absence of elevated creatine kinase.