Primary Evaluation and Management of Statin Therapy Complications

Dean A. Seehusen, MD, MPH, FAAFP; Chad A. Asplund, MD; Dawn R. Johnson, DO; Kevin Horde, A. DO

Disclosures

South Med J. 2006;99(3):250-254. 

In This Article

The Role of Coenzyme Q10

While the cause of statin-associated myopathy is controversial, a central role for coenzyme Q10 (CoQ10 or ubiquinone) is slowly gaining acceptance. Statins have been shown to create an acquired CoQ10 deficiency.[20,21] This enzyme is essential to mitochondrial ATP generation and antioxidant function in lipid and mitochondrial membranes.[2,20] This acquired deficiency may lead to myopathy by inhibiting the biosynthesis of cholesterol.[22,23] Statin-induced CoQ10 deficiency is more prevalent in patients with a pre-existing deficiency such as the elderly,[24,25] as CoQ10 decreases with age, congestive heart failure,[25] or those with unmasked mitochondrial defects.[2]

CoQ10 deficiency can be corrected with exogenous supplementation, as dietary sources are insufficient.[25] Prophylactic therapy may be considered with CoQ10 (60 mg/d to 120 mg/d)[2,20,25] at the initiation of statin therapy. For treatment of statin-associated myalgias, temporarily discontinue the drug and institute a CoQ10 trial before statin reintroduction. If the symptoms are due to CoQ10 deficiency, repletion may improve symptoms in as little as 3 days, or may take up to 8 weeks.[2,20,25]

CoQ10 supplementation is generally well tolerated. Although CoQ10 may cause gastrointestinal side effects in less than 1% of patients, no significant adverse effects have been reported in clinical studies. Case reports have documented interference with warfarin anticoagulation and CoQ10 may enhance the blood pressure-lowering effects of antihypertensive medication.[26]

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