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Original Contribution
June 2004

Atorvastatin Decreases the Coenzyme Q10 Level in the Blood of Patients at Risk for Cardiovascular Disease and Stroke

Author Affiliations

From the Department of Neurology, Columbia University College of Physicians & Surgeons, New York, NY. Dr Sacco has received honoraria for lecturing and consulting from Pfizer Inc. Pfizer Inc had no involvement in data analysis or manuscript preparation.

Arch Neurol. 2004;61(6):889-892. doi:10.1001/archneur.61.6.889
Abstract

Background  Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are widely used for the treatment of hypercholesterolemia and coronary heart disease and for the prevention of stroke. There have been various adverse effects, most commonly affecting muscle and ranging from myalgia to rhabdomyolysis. These adverse effects may be due to a coenzyme Q10 (CoQ10) deficiency because inhibition of cholesterol biosynthesis also inhibits the synthesis of CoQ10.

Objective  To measure CoQ10 levels in blood from hypercholesterolemic subjects before and after exposure to atorvastatin calcium, 80 mg/d, for 14 and 30 days.

Design  Prospective blinded study of the effects of short-term exposure to atorvastatin on blood levels of CoQ10.

Setting  Stroke center at an academic tertiary care hospital.

Patients  We examined a cohort of 34 subjects eligible for statin treatment according to National Cholesterol Education Program: Adult Treatment Panel III criteria.

Results  The mean ± SD blood concentration of CoQ10 was 1.26 ± 0.47 µg/mL at baseline, and decreased to 0.62 ± 0.39 µg/mL after 30 days of atorvastatin therapy (P<.001). A significant decrease was already detectable after 14 days of treatment (P<.001).

Conclusions  Even brief exposure to atorvastatin causes a marked decrease in blood CoQ10 concentration. Widespread inhibition of CoQ10 synthesis could explain the most commonly reported adverse effects of statins, especially exercise intolerance, myalgia, and myoglobinuria.

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