TY - JOUR
T1 - Atorvastatin decreases the coenzyme Q10 level in the blood of patients at risk for cardiovascular disease and stroke
AU - Rundek, Tatjana
AU - Naini, Ali
AU - Sacco, Ralph
AU - Coates, Kristen
AU - DiMauro, Salvatore
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2004/6
Y1 - 2004/6
N2 - 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 Q 10 (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.
AB - 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 Q 10 (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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U2 - 10.1001/archneur.61.6.889
DO - 10.1001/archneur.61.6.889
M3 - Article
C2 - 15210526
AN - SCOPUS:2942587374
VL - 61
SP - 889
EP - 892
JO - Archives of Neurology
JF - Archives of Neurology
SN - 0003-9942
IS - 6
ER -