Author/Authors :
Barry E. Bleske، نويسنده , , Richard A. Willis، نويسنده , , Mark Anthony ، نويسنده , , Nicole Casselberry، نويسنده , , Meeta Datwani، نويسنده , , Virginia E. Uhley، نويسنده , , Stephanie G. Secontine، نويسنده , , Michael J. Shea، نويسنده ,
Abstract :
Background Coenzyme Q10 (CoQ10) is an antioxidant and plays an important role in the synthesis of adenosine triphosphate. Studies suggest that 3-hydroxy-3-methylglutaryl–coenzyme A (HMG-CoA) reductase inhibitors reduce CoQ10 levels; however, no studies have directly compared HMG-CoA reductase inhibitors in a randomized crossover fashion. Methods Twelve healthy volunteers received either 20 mg pravastatin (P) or 10 mg atorvastatin (A) for 4 weeks in a randomized crossover fashion. There was a 4- to 8-week washout period between the 2 phases. CoQ10 levels and a lipid profile were obtained. Results There was no difference in CoQ10 levels from baseline to post–drug therapy for either P or A (0.61 ± 0.14 vs 0.62 ± 0.2 μg/mL and 0.65 ± 0.22 vs 0.6 ± 0.12 μg/mL, respectively; P > .05). There was a significant difference in low-density lipoprotein (LDL) levels from baseline to post–drug therapy for both P and A (97 ± 21 vs 66 ± 19 mg/dL and 102 ± 21 vs 52 ± 14 mg/dL, respectively; P < .01). There was no significant correlation between LDL and CoQ10. Conclusions P and A did not decrease CoQ10 despite a significant decrease in LDL levels. These findings suggest that HMG-CoA reductase inhibitors do not significantly decrease the synthesis of circulating CoQ10 in healthy subjects. Routine supplementation of CoQ10 may not be necessary when HMG-CoA reductase inhibitor therapy is administered. (Am Heart J 2001;142:e2.)