Coenzyme Q10 and statins:: Biochemical and clinical implications

Statins are drugs of known and undisputed efficacy in the treatment of hypercholesterolemia, usually well tolerated by most patients. In some cases treatment with statins produces skeletal muscle complaints, and/or mild serum CK elevation; the incidence of rhabdomyolysis is very low. As a result of the common biosynthetic pathway Coenzyme Q (ubiquinone) and dolichol levels are also affected, to a certain degree, by the treatment with these HMG-CoA reductase inhibitors. Plasma levels of CoQro are lowered in the course of statin treatment. This could be related to the fact that statins lower plasma LDL levels, and CoQ(10) is mainly transported by LDL, but a decrease is also found in platelets and in lymphocytes of statin treated patients, therefore it could truly depend on inhibition of CoQro synthesis. There are also some indications that statin treatment affects muscle ubiquinone levels, although it is not yet clear to which extent this depends on some effect on mitochondrial biogenesis. Some papers indicate that CoQ(10) depletion during statin therapy might be associated with subclinical cardiomyopathy and this situation is reversed upon CoQro treatment. We can reasonably hypothesize that in some conditions where other CoQ(10) depleting situations exist treatment with statins may seriously impair plasma and possible tissue levels of coenzyme Q(10). While waiting for a large scale clinical trial where patients treated with statins are also monitored for their CoQ(10) status, with a group also being given CoQro, physicians should be aware of this drug-nutrient interaction and be vigilant to the possibility that statin drugs may, in some cases, impair skeletal muscle and myocardial bioenergetics. (c) 2007 Elsevier B.V. and Mitochondria Research Society. All rights reserved.