A Study of Effects of Addition of Coenzyme Q 10 to High Dose Statins in Patients of Coronary Artery Disease with Special Reference to Oxidative Balance
This article was originally published by Thieme Medical and Scientific Publishers Private Ltd. and was migrated to Scientific Scholar after the change of Publisher.
Background: Oxidative stress is one of the most potent inductors of endothelial dysfunction and is involved at all stages of atherosclerotic plaque evolution. Statins are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors and are potent inhibitors of cholesterol biosynthesis. In clinical trials, statins are beneficial in the primary and secondary prevention of coronary heart disease. Statins also possess direct free radical scavenging activity. However, the prooxidant effect of statins has also been reported as statins block the mevalonate pathway and the synthesis coenzyme Q10. This Additional Coenzyme Q10 depletion by statins in patients with coronary artery disease (CAD) may be a critical issue as it may reduce absolute benefits of statins.
Objectives: The purpose of this study was to investigate the effects of high dose statins on plasma Malondialdehyde (MDA) levels and plasma glutathione levels in CAD patients who underwent recent PCI and to study whether addition of coenzyme Q10 (100 mg/d) has any additional effect on plasma Malondialdehyde (MDA) levels and plasma glutathione levels in patients already receiving high dose statin therapy.
Methods: Twenty-one consecutive patients who underwent percutaneous transluminal coronary angioplasty (PTCA) in Department of Cardiology at our institute were studied. The cases (n = 21) were given high dose statins for first 1 week and then coenzyme Q10 (100 md /day) is added for next 1 week. Plasma Malondialdehyde(MDA) levels and plasma glutathione levels were analyzed at the time of admission before giving statins and at the end of 1 week of statin therapy and again after 1 week of Co-Q therapy.
Results: Our results indicate that a relation exists between high plasma Malondialdehyde (MDA) levels and low plasma glutathione levels with coronary artery disease. High dose statins decrease MDA levels and increase plasma glutathione levels, even though they decrease coenzyme q levels in the body. It was also shown that addition of Coenzyme Q10 at 100 mg/d enhances plasma glutathione levels and decreases plasma MDA level still further in patients who have CAD, already receiving high dose statin therapy.
Conclusions: Addition of Coenzyme Q10 at 100 mg/d has an additive effect with high dose statins in decreasing oxidative stress. Particularly in light of the excellent tolerance and affordability of this natural physiological compound, supplemental Coenzyme Q10 may emerge as an attractive option in future, and merits evaluation in additional large studies.