Author + information
- Malleswara Rao Dangeti1,
- Maddury Jyotsna1,
- Vijay Kumar Kultala1,
- Indrani Garre1 and
- Janaswamy Vibhav Sri Narayana2
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 pro-oxidant effect of statins has also been reported as statins block the mevalonate pathway and the synthesis coenzyme Q 10. This Additional Coenzyme Q 10 depletion by statins in patients with coronary artery disease (CAD) may be a critical issue as it may reduce absolute benefits of statins. The purpose of this study was to investigate the effects of high dose statins on plasma malonaldehyde (MDA) levels and plasma glutathione levels in CAD patients who underwent recent PCI and to study whether addition of coenzyme Q 10 (100 mg/d) has any additional effect on plasma malonaldehyde (MDA) levels and plasma glutathione levels in patients already receiving high-dose statin therapy.
Twenty-one consecutive patients who underwent percutaneous transluminal coronary angioplasty (PTCA) in Department of Cardiology at Nizam's Institute of Medical Sciences were studied. The cases (n=21) were given high-dose statins for first 1 week and then coenzyme Q 10 (100 mg/day) is added for next 1 week along with high dose statins. Plasma malonaldehyde (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.
The mean age of these 21 patients were 57.5 ± 8.5 years. hypertension, diabetes and smoking were present in 76.2%, 52.4%, and 52.4% respectively. 42.9% of patients presented with stable angina, 33.3% with unstable angina and 23.8% with MI. The majority (80.95%) are in NYHA functional class 1 or 2.
Our results indicate that a relation exists between high plasma malonaldehyde (MDA) (3.2 ± 0.6 nmoles/ml) levels and low plasma glutathione levels (290 ± 41 μM/L) with coronary artery disease. High-dose statins decrease MDA levels (2.6 ± 0.7 nmoles/ml, p=0.001) and increase plasma glutathione levels (346.7 ± 62.4 μM/L, p=0.008), even though they decrease coenzyme q levels in the body. It was also shown that addition of Coenzyme Q 10 at 100 mg/d enhances plasma glutathione levels (376.4 ± 110.2 μM/L, p=0.0001) and decreases plasma MDA (1.99 ± 0.4 nmoles/ml, p=0.2) level still further in patients who have CAD, already receiving high-dose statin therapy.
The addition of Coenzyme Q 10 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 Q 10 may emerge as an attractive option in future, and merits evaluation in additional large studies.