Coenzyme Q as a Marker of Oxidative Stress in Coronary Artery Disease

Coenzyme Q ◽  
2000 ◽  
pp. 287-292
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Coenzyme Q ◽  
Artery Disease

scholarly journals 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

2017 ◽  
Vol 02 (01) ◽  
pp. 006-013
Author(s):  
Malleswara Dangeti ◽  
Siva Katkam ◽  
Raghu Galla ◽  
Ravi Kiran ◽  
Indrani Garre
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Statin Therapy ◽  
Coenzyme Q10 ◽  
Coenzyme Q ◽  
High Dose ◽  
Plasma Glutathione ◽  
Artery Disease ◽  
Plasma Malondialdehyde

AbstractBackground: 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.

Oxidative stress as a predictor of cardiovascular events in coronary artery disease patients

2012 ◽  
Vol 50 (8) ◽  
Author(s):  
Cristina Vassalle ◽  
Sara Bianchi ◽  
Fabrizio Bianchi ◽  
Patrizia Landi ◽  
Debora Battaglia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Cardiovascular Events ◽  
Artery Disease

Altered DNA repair, oxidative stress and antioxidant status in coronary artery disease

2013 ◽  
Vol 38 (2) ◽  
pp. 385-389 ◽  
Author(s):  
A Supriya Simon ◽  
V Chithra ◽  
Anoop Vijayan ◽  
Roy D Dinesh ◽  
T Vijayakumar
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery Disease ◽  
Dna Repair ◽  
Coronary Artery ◽  
Antioxidant Status ◽  
Artery Disease

scholarly journals A randomized controlled trial of metformin on left ventricular hypertrophy in patients with coronary artery disease without diabetes: the MET-REMODEL trial

2019 ◽  
Vol 40 (41) ◽  
pp. 3409-3417 ◽  
Author(s):  
Mohapradeep Mohan ◽  
Shaween Al-Talabany ◽  
Angela McKinnie ◽  
Ify R Mordi ◽  
Jagdeep S S Singh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery Disease ◽  
Body Weight ◽  
Coronary Artery ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Haemoglobin A1c ◽  
Metformin Treatment ◽  
Artery Disease

Abstract Aim We tested the hypothesis that metformin may regress left ventricular hypertrophy (LVH) in patients who have coronary artery disease (CAD), with insulin resistance (IR) and/or pre-diabetes. Methods and results We randomly assigned 68 patients (mean age 65 ± 8 years) without diabetes who have CAD with IR and/or pre-diabetes to receive either metformin XL (2000 mg daily dose) or placebo for 12 months. Primary endpoint was change in left ventricular mass indexed to height1.7 (LVMI), assessed by magnetic resonance imaging. In the modified intention-to-treat analysis (n = 63), metformin treatment significantly reduced LVMI compared with placebo group (absolute mean difference −1.37 (95% confidence interval: −2.63 to −0.12, P = 0.033). Metformin also significantly reduced other secondary study endpoints such as: LVM (P = 0.032), body weight (P = 0.001), subcutaneous adipose tissue (P = 0.024), office systolic blood pressure (BP, P = 0.022) and concentration of thiobarbituric acid reactive substances, a biomarker for oxidative stress (P = 0.04). The glycated haemoglobin A1C concentration and fasting IR index did not differ between study groups at the end of the study. Conclusion Metformin treatment significantly reduced LVMI, LVM, office systolic BP, body weight, and oxidative stress. Although LVH is a good surrogate marker of cardiovascular (CV) outcome, conclusive evidence for the cardio-protective role of metformin is required from large CV outcomes trials.

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