ubiquinol and Coronary-Artery-Disease

The oxidation of low density lipoprotein (LDL) is now commonly regarded as an important early event in atherogenesis. As such there is considerable interest in the ability of antioxidant supplementation to attenuate LDL oxidation and hence atherosclerosis. A majority of studies on LDL antioxidation have focused on alpha-tocopherol (alpha-TOH), biologically and chemically the most active form of vitamin E and quantitatively the major lipid-soluble antioxidant in extracts prepared from human LDL. In addition to alpha-TOH, circulating LDL also contains low levels of ubiquinol-10 (CoQ10H2; the reduced form of coenzyme Q). Recent studies have shown that in intact, isolated LDL, alpha-TOH can act as either an anti- or prooxidant for the lipoprotein's lipids. This article reviews the molecular action of alpha-TOH in LDL undergoing radical-initiated oxidation, and how the presence of CoQ10H2 suppresses the pro-oxidant or complements the antioxidant activity of the vitamin. We also comment on the plasma and intimal levels of alpha-TOH and CoQ10H2 in patients suffering from coronary artery disease and discuss the potential implications of these results for atherogenesis.

Topics: Antioxidants; Arteriosclerosis; Coronary Artery Disease; Diet; Humans; Lipid Peroxidation; Lipoproteins, LDL; Models, Biological; Oxidation-Reduction; Peroxides; Ubiquinone; Vitamin E

Coenzyme Q10 levels are low in patients with coronary artery disease (CAD), and increasing or preserving coenzyme Q10 could be a beneficial strategy. Exercise and statins improve high-density lipoprotein cholesterol (HDL-C) levels. However, statins inhibit coenzyme Q10 biosynthesis, and the combination of statins with coenzyme Q10 supplementation increases HDL-C compared to statins alone. We compared the effects of two statins (rosuvastatin and atorvastatin) combined with exercise on coenzyme Q10 and HDL-C levels in CAD patients.. After randomizing 28 CAD patients to rosuvastatin (n=14) and atorvastatin (n=14) groups, patients performed weekly in-hospital aerobic exercise and daily home exercise for 20 weeks. We measured serum lipids, ubiquinol, and exercise capacity.. Both statins equally improved exercise capacity and lowered low-density lipoprotein cholesterol and triglyceride levels. Rosuvastatin significantly increased HDL-C (rosuvastatin, +12 ± 9 mg/dL [+30%], atorvastatin, +5 ± 5 mg/dL [+13%], p=0.014) and apolipoprotein A1 (ApoA1) (rosuvastatin, +28.3 ± 20.7 mg/dL, atorvastatin, +13.4 ± 12.0 mg/dL, p=0.030) compared to atorvastatin. Atorvastatin significantly decreased serum ubiquinol (731 ± 238 to 547 ± 219 nmol/L, p=0.001), but rosuvastatin (680±233 to 668 ± 299 nmol/L, p=0.834) did not. There was a significant positive correlation between changes in ubiquinol and ApoA1 (r=0.518, p=0.005). Multivariate regression analysis showed that changes in ubiquinol correlated significantly with changes in ApoA1 after adjusting for age, sex, body mass index, and smoking (β=0.502, p=0.008).. Compared to atorvastatin, rosuvastatin combined with exercise significantly preserved ubiquinol levels associated with an increase in HDL-C. Rosuvastatin with regular exercise could be beneficial for CAD patients.

Topics: Aged; Atorvastatin; Cholesterol, HDL; Coronary Artery Disease; Echocardiography; Exercise; Female; Fluorobenzenes; Heptanoic Acids; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Middle Aged; Multivariate Analysis; Pyrimidines; Pyrroles; Risk; Rosuvastatin Calcium; Smoking; Sulfonamides; Ubiquinone

Information concerning un-supplemented plasma concentrations of ubiquinol-10 in coronary artery disease patients is still controversial. The aim of this study is to determine the levels of plasma ubiquinol-10 and ratios of ubiquinol-10 to plasma lipids in consecutive patients with different angiographic findings.. Thirty-six consecutive patients who underwent coronary angiography were split in two groups with different atherosclerotic changes. These patients were un-supplemented with antioxidants and were not treated by lipid-lowering medication. We have measured a plasma level of ubiquinol-10 using high-performance liquid chromatography with coulometric detection. Conventional plasma lipids, markers of oxidative stress and other widely accepted risk factors of atherosclerosis have been determined too.. Plasma ubiquinol-10 to low-density lipoprotein cholesterol (LDL-C) ratios in patients with different angiographic findings have been found as 180+/-69 and 132+/-43, respectively (p=0.020). The ubiquinol-10/LDL-C ratio was significantly lower in angiographically positive patients. There were also significant differences in ubiquinol-10 per total cholesterol (109+/-47 and 80+/-26, respectively; p=0.031), per triglycerides (426+/-191 and 237+/-86, respectively; p=0.002) and per the sum of triglycerides and total cholesterol (86+/-35 and 61+/-20, respectively; p=0.013).. There have not been found any significant differences between levels of widely accepted risk factors for genesis and progress of atherosclerotic changes in these two groups of patients. Only the level of triglycerides and the total cholesterol minus high-density lipoprotein cholesterol/high-density lipoprotein cholesterol ratio were significantly higher in patients with stenosis. This ratio correlated with the ubiquinol-10/LDL-C ratio, which was significantly lower in patients with stenosis. Our results indicate that the ratio of ubiquinol-10/LDL-C is likely to be a risk factor for atherogenesis.

Topics: Adult; Aged; Aged, 80 and over; Antioxidants; Biomarkers; Coronary Angiography; Coronary Artery Disease; Female; Humans; Lipids; Male; Middle Aged; Risk Factors; Ubiquinone; Vitamin E