ubiquinone and Coronary-Artery-Disease

Systemic inflammation and oxidative stress significantly contribute in developing coronary artery disease (CAD). This systematic review and meta-analysis was aimed to determine the effects of coenzyme Q10 (CoQ10) supplementation on biomarkers of inflammation and oxidative stress among patients with CAD.. The electronic databases including MEDLINE, EMBASE, Scopus, Web of Science, and Cochrane Library databases were systematically searched until Oct 2018. The quality assessment and heterogeneity of the selected randomized clinical Trials (RCTs) were examined using the Cochrane Collaboration risk of bias tool, and Q and I. Overall, this meta-analysis demonstrated CoQ10 supplementation increased SOD and CAT, and decreased MDA and diene levels, but did not affect CRP, TNF-α, IL-6, and GPx levels among patients with CAD.

Topics: Animals; Biomarkers; Coronary Artery Disease; Dietary Supplements; Humans; Inflammation; Oxidative Stress; Randomized Controlled Trials as Topic; Ubiquinone

Chronic inflammation and increased oxidative stress significantly contribute in developing coronary artery disease (CAD). Hence, antioxidant supplementation might be an appropriate approach to decrease the incidence of CAD. This systematic review and meta-analysis was aimed to determine the effects of coenzyme Q10 (CoQ10) supplementation on lipid profile, as one of the major triggers for CAD, among patients diagnosed with coronary artery disease.. EMBASE, Scopus, PubMed, Cochrane Library, and Web of Science were searched for studies prior to May 20th, 2018. Cochrane Collaboration risk of bias tool was applied to assess the methodological quality of included trials. I-square and Q-tests were used to measure the existing heterogeneity across included studies. Considering heterogeneity among studies, fixed- or random-effect models were applied to pool standardized mean differences (SMD) as overall effect size.. A total of eight trials (267 participants in the intervention group and 259 in placebo group) were included in the current meta-analysis. The findings showed that taking CoQ10 by patients with CAD significantly decreased total-cholesterol (SMD -1.07; 95% CI, - 1.94, - 0.21, P = 0.01) and increased HDL-cholesterol levels (SMD 1.30; 95% CI, 0.20, 2.41, P = 0.02). We found no significant effects of CoQ10 supplementation on LDL-cholesterol (SMD -0.37; 95% CI, - 0.87, 0.13, P = 0.14), lipoprotein (a) [Lp(a)] levels (SMD -1.12; 95% CI, - 2.84, 0.61, P = 0.20) and triglycerides levels (SMD 0.01; 95% CI, - 0.22, 0.24, P = 0.94).. This meta-analysis demonstrated the promising effects of CoQ10 supplementation on lowering lipid levels among patients with CAD, though it did not affect triglycerides, LDL-cholesterol and Lp(a) levels.

Topics: Cholesterol, HDL; Cholesterol, LDL; Coronary Artery Disease; Dietary Supplements; Humans; Lipids; Lipoprotein(a); Randomized Controlled Trials as Topic; Triglycerides; Ubiquinone

A short review is given of the potential role of selenium deficiency and selenium intervention trials in atherosclerotic heart disease. Selenium is an essential constituent of several proteins, including the glutathione peroxidases and selenoprotein P. The selenium intake in Europe is generally in the lower margin of recommendations from authorities. Segments of populations in Europe may thus have a deficient intake that may be presented by a deficient anti-oxidative capacity in various illnesses, in particular atherosclerotic disease, and this may influence the prognosis of the disease. Ischemic heart disease and heart failure are two conditions where increased oxidative stress has been convincingly demonstrated. Some of the intervention studies of anti-oxidative substances that have focused on selenium are discussed in this review. The interrelationship between selenium and coenzyme Q10, another anti-oxidant, is presented, pointing to a theoretical advantage in using both substances in an intervention if there are deficiencies within the population. Clinical results from an intervention study using both selenium and coenzyme Q10 in an elderly population are discussed, where reduction in cardiovascular mortality, a better cardiac function according to echocardiography, and finally a lower concentration of the biomarker NT-proBNP as a sign of lower myocardial wall tension could be seen in those on active treatment, compared to placebo.

Topics: Animals; Antioxidants; Ataxia; Cardiovascular Diseases; Coronary Artery Disease; Deficiency Diseases; Diet; Dietary Supplements; Europe; Humans; Mitochondrial Diseases; Muscle Weakness; Nutritional Status; Oxidative Stress; Selenium; Ubiquinone

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

Im Rahmen der vorliegenden Studie sollte der Einfluss des Weichteilschadens auf das klinische Ergebnis nach offener Ellenbogenluxation untersucht werden.. Von Oktober 2008 bis August 2015 wurden insgesamt 230 Patienten mit Ellenbogenluxation behandelt. Diese retrospektive Studie umfasst 21 Fälle von offenen Ellenbogenluxationen. Das Durchschnittsalter der Patienten betrug 49 Jahre alt (20–83 Jahre), 6 Patienten waren weiblich (29%), 15 männlich (71%). Das Bewegungsausmaß des verletzten und unverletzten Ellenbogens wurde erhoben und das funktionelle Ergebnis u. a. mittels Mayo Elbow Performance Score (MEPS), Mayo Wrist Score (MWS) und dem Disability of Arm, Shoulder and Hand (DASH) Score erfasst. Zusätzlich wurden Komplikationen und Revisionsoperationen aufgezeichnet. Der Einfluss des Weichteilschadens (I°/II° offen vs. III° offen) und des Luxationstyps (einfach vs. komplex) auf das klinische Ergebnis wurde analysiert.. Offene Ellenbogenluxationen können mit einem zufriedenstellenden klinischen Ergebnis einhergehen. Insbesondere komplexe offene Ellenbogenluxationen sind jedoch sehr komplikationsbehaftet, wobei neurovaskuläre Komplikationen am häufigsten auftreten.. The current high rate of multidrug-resistant gram-negative bacteria infections among hospitalised patients with cUTIs in the studied area is alarming. Our predictive model could be useful to avoid inappropriate antibiotic treatment and implement antibiotic stewardship policies that enhance the use of carbapenem-sparing regimens in patients at low risk of multidrug-resistance.. The results indicated differential patterns of Inhibition of Return between the High and Low shape/weight based self-worth groups. The High group displayed increased inhibition of return for the shape/weight stimuli relative to control stimuli, while the Low group displayed reduced inhibition of return for the shape/weight stimuli compared to control stimuli. The ED group displayed a similar pattern of results to the High group, but this did not reach significance.. The current findings indicate that young women without an eating disorder who base their self-worth on shape/weight display a pattern of avoidance of shape/weight stimuli that is in direct contrast to those at low risk of developing eating disorders. The possible implications of these specific patterns of inhibition of return across those at varying levels of risk for an eating disorder are discussed along with their implications for intervention approaches.. These results indicated that Sr. An unusually high HbA

Topics: Activities of Daily Living; Acute Disease; Adalimumab; Adaptation, Physiological; Adenosine Triphosphate; Adipose Tissue; Administration, Intravaginal; Adolescent; Adsorption; Adult; Adverse Childhood Experiences; Age Distribution; Age Factors; Aged; Aged, 80 and over; Air Pollution, Indoor; Aldehyde Oxidase; Alginates; Alloys; alpha-Globins; Aluminum Hydroxide; Alveolar Bone Loss; Anaerobiosis; Anesthesia, General; Anesthetics; Animals; Anovulation; Anti-Bacterial Agents; Anti-Infective Agents; Anti-Inflammatory Agents, Non-Steroidal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Apoptosis; Bacillus cereus; Bacterial Typing Techniques; Bacteroidetes; Base Composition; Biocompatible Materials; Biofilms; Biological Availability; Biological Transport; Biosensing Techniques; Bipolar Disorder; Blood Glucose; Body Mass Index; Bone Regeneration; Boranes; Brachial Artery; Butyric Acid; Candida albicans; Carbon; Carcinoembryonic Antigen; Cell Differentiation; Cell Line, Tumor; 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High oxidative stress and chronic inflammation can contribute to the pathogenesis of coronary artery disease (CAD). Coenzyme Q10 is an endogenous lipid-soluble antioxidant. Statins therapy can reduce the biosynthesis of coenzyme Q10. The purpose of this study was to investigate the effects of a coenzyme Q10 supplement (300 mg/d; 150 mg/b.i.d) on antioxidation and anti-inflammation in patients who have CAD during statins therapy.. Patients who were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery and who were treated with statins for at least one month were enrolled in this study. The subjects (n = 51) were randomly assigned to the placebo (n = 24) and coenzyme Q10 groups (Q10-300 group, n = 27). The intervention was administered for 12 weeks. The concentrations of coenzyme Q10, vitamin E, antioxidant enzymes activities (superoxide dismutase, catalase, and glutathione peroxidase), and inflammatory markers [C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6)] were measured in the 42 subjects (placebo, n = 19; Q10-300, n = 23) who completed the study.. The levels of the plasma coenzyme Q10 (P < 0.001) and antioxidant enzymes activities (P < 0.05) were significantly higher after coenzyme Q10 supplementation. The levels of inflammatory markers (TNF-α, P = 0.039) were significantly lower after coenzyme Q10 supplementation. The subjects in the Q10-300 group had significantly higher vitamin E (P = 0.043) and the antioxidant enzymes activities (P < 0.05) than the placebo group at week 12. The level of plasma coenzyme Q10 was significantly positively correlated with vitamin E (P = 0.008) and antioxidant enzymes activities (P < 0.05) and was negatively correlated with TNF-α (P = 0.034) and IL-6 (P = 0.027) after coenzyme Q10 supplementation.. Coenzyme Q10 supplementation at 300 mg/d significantly enhances antioxidant enzymes activities and lowers inflammation in patients who have CAD during statins therapy.. ClinicalTrials.gov Identifier: NCT01424761.

Topics: Aged; Aged, 80 and over; C-Reactive Protein; Catalase; Coronary Artery Disease; Dietary Supplements; Dose-Response Relationship, Drug; Female; Glutathione Peroxidase; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Inflammation; Interleukin-6; Male; Middle Aged; Oxidative Stress; Single-Blind Method; Superoxide Dismutase; Tumor Necrosis Factor-alpha; Ubiquinone

The purpose of this study was to investigate the effect of coenzyme Q10 supplementation on oxidative stress and antioxidant enzyme activity in patients with coronary artery disease (CAD).. This was an intervention study. Patients who were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery or receiving percutaneous transluminal coronary angioplasty (n = 51) were randomly assigned to the placebo group (n = 14) or one of the two coenzyme Q10-supplemented groups (60 mg/d, n = 19 [Q10-60 group]; 150 mg/d, n = 18 [Q10-150 group]). Intervention was administered for 12 wk. Patients' blood samples were analyzed every 4 wk for plasma coenzyme Q10 concentrations, malondialdehyde (MDA), and antioxidant enzyme (catalase [CAT], superoxide dismutase [SOD], glutathione peroxidase) activity.. Forty-three subjects with CAD completed intervention study. Plasma coenzyme Q10 concentration increased significantly after coenzyme the Q10-150 intervention (P < 0.01). The MDA levels were significantly lower than baseline in the Q10-150 group at week 4 (P = 0.03). The Q10-150 group had significantly lower MDA levels than the placebo group at week 8 (P = 0.03). With respect to antioxidant enzyme activity, subjects in the Q10-150 group had significantly higher CAT (P = 0.03) and SOD (P = 0.03) activity than the placebo group at week 12. The plasma coenzyme Q10 concentration was significantly correlated with MDA levels (r = -0.35, P = 0.02) and CAT (r = 0.43, P = 0.01) and SOD activity (r = 0.39, P = 0.01). The ratio of plasma coenzyme Q10 to total cholesterol was significantly correlated with SOD activity (r = 0.39, P = 0.02). The ratio of plasma coenzyme Q10 to low-density lipoprotein was significantly correlated with CAT (r = 0.35, P = 0.04) and SOD (r = 0.45, P = 0.01) activity. However, there was no relation between coenzyme Q10 concentration and glutathione peroxidase activity.. Coenzyme Q10 supplements at a dose of 150 mg can decrease oxidative stress and increase antioxidant enzyme activity in patients with CAD. A higher dose of coenzyme Q10 supplements (>150 mg/d) might promote rapid and sustainable antioxidation in patients with CAD.

Topics: Aged; Aged, 80 and over; Angioplasty, Balloon, Coronary; Antioxidants; Catalase; Coronary Artery Disease; Dietary Supplements; Female; Glutathione Peroxidase; Humans; Male; Malondialdehyde; Oxidative Stress; Postmenopause; Superoxide Dismutase; Ubiquinone

The purpose of this study was to investigate the effects of coenzyme Q10 supplementation on inflammatory markers (high-sensitivity C-reactive protein [hs-CRP], interleukin-6 [IL-6], and homocysteine) in patients with coronary artery disease (CAD).. Patients with CAD (n = 51) were randomly assigned to a placebo group (n = 14) or one of two coenzyme Q10-supplemented groups (60 mg/d, Q10-60 group, n = 19; 150 mg/d, Q10-150 group, n = 18). The intervention was administered for 12 wk. Plasma coenzyme Q10 concentration, inflammatory markers (hs-CRP, IL-6, and homocysteine), malondialdehyde, and superoxide dismutase activities were measured.. Forty subjects with CAD completed the intervention study. The plasma coenzyme Q10 concentration increased significantly in the Q10-60 and Q10-150 groups (P < 0.01). After 12 wk of intervention, the inflammatory marker IL-6 (P = 0.03) was decreased significantly in the Q10-150 group. Subjects in the Q10-150 group had significantly lower malondialdehyde levels and those in the Q10-60 (P = 0.05) and Q10-150 (P = 0.06) groups had greater superoxide dismutase activities. Plasma coenzyme Q10 was inversely correlated with hs-CRP (r = -0.20, P = 0.07) and IL-6 (r = -0.25, P = 0.03) at baseline. After supplementation, plasma coenzyme Q10 was significantly correlated with malondialdehyde (r = -0.35, P < 0.01) and superoxide dismutase activities (r = 0.52, P < 0.01). However, there was no correlation between coenzyme Q10 and homocysteine.. Coenzyme Q10 supplementation at a dosage of 150 mg appears to decrease the inflammatory marker IL-6 in patients with CAD.

Topics: Aged; Aged, 80 and over; Anti-Inflammatory Agents, Non-Steroidal; C-Reactive Protein; Coronary Artery Disease; Dietary Supplements; Female; Homocysteine; Humans; Inflammation Mediators; Interleukin-6; Male; Malondialdehyde; Patient Dropouts; Superoxide Dismutase; Ubiquinone

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

The hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) are effective cholesterol lowering medications, however, statins may interfere with CoQ(10) biosynthesis. We examined the effect of statin therapy as well as nutritional supplements on plasma, cardiac and skeletal muscle concentrations of CoQ(10).. Forty patients with left ventricular dysfunction had fasting blood samples collected at baseline and following four weeks of supplementation (150mg/day of CoQ(10)). Cardiac and skeletal muscle biopsies were collected at the time of surgery and frozen in liquid nitrogen until analyzed for CoQ(10) levels by high performance liquid chromatography.. Nutrient supplementation significantly increased plasma [(1.8 (1.2, 2.7) vs 0.8 (0.6, 0.94) mug/ml plasma, median+IQR; p=0.001)] and cardiac tissue concentrations of CoQ(10) [(120.5 (76.5, 177.1) vs 87.3 (60.5, 110.8) nmol/g wet weight, p=0.04)]. No effect of supplementation was seen on samples of skeletal muscle from the chest wall. Statin therapy was not found to influence plasma, cardiac or chest wall levels of CoQ(10).. Nutrient supplementation significantly increased plasma and cardiac tissue levels of CoQ(10) but did not influence chest wall muscle concentrations. Statin therapy did not significantly influence tissue concentrations of CoQ(10). Longer term studies are needed to confirm this observation.

Topics: Aged; Coenzymes; Coronary Artery Bypass; Coronary Artery Disease; Dietary Supplements; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Middle Aged; Muscle, Skeletal; Myocardium; Preoperative Care; Treatment Outcome; Ubiquinone; Up-Regulation

There is conflicting clinical evidence whether administration of coenzyme Q10 (CoQ10) improves function following coronary artery bypass graft surgery (CABG). Using a swine model of hibernating myocardium, we tested whether daily CoQ10 would improve contractile function by MRI at 4-week post-CABG. Twelve pigs underwent a thoracotomy and had a constrictor placed on the left anterior descending (LAD). At 12 weeks, they underwent off-pump bypass and received daily dietary supplements of either CoQ10 (10 mg/kg/day) or placebo. At 4-week post-CABG, circumferential strain measurements in the hibernating LAD region from placebo and CoQ10 groups were not different and increased to a similar extent with dobutamine (-14.7 ± 0.6 versus -14.8 ± 0.1, respectively (NS)). Post-sacrifice, oxidant stress markers were obtained in the mitochondrial isolates and protein carbonyl in the placebo, and CoQ10 groups were 6.14 ± 0.36 and 5.05 ± 0.32 nmol/mg, respectively (NS). In summary, CoQ10 did not improve contractile reserve or reduce oxidant stress at 4-week post-CABG.

Topics: Animals; Biomarkers; Biomechanical Phenomena; Cardiotonic Agents; Coronary Artery Bypass, Off-Pump; Coronary Artery Disease; Disease Models, Animal; Female; Magnetic Resonance Imaging; Mitochondria, Heart; Myocardial Contraction; Myocardial Stunning; Myocardium; Oxidative Stress; Protein Carbonylation; Recovery of Function; Stress, Mechanical; Sus scrofa; Time Factors; Ubiquinone

A meta-analysis of younger patients included in randomized trials found good evidence that statins reduce vascular events and mortality in people with high cholesterol and the risk of coronary heart disease. The use pf statin in the elderly prevents the disease but can exert considerable side effects.

Topics: Age Factors; Aged; Cause of Death; Cholesterol; Coronary Artery Disease; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; ras Proteins; Reference Values; Risk Factors; Ubiquinone

A higher oxidative stress may contribute to the pathogenesis of coronary artery disease (CAD). The purpose of this study was to investigate the relationship between coenzyme Q10 concentration and lipid peroxidation, antioxidant enzymes activities and the risk of CAD. Patients who were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery were assigned to the case group (n = 51). The control group (n = 102) comprised healthy individuals with normal blood biochemical values. The plasma coenzyme Q10, malondialdehyde (MDA) and antioxidant enzymes activities (catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx)) were measured. Subjects with CAD had significant lower plasma coenzyme Q10, CAT and GPx activities and higher MDA and SOD levels compared to those of the control group. The plasma coenzyme Q10 was positively correlated with CAT and GPx activities and negatively correlated with MDA and SOD. However, the correlations were not significant after adjusting for the potential confounders of CAD with the exception of SOD. A higher level of plasma coenzyme Q10 (≥ 0.52 μmol/L) was significantly associated with reducing the risk of CAD. Our results support the potential cardioprotective impact of coenzyme Q10.

Topics: Adult; Aged; Antioxidants; Catalase; Constriction, Pathologic; Coronary Artery Disease; Female; Glutathione Peroxidase; Humans; Lipid Peroxidation; Male; Malondialdehyde; Middle Aged; Oxidative Stress; Risk; Superoxide Dismutase; Ubiquinone

The correlation of coronary artery disease (CAD) with pro-oxidant/antioxidant balance and oxidative DNA damage was investigated. Seventy-seven patients with CAD and 44 healthy individuals as control were included in this study. The comparative ratios of ubiquinol-10/ubiquinone-10, 8-hydroxy-2(')-deoxyguanosine/deoxyguanosine and the level of MDA measured by HPLC and the activities of GPX and SOD by colorimetric approach in blood samples obtained from patients with CAD were unraveled.8-OHdG/dG ratios, serum MDA level and GPX activity were found significantly elevated level in serum of CAD patients compared to control group. The SOD activity was observed in stable levels in CAD patients. Ubiquinol-10/ubiquinone-10 ratio was significantly lower in patients with CAD than the controls. The positive correlation was observed between 8-OHdG/dG ratios in both MDA levels and GPX activity, while the significant negative correlation was seemed between the ratio of 8-OHdG/dG and ubiquinol-10/ubiquinone-10 as well as MDA levels and ubiquinol-10/ubiquinone-10 ratio. We conclude that, both the disruption of pro-oxidant/antioxidant balance and oxidative stress in DNA may play an important role in the pathogenesis of coronary artery disease.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Case-Control Studies; Chromatography, High Pressure Liquid; Coronary Artery Disease; Deoxyguanosine; DNA Damage; Female; Glutathione Peroxidase; Humans; Male; Middle Aged; Oxidative Stress; Superoxide Dismutase; Ubiquinone

Coronary artery disease (CAD) is the leading cause of death worldwide. The purpose of this study was to investigate the relationship between plasma levels of coenzyme Q10 and vitamin B-6 and the risk of CAD. Patients with at least 50% stenosis of one major coronary artery identified by cardiac catheterization were assigned to the case group (n = 45). The control group (n = 89) comprised healthy individuals with normal blood biochemistry. The plasma concentrations of coenzyme Q10 and vitamin B-6 (pyridoxal 5'-phosphate) and the lipid profiles of the participants were measured. Subjects with CAD had significantly lower plasma levels of coenzyme Q10 and vitamin B-6 compared to the control group. The plasma coenzyme Q10 concentration (β = 1.06, P = .02) and the ratio of coenzyme Q10 to total cholesterol (β = .28, P = .01) were positively correlated with vitamin B-6 status. Subjects with higher coenzyme Q10 concentration (≥516.0 nmol/L) had a significantly lower risk of CAD, even after adjusting for the risk factors for CAD. Subjects with higher pyridoxal 5'-phosphate concentration (≥59.7 nmol/L) also had a significantly lower risk of CAD, but the relationship lost its statistical significance after adjusting for the risk factors of CAD. There was a significant correlation between the plasma levels of coenzyme Q10 and vitamin B-6 and a reduced risk of CAD. Further study is needed to examine the benefits of administering coenzyme Q10 in combination with vitamin B-6 to CAD patients, especially those with low coenzyme Q10 level.

Topics: Adult; Aged; Aged, 80 and over; Case-Control Studies; Cholesterol; Constriction, Pathologic; Coronary Artery Disease; Coronary Vessels; Female; Humans; Male; Middle Aged; Nutritional Status; Pyridoxal Phosphate; Reference Values; Ubiquinone; Vitamins

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a medical illness characterized by disorders in inflammatory and oxidative and nitrosative (IO&NS) pathways.. This paper examines the role of Coenzyme Q10 (CoQ10), a mitochondrial nutrient which acts as an essential cofactor for the production of ATP in mitochondria and which displays significant antioxidant activities. Plasma CoQ10 has been assayed in 58 patients with ME/CFS and in 22 normal controls; the relationships between CoQ10 and the severity of ME/CFS as measured by means of the FibroFatigue (FF) scale were measured.. Plasma CoQ10 was significantly (p=0.00001) lower in ME/CFS patients than in normal controls. Up to 44.8% of patients with ME/CFS had values beneath the lowest plasma CoQ10 value detected in the normal controls, i.e. 490 microg/L. In ME/CFS, there were significant and inverse relationships between CoQ10 and the total score on the FF scale, fatigue and autonomic symptoms. Patients with very low CoQ10 (<390 microg/L) suffered significantly more from concentration and memory disturbances.. The results show that lowered levels of CoQ10 play a role in the pathophysiology of ME/CFS and that symptoms, such as fatigue, and autonomic and neurocognitive symptoms may be caused by CoQ10 depletion. Our results suggest that patients with ME/CFS would benefit from CoQ10 supplementation in order to normalize the low CoQ10 syndrome and the IO&NS disorders. The findings that lower CoQ10 is an independent predictor of chronic heart failure (CHF) and mortality due to CHF may explain previous reports that the mean age of ME/CFS patients dying from CHF is 25 years younger than the age of those dying from CHF in the general population. Since statins significantly decrease plasma CoQ10, ME/CFS should be regarded as a relative contraindication for treatment with statins without CoQ10 supplementation.

Topics: Adult; Autonomic Nervous System; Cognition Disorders; Coronary Artery Disease; Fatigue Syndrome, Chronic; Female; Heart Failure; Humans; Male; Middle Aged; Oxidative Stress; Risk Factors; Ubiquinone; Vasculitis

Inhibition of squalene synthesis could transform unstable, macrophage/lipid-rich coronary plaques into stable, fibromuscular plaques. We have here treated WHHLMI rabbits, a model for coronary atherosclerosis and myocardial infarction, with a novel squalene synthase inhibitor, lapaquistat acetate (TAK-475).. Young male WHHLMI rabbits were fed a diet supplemented with lapaquistat acetate (100 or 200 mg per kg body weight per day) for 32 weeks. Serum lipid levels were monitored every 4 weeks. After the treatment, lipoprotein lipid and coenzyme Q10 levels were assayed, and coronary atherosclerosis and xanthomas were examined histopathologically or immunohistochemically. From histopathological and immunohistochemical sections, the composition of the plaque was analysed quantitatively with computer-assisted image analysis. Xanthoma was evaluated grossly.. Lapaquistat acetate decreased plasma cholesterol and triglyceride levels, by lowering lipoproteins containing apoB100. Development of atherosclerosis and xanthomatosis was suppressed. Accumulation of oxidized lipoproteins, macrophages and extracellular lipid was decreased in coronary plaques of treated animals. Treatment with lapaquistat acetate increased collagen concentration and transformed coronary plaques into fibromuscular plaques. Lapaquistat acetate also suppressed the expression of matrix metalloproteinase-1 and plasminogen activator inhibitor-1 in the plaque and increased peripheral coenzyme Q10 levels. Increased coenzyme Q10 levels and decreased very low-density lipoprotein cholesterol levels were correlated with improvement of coronary plaque composition.. Inhibition of squalene synthase by lapaquistat acetate delayed progression of coronary atherosclerosis and changed coronary atheromatous plaques from unstable, macrophage/lipid accumulation-rich, lesions to stable fibromuscular lesions.

Topics: Animals; Apolipoprotein B-100; Cholesterol; Collagen; Coronary Artery Disease; Disease Models, Animal; Disease Progression; Dose-Response Relationship, Drug; Enzyme Inhibitors; Farnesyl-Diphosphate Farnesyltransferase; Hypercholesterolemia; Hypolipidemic Agents; Image Interpretation, Computer-Assisted; Immunohistochemistry; Lipid Metabolism; Lipoproteins, LDL; Macrophages; Male; Matrix Metalloproteinase 1; Oxazepines; Piperidines; Plasminogen Activator Inhibitor 1; Rabbits; Triglycerides; Ubiquinone; Xanthomatosis

The beneficial effects of statins in patients with coronary artery disease (CAD) may be balanced by concerns that statins can depress production of ubiquinone (CoQ10), which serves as a component of mitochondrial energy production and an antioxidant. Accordingly, the effects of atorvastatin (ATO)-induced changes in plasma CoQ10 on BNP and oxidative stress were investigated. In 29 patients with CAD, the plasma levels of CoQ10 and BNP and urinary excretion of 8-iso-prostaglandin F2alpha (8-iso-PGF) were determined before and after 3-month treatment with ATO. Ten patients had received pravastatin and 10 patients fluvastatin, while 9 patients had not received any statin before ATO. There was a linear correlation between ATO-induced changes in total cholesterol and CoQ10 (r = 0.632, P < 0.01), and an inverse correlation between ATO-induced changes in CoQ10 and BNP (r = -0.497, P < 0.01). There was no significant correlation between ATO-induced changes in CoQ10 and 8-iso-PGF. Multivariate analysis revealed that ATO-induced decreases in plasma CoQ10 were significantly associated with increasing BNP levels. In conclusion, long-term treatment with ATO might increase plasma levels of BNP in patients with CAD when it is accompanied by a greater reduction in plasma CoQ10. However, ATO-induced decreases in CoQ10 might not increase oxidative stress.

Topics: Aged; Atorvastatin; Chromatography, High Pressure Liquid; Coronary Artery Disease; Dose-Response Relationship, Drug; Follow-Up Studies; Heptanoic Acids; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Immunoassay; Natriuretic Peptide, Brain; Oxidative Stress; Pyrroles; Treatment Outcome; 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

In order to assess efficacy of one of natural antioxidants--coenzyme Q10 (90 mg daily) and its combination with simvastatin (10 mg daily) 44 outpatients with coronary atherosclerosis were examined. Twenty four patients had undergone coronary artery bypass surgery, 12--coronary angioplasty and in 8 coronary heart disease was confirmed by angiography. Duration of treatment was 12 weeks. Positive effects of coenzyme Q10 was particularly expressed in relation to antiatherogenic fraction of cholesterol which increased by 23%. Index of atherogenicity decreased by 27%. At the background of coenzyme Q10 treatment 30% reduction in plasma lipoperoxide levels occurred demonstrating potentially independent role of coenzyme Q10 in positive modification of oxidative stress. Coenzyme Q10 revealed antiaggregatory ability. It was not related to the improvement of endothelial function. Normalization of plasma nitric oxide concentrations was achieved only with combination of coenzyme Q10 and simvastatin. This fact may be explained by positive action of statins on endothelial function.

Topics: Adult; Aged; Antioxidants; Coenzymes; Coronary Angiography; Coronary Artery Disease; Cytoprotection; Drug Therapy, Combination; Female; Follow-Up Studies; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Lipid Peroxides; Male; Middle Aged; Nitric Oxide; Oxidative Stress; Simvastatin; Treatment Outcome; Ubiquinone

The goal of the present research was to assess the efficacy of combination treatment with antioxidant coenzyme Q10 and simvastatin as well as coenzyme Q10 without statin therapy in order to prevent coronary atherosclerosis. 42 outpatients were divided into 2 groups: receiving coenzyme Q10 (Hasco-Lek, Poland) 60mg daily and its combination with simvastatin (zocor, vasilip) 10mg daily for an 8-week period. The treatment with coenzyme Q10 demonstrated its potential independent role in positive modification of oxidative stress, antiatherogenic fraction of lipid profile, atherogenic ratio, platelet aggregability. Taking into consideration the obtained results the study supports the use of coenzyme Q10 in combination with statins. Suggested attractive approach may result in complete correction of dislipidemia, reverse of endothelial dysfunction, reduce degree of oxidative stress and platelet aggregability. Consequently such a combination may be beneficial in preventing of further development of atherosclerosis in native coronary arteries as well as in bypass grafts in all coronary heart disease patients with or without myocardial revascularization.

Topics: Antioxidants; Coenzymes; Coronary Artery Bypass; Coronary Artery Disease; Coronary Disease; Data Interpretation, Statistical; Drug Therapy, Combination; Female; Humans; Hypolipidemic Agents; Lipids; Male; Middle Aged; Nitric Oxide; Oxidative Stress; Platelet Aggregation; Simvastatin; Time Factors; Treatment Outcome; Triglycerides; Ubiquinone

Ubiquinone-10 (CoQ10: the oxidized form of Coenyzme Q) is recognized as an antioxidant in the mitochondrial membrane and considered an anti-risk factor for coronary artery disease (CAD). The aim of this report is to determine the levels of plasma CoQ10 and the ratios of CoQ10 to plasma lipids in CAD patients and to compare them to a matched control group.. Sixty-four consecutive patients with CAD were studied and compared to 34 clinically healthy individuals. In addition to conventional lipid and lipoprotein analyses, plasma CoQ10 concentrations were measured by electrochemical high pressure liquid chromatography (EC-HPLC) after extraction of plasma with hexane-ethanol.. Plasma CoQ10 concentrations in patients with CAD and controls were found as 0.77 and 0.41 micromol/l, respectively (P < 0.01). Also, the ratio of CoQ10 to low density lipoprotein (LDL) was found significantly lower in patients with CAD when compared to controls (P < 0.01).. Our results indicate that a relation exists between low plasma CoQ10 concentration and coronary artery disease, yet this correlation is not strong enough to indicate a causal relationship.

Topics: Adult; Cholesterol; Chromatography, High Pressure Liquid; Coenzymes; Coronary Artery Disease; Edetic Acid; Humans; Lipid Metabolism; Lipids; Membrane Potentials; Middle Aged; Mitochondria; Risk Factors; Ubiquinone

Coenzyme Q10 (CoQ10) is an important mitochondrial electron transfer component and has been postulated to function as a powerful antioxidant protecting LDL from oxidative damage. It could thus reduce the risk of cardiovascular disease. Thus far, beneficial effects of supplementation with CoQ10 have been reported. To study the relation between unsupplemented concentrations of plasma CoQ10 and coronary atherosclerosis, we performed a case-control study among 71 male cases with angiographically documented severe coronary atherosclerosis and 69 healthy male controls free from symptomatic cardiovascular disease and without atherosclerotic plaques in the carotid artery. Plasma CoQ10 concentrations (mean +/- SE) were 0.86+/-0.04 vs. 0.83+/-0.04 micromol/l for cases and controls, respectively. The CoQ10/LDL-cholesterol ratio (micromol/ mmol) was slightly lower in cases than in controls (0.22+/-0.01 vs. 0.26+/-0.03). Differences in CoQ10 concentrations and CoQ10/LDL-cholesterol ratio did not reach significance. The odds ratios (95% confidence interval) for the risk of coronary atherosclerosis calculated per micromol/l increase of CoQ10 was 1.12 (0.28-4.43) after adjustment for age, smoking habits, total cholesterol and diastolic blood pressure. We conclude that an unsupplemented plasma CoQ10 concentration is not related to risk of coronary atherosclerosis.

Topics: Aged; Antioxidants; Case-Control Studies; Cholesterol, LDL; Coenzymes; Coronary Artery Disease; Electron Transport; Humans; Male; Middle Aged; Oxidation-Reduction; Risk Factors; Ubiquinone