Coenzyme Q(10) An Independent Predictor of Mortality in Chronic Heart Failure

Clinical Biochemistry Unit, Canterbury Health Laboratories, Christchurch, New Zealand.
Journal of the American College of Cardiology (Impact Factor: 16.5). 11/2008; 52(18):1435-41. DOI: 10.1016/j.jacc.2008.07.044
Source: PubMed


The aim of this study was to investigate the relationship between plasma coenzyme Q(10) (CoQ(10)) and survival in patients with chronic heart failure (CHF).
Patients with CHF have low plasma concentrations of CoQ(10), an essential cofactor for mitochondrial electron transport and myocardial energy supply. Additionally, low plasma total cholesterol (TC) concentrations have been associated with higher mortality in heart failure. Plasma CoQ(10) is closely associated with low-density lipoprotein cholesterol (LDL-C), which might contribute to this association. Therefore we tested the hypothesis that plasma CoQ(10) is a predictor of total mortality in CHF and could explain this association.
Plasma samples from 236 patients admitted to the hospital with CHF, with a median (range) duration of follow-up of 2.69 (0.12 to 5.75) years, were assayed for LDL-C, TC, and total CoQ(10).
Median age at admission was 77 years. Median (range) CoQ(10) concentration was 0.68 (0.18 to 1.75) micromol/l. The optimal CoQ(10) concentration for prediction of mortality (established with receiver-operator characteristic [ROC] curves) was 0.73 micromol/l. Multivariable analysis allowing for effects of standard predictors of survival--including age at admission, gender, previous myocardial infarction, N-terminal peptide of B-type natriuretic peptide, and estimated glomerular filtration rate (modification of diet in renal disease)--indicated CoQ(10) was an independent predictor of survival, whether dichotomized at the ROC curve cut-point (hazard ratio [HR]: 2.0; 95% confidence interval [CI]: 1.2 to 3.3) or the median (HR: 1.6; 95% CI: 1.0 to 2.6).
Plasma CoQ(10) concentration was an independent predictor of mortality in this cohort. The CoQ(10) deficiency might be detrimental to the long-term prognosis of CHF, and there is a rationale for controlled intervention studies with CoQ(10).

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Available from: Peter Myles George, May 24, 2014
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    • "CoQ10 is a molecule especially important in tissues with high metabolic requirements, like the liver, brain and heart. A clear association between low plasma levels of CoQ10 and heart failure has been established [4], and it has also been established as an independent predictor of greater mortality among patients with heart failure [5]. In addition, many cases of inherited CoQ10 deficiency have been described, caused by autosomal recessive mutations of genes involved in its synthesis. "
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    ABSTRACT: Coenzyme Q10 (CoQ10) is a lipid-soluble antioxidant that could have beneficial effects in patients undergoing cardiac surgery with cardiopulmonary bypass. There is no clear evidence about its clinical effects or a systematic review published yet. We aimed to conduct a systematic review and meta-analysis of the literature to elucidate the role of coenzyme Q10 in preventing complications in patients undergoing cardiac surgery with cardiopulmonary bypass. We searched the PubMed Database using the following keywords: Coenzyme Q10, ubiquinone, ubiquinol, CoQ10, Heart Surgery, Cardiac surgery. Articles were systematically retrieved, selected, assessed and summarized for this review. We performed separate meta-analyses for different outcomes (inotropic drug requirements after surgery, incidence of ventricular arrhythmias and atrial fibrillation, cardiac index 24 h after surgery and hospital stay), estimating pooled odds ratios (ORs) or mean differences of the association of CoQ10 administration with the risk of these outcomes. Eight clinical trials met our inclusion criteria. Patients with CoQ10 treatment were significantly less likely to require inotropic drugs after surgery {OR [95% confidence interval (CI) 0.47 (0.27-0.81)]}, and to develop ventricular arrhythmias after surgery [OR (95% CI) 0.05 (0.01-0.31)]. However, CoQ10 treatment was not associated with Cardiac index 24 h after surgery [mean difference (95% CI) 0.06 (-0.30 to 0.43)], hospital stay (days) [mean difference (95% CI) -0.61 (-4.61 to 3.39)] and incidence of atrial fibrillation [OR (95% CI) 1.06 (0.19-6.04)]. Since none of the clinical trials included in this review report any adverse effects associated to CoQ10 administration, and coenzyme Q10 has been demonstrated to be safe even at much higher doses in other studies, we conclude that CoQ10 should be considered as a prophylactic treatment for preventing complications in patients undergoing cardiac surgery with cardiopulmonary bypass. However, better quality randomized, controlled trials are needed to clarify the role of CoQ10 in patients undergoing cardiac surgery with cardiopulmonary bypass.
    Interactive Cardiovascular and Thoracic Surgery 10/2014; 20(2). DOI:10.1093/icvts/ivu334 · 1.16 Impact Factor
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    • "CoQ10 is one of several nutritional components that have been recorded to be inadequate in diabetic states [6]–[9]. The CoQ10 deficiency is possibly due to the impaired mitochondrial substrate metabolism and/or increased oxidative stress [10] that may be linked with the impairment of β-cells and the development of IR [11]. "
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    ABSTRACT: As a nutritional supplement, coenzyme Q10 (CoQ10) was tested previously in several models of diabetes and/or insulin resistance (IR); however, its exact mechanisms have not been profoundly explicated. Hence, the objective of this work is to verify some of the possible mechanisms that underlie its therapeutic efficacy. Moreover, the study aimed to assess the potential modulatory effect of CoQ10 on the antidiabetic action of glimebiride. An insulin resistance/type 2 diabetic model was adopted, in which rats were fed high fat/high fructose diet (HFFD) for 6 weeks followed by a single sub-diabetogenic dose of streptozotocin (35 mg/kg, i.p.). At the end of the 7(th) week animals were treated with CoQ10 (20 mg/kg, p.o) and/or glimebiride (0.5 mg/kg, p.o) for 2 weeks. CoQ10 alone opposed the HFFD effect and increased the hepatic/muscular content/activity of tyrosine kinase (TK), phosphatidylinositol kinase (PI3K), and adiponectin receptors. Conversely, it decreased the content/activity of insulin receptor isoforms, myeloperoxidase and glucose transporters (GLUT4; 2). Besides, it lowered significantly the serum levels of glucose, insulin, fructosamine and HOMA index, improved the serum lipid panel and elevated the levels of glutathione, sRAGE and adiponectin. On the other hand, CoQ10 lowered the serum levels of malondialdehyde, visfatin, ALT and AST. Surprisingly, CoQ10 effect surpassed that of glimepiride in almost all the assessed parameters, except for glucose, fructosamine, TK, PI3K, and GLUT4. Combining CoQ10 with glimepiride enhanced the effect of the latter on the aforementioned parameters. These results provided a new insight into the possible mechanisms by which CoQ10 improves insulin sensitivity and adjusts type 2 diabetic disorder. These mechanisms involve modulation of insulin and adiponectin receptors, as well as TK, PI3K, glucose transporters, besides improving lipid profile, redox system, sRAGE, and adipocytokines. The study also points to the potential positive effect of CoQ10 as an adds- on to conventional antidiabetic therapies.
    PLoS ONE 02/2014; 9(2):e89169. DOI:10.1371/journal.pone.0089169 · 3.23 Impact Factor
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    • "CoQ10 localized in the mitochondria and plasma membrane functions as an efficient antioxidant either by direct conjugation with reactive oxygen species (ROS) or by regeneration of cellular antioxidants such as tocopherol and ascorbic acid (Crane, 2001). Moreover, tissue or blood levels of CoQ10 are significantly lower in patients with cardiovascular disease, including chronic heart failure and type II diabetes (Mortensen et al., 1990; Molyneux et al., 2008; Miyake et al., 1999). Decreased CoQ10 levels are a pathological marker of the increased oxidative stress in congestive heart failure, coronal artery disease (Chagan et al., 2002; Sarter, 2002), and diabetes (Hodgson et al., 2002). "
    Dataset: COQ10

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