Coenzyme Q10 for heart failure

Heart failure is a term used to describe the state that develops when the heart cannot maintain adequate cardiac output or can do so only at the expense of overfilling the heart chambers. People with heart failure commonly experience a relapsing and remitting disease course, with periods of stability and episodes of decompensation (failure to cope with heart damage) leading to worsening symptoms that necessitate hospitalisation. Treatment options for heart failure range from drugs to heart transplantation, with each having its own limitations. Coenzyme Q10 (or ubiquinone) has been suggested as a treatment option in some trials. Coenzyme Q10 is a non-prescription nutritional supplement. It is a fat-soluble molecule that has a role in energy production within the cells of the body. It may also have antioxidant properties. Low levels of conequme Q10 may be related to the severity of heart failure. Coenzyme Q10 has been found in all tissues and organs in the body, with the highest concentrations in the heart. Emerging data have suggested that the harmful effects of reactive oxygen species are increased in patients with heart failure and coenzyme Q10, given its antioxidant activity, may help to reduce these toxic effects, which damage the components of the cardiac cells and disrupt cellular signalling. Coenzyme Q10 also has a role in stabilising myocardial calcium-dependent ion channels and preventing the consumption of metabolites essential for adenosine-5'-triphosphate (ATP) synthesis. The concentration of coenzyme Q10 has been inversely related to the severity of heart failure. Supplementation with coenzyme Q10 may improve heart failure. Coenzyme Q10 is sometimes used because it is thought to have an acceptable safety profile with no significant side effects.

We conducted this review to assess the available evidence on the effects of coenzyme Q10 in heart failure patients. We included seven small randomised controlled trials in this review, that were at a risk of bias. Due to the variation in the way that the studies were done we were not able to combine many of the data in our review, meaning that it is difficult to explore the impact of this variation on the results of this review. Only one study reported on mortality, majro cardiovascular evetns and hospitalisation. The evidence collected in this review shows no clear effect of coenzyme Q10 on the improvement of clinical status (using the New York Heart Association (NYHA) classification) or on exercise capacity. There is no convincing evidence to support or refute the use of coenzyme Q10 for heart failure.

Authors' conclusions: 

No conclusions can be drawn on the benefits or harms of coenzyme Q10 in heart failure at this time as trials published to date lack information on clinically relevant endpoints. Furthermore, the existing data are derived from small, heterogeneous trials that concentrate on physiological measures: their results are inconclusive. Until further evidence emerges to support the use of coenzyme Q10 in heart failure, there might be a need to re-evaluate whether further trials testing coenzyme Q10 in heart failure are desirable.

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Background: 

Coenzyme Q10, or ubiquinone, is a non-prescription nutritional supplement. It is a fat-soluble molecule that acts as an electron carrier in mitochondria and as a coenzyme for mitochondrial enzymes. Coenzyme Q10 deficiency may be associated with a multitude of diseases including heart failure. The severity of heart failure correlates with the severity of coenzyme Q10 deficiency. Emerging data suggest that the harmful effects of reactive oxygen species are increased in patients with heart failure and coenzyme Q10 may help to reduce these toxic effects because of its antioxidant activity. Coenzyme Q10 may also have a role in stabilising myocardial calcium-dependent ion channels and preventing the consumption of metabolites essential for adenosine-5'-triphosphate (ATP) synthesis. Coenzyme Q10, although not a primary recommended treatment, could be beneficial to patients with heart failure. Several randomised controlled trials have compared coenzyme Q10 to other therapeutic modalities, but no systematic review of existing randomised trials has been conducted.

Objectives: 

To review the safety and efficacy of coenzyme Q10 in heart failure.

Search strategy: 

We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (2012, Issue 12); MEDLINE OVID (1950 to January Week 3 2013) and EMBASE OVID (1980 to 2013 Week 03) on 24 January 2013; Web of Science with Conference Proceedings (1970 to January 2013) and CINAHL Plus (1981 to January 2013) on 25 January 2013; and AMED (Allied and Complementary Medicine) (1985 to January 2013) on 28 January 2013. We applied no language restrictions.

Selection criteria: 

We included randomised controlled trials of either parallel or cross-over design that assessed the beneficial and harmful effects of coenzyme Q10 in patients with heart failure. When cross-over studies were identified, we considered data only from the first phase.

Data collection and analysis: 

Two authors independently extracted data from the included studies onto a pre-designed data extraction form. We then entered the data into Review Manager 5.2 for analysis. We assessed study risk of bias using the Cochrane 'Risk of bias' tool. For dichotomous data, we calculated the risk ratio and for continuous data the mean difference (MD). Where appropriate data were available, we performed meta-analysis. For this review we prioritised data from pooled analyses only. Where meta-analysis was not possible, we wrote a narrative synthesis. We provided a QUOROM flow chart to show the flow of papers.

Main results: 

We included seven studies with 914 participants comparing conenzyme Q10 versus placebo. There were no data on clinical events from published randomised trials. The included studies had small sample sizes. Meta-analysis was only possible for a few physiological measures and there was substantial heterogeneity.

Only one study reported on total mortality, major cardiovascular events and hospitalisation. Five trials reported on the New York Heart Association (NYHA) classification of clinical status, but it was impossible to pool data due to heterogeneity. None of the included trials considered quality of life, exercise variables, adverse events or cost-effectiveness as outcome measures. Pooled analysis suggests that the use of coenzyme Q10 has no clear effect on left ventricular ejection fraction (MD -2.26; 95% confidence interval (CI) -15.49 to 10.97, n = 60) or exercise capacity (MD 12.79; 95% CI -140.12 to 165.70, n = 85). Pooled data did indicate that supplementation increased blood levels of coenzyme Q10 (MD 1.46; 95% CI 1.19 to 1.72, n = 112). However, there are only a small number of small studies with a risk of bias, so these results should be interpreted with caution.

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