By Harold L. Karpman, FACC, FACP
Clinical Professor of Medicine,
UCLA School of Medicine
Dr. Karpman reports no financial relationships relevant to this field of study.
SYNOPSIS: Treatment with coenzyme Q10 in addition to standard therapy for patients with moderate to severe HF is safe, well tolerated, and associated with a reduction in symptoms and major adverse cardiovascular events.
SOURCE: Mortensen SA, et al. The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure. J Amer Coll Card Heart Failure 2014;2:641-649.
Many research groups have attempted to elucidate the pathways, deficiencies, and enhancement of the energy-generation centers of the myocardial cells, the mitochondria.1 Coenzyme Q10 (CoQ10) influences mitochondrial function by contributing to oxidative phosphorylation and the generation of adenosine triphosphate, thereby augmenting energy production and enhancing efficient energy utilization.2 Previously published meta-analyses of randomized, controlled trials using CoQ10 in patients with heart failure (HF) have mostly revealed that the drug had a positive effect on left ventricular ejection fraction (EF) whether or not improvement of the New York Heart Association (NYHA) functional class occurs.3-5
Mortensen and his associates6 performed a prospective, randomized, double-blind, placebo-controlled, multicenter trial of CoQ10 as adjunctive treatment of chronic HF focusing on changes in symptoms, biomarker status, and long-term outcomes. Patients were enrolled in 17 European, Asian, and Australian centers from 2003 to 2010. The treatment group received CoQ10 in a dosage of 100 mg three times daily. The short-term (i.e., 16 weeks) aim of the study was a blinded evaluation of patient symptoms and functional status and the long-term (106 weeks) goal of the study was to test whether CoQ10 could reduce cardiovascular mortality and morbidity in HF patients as a composite endpoint. CoQ10-treated patients compared with the placebo group were found to have a significantly lower cardiovascular mortality, all-cause mortality, and a reduced incidence of hospital stays for HF. A significant improvement in NYHA class was also found to occur in the CoQ10-treated group.
Despite significant improvements in pharmacological HF therapy, Mortensen and colleagues have clearly demonstrated that adding 300 mg of CoQ10 daily significantly reduced cardiovascular death by 43% and all-cause mortality by 42%. Furthermore, CoQ10 supplementation improved symptoms according to positive changes in the NYHA functional classification after 2 years of therapy. The biological mechanisms behind the improvement of symptoms and survival in the HF patients who received CoQ10 may be multiple.7-9 These include increased energy production in the failing heart, changes in oxidative phosphorylation, and improvement in endothelial function.10 In addition, it has been demonstrated that CoQ10 may protect the myocardium against ischemia.11 Many patients with HF are malnourished as a result of defects in substrate utilization and energy supply,12 but whether a patient is malnourished or not, multiple metabolic dysfunctions may be present. It should be recognized that this trial of chronic HF recruited 420 patients over an 8-year period in nine countries in 17 centers; clearly, this trial had significant recruitment and performance issues, but the final results are clearly positive and should not be ignored. It is obvious that more research is required for further elucidation of the many molecular causes of heart failure that may be influenced in a positive way by CoQ10 or other drugs that become available in future years.
In summary, the results of the Mortensen study demonstrated that treatment with CoQ10 in addition to standard therapy in patients with moderate or even severe HF is safe, well-tolerated, and appears to be associated with a reduction in symptoms, with improvement of the NYHA functional class after 2 years of therapy.
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