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Coenzyme Q10 for the treatment of heart failure: a review of the literature
Coenzyme Q10 (CoQ10) is an endogenously synthesised and diet-supplied lipid-soluble cofactor that functions in the mitochondrial inner membrane to transfer electrons from complexes I and II to complex III. In addition, its redox activity enables CoQ10 to act as a membrane antioxidant. In patients wi...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BMJ Publishing Group
2015
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4620231/ https://www.ncbi.nlm.nih.gov/pubmed/26512330 http://dx.doi.org/10.1136/openhrt-2015-000326 |
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author | DiNicolantonio, James J Bhutani, Jaikrit McCarty, Mark F O'Keefe, James H |
author_facet | DiNicolantonio, James J Bhutani, Jaikrit McCarty, Mark F O'Keefe, James H |
author_sort | DiNicolantonio, James J |
collection | PubMed |
description | Coenzyme Q10 (CoQ10) is an endogenously synthesised and diet-supplied lipid-soluble cofactor that functions in the mitochondrial inner membrane to transfer electrons from complexes I and II to complex III. In addition, its redox activity enables CoQ10 to act as a membrane antioxidant. In patients with congestive heart failure, myocardial CoQ10 content tends to decline as the degree of heart failure worsens. A number of controlled pilot trials with supplemental CoQ10 in heart failure found improvements in functional parameters such as ejection fraction, stroke volume and cardiac output, without side effects. Subsequent meta-analyses have confirmed these findings, although the magnitude of benefit tends to be less notable in patients with severe heart failure, or within the context of ACE inhibitor therapy. The multicentre randomised placebo-controlled Q-SYMBIO trial has assessed the impact of supplemental CoQ10 on hard endpoints in heart failure. A total of 420 patients received either CoQ10 (100 mg three times daily) or placebo and were followed for 2 years. Although short-term functional endpoints were not statistically different in the two groups, CoQ10 significantly reduced the primary long-term endpoint—a major adverse cardiovascular event—which was observed in 15% of the treated participants compared to 26% of those receiving placebo (HR=0.50, CI 0.32 to 0.80, p=0.003). Particularly in light of the excellent tolerance and affordability of this natural physiological compound, supplemental CoQ10 has emerged as an attractive option in the management of heart failure, and merits evaluation in additional large studies. |
format | Online Article Text |
id | pubmed-4620231 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BMJ Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-46202312015-10-28 Coenzyme Q10 for the treatment of heart failure: a review of the literature DiNicolantonio, James J Bhutani, Jaikrit McCarty, Mark F O'Keefe, James H Open Heart Review Coenzyme Q10 (CoQ10) is an endogenously synthesised and diet-supplied lipid-soluble cofactor that functions in the mitochondrial inner membrane to transfer electrons from complexes I and II to complex III. In addition, its redox activity enables CoQ10 to act as a membrane antioxidant. In patients with congestive heart failure, myocardial CoQ10 content tends to decline as the degree of heart failure worsens. A number of controlled pilot trials with supplemental CoQ10 in heart failure found improvements in functional parameters such as ejection fraction, stroke volume and cardiac output, without side effects. Subsequent meta-analyses have confirmed these findings, although the magnitude of benefit tends to be less notable in patients with severe heart failure, or within the context of ACE inhibitor therapy. The multicentre randomised placebo-controlled Q-SYMBIO trial has assessed the impact of supplemental CoQ10 on hard endpoints in heart failure. A total of 420 patients received either CoQ10 (100 mg three times daily) or placebo and were followed for 2 years. Although short-term functional endpoints were not statistically different in the two groups, CoQ10 significantly reduced the primary long-term endpoint—a major adverse cardiovascular event—which was observed in 15% of the treated participants compared to 26% of those receiving placebo (HR=0.50, CI 0.32 to 0.80, p=0.003). Particularly in light of the excellent tolerance and affordability of this natural physiological compound, supplemental CoQ10 has emerged as an attractive option in the management of heart failure, and merits evaluation in additional large studies. BMJ Publishing Group 2015-10-19 /pmc/articles/PMC4620231/ /pubmed/26512330 http://dx.doi.org/10.1136/openhrt-2015-000326 Text en Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ |
spellingShingle | Review DiNicolantonio, James J Bhutani, Jaikrit McCarty, Mark F O'Keefe, James H Coenzyme Q10 for the treatment of heart failure: a review of the literature |
title | Coenzyme Q10 for the treatment of heart failure: a review of the literature |
title_full | Coenzyme Q10 for the treatment of heart failure: a review of the literature |
title_fullStr | Coenzyme Q10 for the treatment of heart failure: a review of the literature |
title_full_unstemmed | Coenzyme Q10 for the treatment of heart failure: a review of the literature |
title_short | Coenzyme Q10 for the treatment of heart failure: a review of the literature |
title_sort | coenzyme q10 for the treatment of heart failure: a review of the literature |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4620231/ https://www.ncbi.nlm.nih.gov/pubmed/26512330 http://dx.doi.org/10.1136/openhrt-2015-000326 |
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