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- Publisher Website: 10.1016/j.atherosclerosis.2011.02.013
- Scopus: eid_2-s2.0-79958002852
- PMID: 21388622
- WOS: WOS:000291343600026
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Article: Reversal of mitochondrial dysfunction by coenzyme Q10 supplement improves endothelial function in patients with ischaemic left ventricular systolic dysfunction: A randomized controlled trial
Title | Reversal of mitochondrial dysfunction by coenzyme Q10 supplement improves endothelial function in patients with ischaemic left ventricular systolic dysfunction: A randomized controlled trial | ||||||
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Authors | |||||||
Keywords | Co-Enzyme Q10 Heart Failure Mitochondrial Function | ||||||
Issue Date | 2011 | ||||||
Publisher | Elsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis | ||||||
Citation | Atherosclerosis, 2011, v. 216 n. 2, p. 395-401 How to Cite? | ||||||
Abstract | Aims: Coronary artery disease (CAD) is associated with endothelial dysfunction and mitochondrial dysfunction (MD). The aim of this study was to investigate whether co-enzyme Q10 (CoQ) supplementation, which is an obligatory coenzyme in the mitochondrial respiratory transport chain, can reverse MD and improve endothelial function in patients with ischaemic left ventricular systolic dysfunction (LVSD). Methods and results: We performed a randomized, double-blind, placebo-controlled trial to determine the effects of CoQ supplement (300. mg/day, n= 28) vs. placebo (controls, n= 28) for 8. weeks on brachial flow-mediated dilation (FMD) in patients with ischaemic LVSD(left ventricular ejection fraction <45%). Mitochondrial function was determined by plasma lactate/pyruvate ratio (LP ratio). After 8. weeks, CoQ-treated patients had significant increases in plasma CoQ concentration (treatment effect 2.20 μg/mL, P< 0.001) and FMD (treatment effect 1.51%, P= 0.03); and decrease in LP ratio (treatment effect -2.46, P= 0.03) compared with controls. However, CoQ treatment did not alter nitroglycerin-mediated dilation, blood pressure, blood levels of fasting glucose, haemoglobin A1c, lipid profile, high-sensitivity C-reactive protein and oxidative stress as determined by serum superoxide dismutase and 8-isoprostane (all P> 0.05). Furthermore, the reduction in LP ratio significantly correlated with improvement in FMD (r= -0.29, P= 0.047). Conclusion: In patients with ischaemic LVSD, 8. weeks supplement of CoQ improved mitochondrial function and FMD; and the improvement of FMD correlated with the change in mitochondrial function, suggesting that CoQ improved endothelial function via reversal of mitochondrial dysfunction in patients with ischaemic LVSD. © 2011 Elsevier Ireland Ltd. | ||||||
Persistent Identifier | http://hdl.handle.net/10722/134158 | ||||||
ISSN | 2023 Impact Factor: 4.9 2023 SCImago Journal Rankings: 1.461 | ||||||
ISI Accession Number ID |
Funding Information: This work was supported by the CRCG Small Project Funding of University of Hong Kong (Project No. 200907176063); and Sun Chieh Yeh Heart Foundation. Jarrow Formulas, Los Angeles, CA, USA kindly supplied the co-enzyme Q10 and matching placebo capsules used in this study. | ||||||
References | |||||||
Grants |
DC Field | Value | Language |
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dc.contributor.author | Dai, YL | en_HK |
dc.contributor.author | Luk, TH | en_HK |
dc.contributor.author | Yiu, KH | en_HK |
dc.contributor.author | Wang, M | en_HK |
dc.contributor.author | Yip, PMC | en_HK |
dc.contributor.author | Lee, SWL | en_HK |
dc.contributor.author | Li, SW | en_HK |
dc.contributor.author | Tam, S | en_HK |
dc.contributor.author | Fong, B | en_HK |
dc.contributor.author | Lau, CP | en_HK |
dc.contributor.author | Siu, CW | en_HK |
dc.contributor.author | Tse, HF | en_HK |
dc.date.accessioned | 2011-06-13T07:20:22Z | - |
dc.date.available | 2011-06-13T07:20:22Z | - |
dc.date.issued | 2011 | en_HK |
dc.identifier.citation | Atherosclerosis, 2011, v. 216 n. 2, p. 395-401 | en_HK |
dc.identifier.issn | 0021-9150 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/134158 | - |
dc.description.abstract | Aims: Coronary artery disease (CAD) is associated with endothelial dysfunction and mitochondrial dysfunction (MD). The aim of this study was to investigate whether co-enzyme Q10 (CoQ) supplementation, which is an obligatory coenzyme in the mitochondrial respiratory transport chain, can reverse MD and improve endothelial function in patients with ischaemic left ventricular systolic dysfunction (LVSD). Methods and results: We performed a randomized, double-blind, placebo-controlled trial to determine the effects of CoQ supplement (300. mg/day, n= 28) vs. placebo (controls, n= 28) for 8. weeks on brachial flow-mediated dilation (FMD) in patients with ischaemic LVSD(left ventricular ejection fraction <45%). Mitochondrial function was determined by plasma lactate/pyruvate ratio (LP ratio). After 8. weeks, CoQ-treated patients had significant increases in plasma CoQ concentration (treatment effect 2.20 μg/mL, P< 0.001) and FMD (treatment effect 1.51%, P= 0.03); and decrease in LP ratio (treatment effect -2.46, P= 0.03) compared with controls. However, CoQ treatment did not alter nitroglycerin-mediated dilation, blood pressure, blood levels of fasting glucose, haemoglobin A1c, lipid profile, high-sensitivity C-reactive protein and oxidative stress as determined by serum superoxide dismutase and 8-isoprostane (all P> 0.05). Furthermore, the reduction in LP ratio significantly correlated with improvement in FMD (r= -0.29, P= 0.047). Conclusion: In patients with ischaemic LVSD, 8. weeks supplement of CoQ improved mitochondrial function and FMD; and the improvement of FMD correlated with the change in mitochondrial function, suggesting that CoQ improved endothelial function via reversal of mitochondrial dysfunction in patients with ischaemic LVSD. © 2011 Elsevier Ireland Ltd. | en_HK |
dc.language | eng | en_US |
dc.publisher | Elsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosis | en_HK |
dc.relation.ispartof | Atherosclerosis | en_HK |
dc.subject | Co-Enzyme Q10 | en_US |
dc.subject | Heart Failure | en_US |
dc.subject | Mitochondrial Function | en_US |
dc.subject.mesh | Aged | en_HK |
dc.subject.mesh | Blood Pressure | en_HK |
dc.subject.mesh | Brachial Artery - pathology | en_HK |
dc.subject.mesh | Cross-Sectional Studies | en_HK |
dc.subject.mesh | Dietary Supplements | en_HK |
dc.subject.mesh | Dinoprost - analogs & derivatives - blood | en_HK |
dc.subject.mesh | Double-Blind Method | en_HK |
dc.subject.mesh | Endothelium, Vascular - metabolism | en_HK |
dc.subject.mesh | Female | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | Male | en_HK |
dc.subject.mesh | Middle Aged | en_HK |
dc.subject.mesh | Nitroglycerin - metabolism | en_HK |
dc.subject.mesh | Placebos | en_HK |
dc.subject.mesh | Risk Factors | en_HK |
dc.subject.mesh | Superoxide Dismutase - blood | en_HK |
dc.subject.mesh | Ubiquinone - administration & dosage - analogs & derivatives - metabolism | en_HK |
dc.subject.mesh | Ventricular Dysfunction, Left - pathology | en_HK |
dc.title | Reversal of mitochondrial dysfunction by coenzyme Q10 supplement improves endothelial function in patients with ischaemic left ventricular systolic dysfunction: A randomized controlled trial | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Yiu, KH:khkyiu@hku.hk | en_HK |
dc.identifier.email | Wang, M:meiwang@hkucc.hku.hk | en_HK |
dc.identifier.email | Siu, CW:cwdsiu@hkucc.hku.hk | en_HK |
dc.identifier.email | Tse, HF:hftse@hkucc.hku.hk | en_HK |
dc.identifier.authority | Yiu, KH=rp01490 | en_HK |
dc.identifier.authority | Wang, M=rp00281 | en_HK |
dc.identifier.authority | Siu, CW=rp00534 | en_HK |
dc.identifier.authority | Tse, HF=rp00428 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1016/j.atherosclerosis.2011.02.013 | en_HK |
dc.identifier.pmid | 21388622 | - |
dc.identifier.scopus | eid_2-s2.0-79958002852 | en_HK |
dc.identifier.hkuros | 225169 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-79958002852&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 216 | en_HK |
dc.identifier.issue | 2 | en_HK |
dc.identifier.spage | 395 | en_HK |
dc.identifier.epage | 401 | en_HK |
dc.identifier.isi | WOS:000291343600026 | - |
dc.publisher.place | Ireland | en_HK |
dc.relation.project | Relationship between mitochondrial dysfunction and vascular function in patients with cardiovascular diseases | - |
dc.identifier.scopusauthorid | Dai, YL=35168927300 | en_HK |
dc.identifier.scopusauthorid | Luk, TH=35170682200 | en_HK |
dc.identifier.scopusauthorid | Yiu, KH=35172267800 | en_HK |
dc.identifier.scopusauthorid | Wang, M=7406690398 | en_HK |
dc.identifier.scopusauthorid | Yip, PMC=36741033300 | en_HK |
dc.identifier.scopusauthorid | Lee, SWL=53881501100 | en_HK |
dc.identifier.scopusauthorid | Li, SW=13807028100 | en_HK |
dc.identifier.scopusauthorid | Tam, S=7202037323 | en_HK |
dc.identifier.scopusauthorid | Fong, B=16507017100 | en_HK |
dc.identifier.scopusauthorid | Lau, CP=7401968501 | en_HK |
dc.identifier.scopusauthorid | Siu, CW=7006550690 | en_HK |
dc.identifier.scopusauthorid | Tse, HF=7006070805 | en_HK |
dc.identifier.citeulike | 8885647 | - |
dc.identifier.issnl | 0021-9150 | - |