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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

TitleReversal of mitochondrial dysfunction by coenzyme Q10 supplement improves endothelial function in patients with ischaemic left ventricular systolic dysfunction: A randomized controlled trial
Authors
KeywordsCo-Enzyme Q10
Heart Failure
Mitochondrial Function
Issue Date2011
PublisherElsevier 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?
AbstractAims: 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 Identifierhttp://hdl.handle.net/10722/134158
ISSN
2015 Impact Factor: 3.942
2015 SCImago Journal Rankings: 1.819
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong Kong200907176063
Sun Chieh Yeh Heart Foundation
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

 

DC FieldValueLanguage
dc.contributor.authorDai, YLen_HK
dc.contributor.authorLuk, THen_HK
dc.contributor.authorYiu, KHen_HK
dc.contributor.authorWang, Men_HK
dc.contributor.authorYip, PMCen_HK
dc.contributor.authorLee, SWLen_HK
dc.contributor.authorLi, SWen_HK
dc.contributor.authorTam, Sen_HK
dc.contributor.authorFong, Ben_HK
dc.contributor.authorLau, CPen_HK
dc.contributor.authorSiu, CWen_HK
dc.contributor.authorTse, HFen_HK
dc.date.accessioned2011-06-13T07:20:22Z-
dc.date.available2011-06-13T07:20:22Z-
dc.date.issued2011en_HK
dc.identifier.citationAtherosclerosis, 2011, v. 216 n. 2, p. 395-401en_HK
dc.identifier.issn0021-9150en_HK
dc.identifier.urihttp://hdl.handle.net/10722/134158-
dc.description.abstractAims: 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.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/atherosclerosisen_HK
dc.relation.ispartofAtherosclerosisen_HK
dc.subjectCo-Enzyme Q10en_US
dc.subjectHeart Failureen_US
dc.subjectMitochondrial Functionen_US
dc.subject.meshAgeden_HK
dc.subject.meshBlood Pressureen_HK
dc.subject.meshBrachial Artery - pathologyen_HK
dc.subject.meshCross-Sectional Studiesen_HK
dc.subject.meshDietary Supplementsen_HK
dc.subject.meshDinoprost - analogs & derivatives - blooden_HK
dc.subject.meshDouble-Blind Methoden_HK
dc.subject.meshEndothelium, Vascular - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshNitroglycerin - metabolismen_HK
dc.subject.meshPlacebosen_HK
dc.subject.meshRisk Factorsen_HK
dc.subject.meshSuperoxide Dismutase - blooden_HK
dc.subject.meshUbiquinone - administration & dosage - analogs & derivatives - metabolismen_HK
dc.subject.meshVentricular Dysfunction, Left - pathologyen_HK
dc.titleReversal of mitochondrial dysfunction by coenzyme Q10 supplement improves endothelial function in patients with ischaemic left ventricular systolic dysfunction: A randomized controlled trialen_HK
dc.typeArticleen_HK
dc.identifier.emailYiu, KH:khkyiu@hku.hken_HK
dc.identifier.emailWang, M:meiwang@hkucc.hku.hken_HK
dc.identifier.emailSiu, CW:cwdsiu@hkucc.hku.hken_HK
dc.identifier.emailTse, HF:hftse@hkucc.hku.hken_HK
dc.identifier.authorityYiu, KH=rp01490en_HK
dc.identifier.authorityWang, M=rp00281en_HK
dc.identifier.authoritySiu, CW=rp00534en_HK
dc.identifier.authorityTse, HF=rp00428en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.atherosclerosis.2011.02.013en_HK
dc.identifier.pmid21388622-
dc.identifier.scopuseid_2-s2.0-79958002852en_HK
dc.identifier.hkuros225169-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79958002852&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume216en_HK
dc.identifier.issue2en_HK
dc.identifier.spage395en_HK
dc.identifier.epage401en_HK
dc.identifier.isiWOS:000291343600026-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridDai, YL=35168927300en_HK
dc.identifier.scopusauthoridLuk, TH=35170682200en_HK
dc.identifier.scopusauthoridYiu, KH=35172267800en_HK
dc.identifier.scopusauthoridWang, M=7406690398en_HK
dc.identifier.scopusauthoridYip, PMC=36741033300en_HK
dc.identifier.scopusauthoridLee, SWL=53881501100en_HK
dc.identifier.scopusauthoridLi, SW=13807028100en_HK
dc.identifier.scopusauthoridTam, S=7202037323en_HK
dc.identifier.scopusauthoridFong, B=16507017100en_HK
dc.identifier.scopusauthoridLau, CP=7401968501en_HK
dc.identifier.scopusauthoridSiu, CW=7006550690en_HK
dc.identifier.scopusauthoridTse, HF=7006070805en_HK
dc.identifier.citeulike8885647-

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