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Article: Mitochondrial dysfunction induced by statin contributes to endothelial dysfunction in patients with coronary artery disease

TitleMitochondrial dysfunction induced by statin contributes to endothelial dysfunction in patients with coronary artery disease
Authors
KeywordsEndothelial dysfunction
Mitochondrial dysfunction
Statin
Issue Date2010
PublisherHumana Press, Inc. The Journal's web site is located at http://www.cardiotox.com
Citation
Cardiovascular Toxicology, 2010, v. 10 n. 2, p. 130-138 How to Cite?
AbstractDespite the use of statin therapy, a significant proportion of patients with coronary artery disease (CAD) still develop cardiovascular events. We hypothesized that development of mitochondrial dysfunction (MD) after statin therapy might be linked to endothelial dysfunction and thus limiting its beneficial effects. We studied the effect of MD on endothelial function in 119 patients with CAD on long-term statins (> 1 year). Brachial artery flow-mediated dilation (FMD) was assessed by high-resolution ultrasonography and blood levels of lactate, pyruvate, fasting glucose, and lipids were measured. MD (defined by a lactate/pyruvate ratio >75th percentile of the age- and sex-matched normal controls, i.e., ≥18) was observed in 43/119(36%) patients. There were no significant differences in age, gender, and clinical characteristics between patients with or without MD (all P > 0.05). Patients with MD received higher dose of statin (23.5 ± 19.3 vs. 17.1 ± 10.5 mg simvastatin-equivalent dose, P = 0.05) and had lower FMD (2.69 ± 2.94 vs. 4.33 ± 2.80%, P = 0.003) than those without MD. Multivariate analysis showed that statin dosage was independently associated with MD (OR:1.03, P = 0.03), and MD significantly predicted an absolute 1.36% decrease in FMD (P = 0.01). In conclusion, a significant proportion of patients with CAD on statin developed MD, which was associated with high-dose statin and with impaired FMD, suggesting that increased statin dosage may induce MD and contribute to endothelial dysfunction in patients with CAD. © Springer Science+Business Media, LLC 2010.
Persistent Identifierhttp://hdl.handle.net/10722/76964
ISSN
2015 Impact Factor: 2.063
2015 SCImago Journal Rankings: 0.759
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong Kong200907176063
Sun Chieh Yeh Heart Foundation
Funding Information:

This study was supported by the CRCG Small Project Funding of University of Hong Kong (Project No. 200907176063) and Sun Chieh Yeh Heart Foundation.

References

 

DC FieldValueLanguage
dc.contributor.authorDai, YLen_HK
dc.contributor.authorLuk, THen_HK
dc.contributor.authorSiu, CWen_HK
dc.contributor.authorYiu, KHen_HK
dc.contributor.authorChan, HTen_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.authorTse, HFen_HK
dc.date.accessioned2010-09-06T07:26:49Z-
dc.date.available2010-09-06T07:26:49Z-
dc.date.issued2010en_HK
dc.identifier.citationCardiovascular Toxicology, 2010, v. 10 n. 2, p. 130-138en_HK
dc.identifier.issn1530-7905en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76964-
dc.description.abstractDespite the use of statin therapy, a significant proportion of patients with coronary artery disease (CAD) still develop cardiovascular events. We hypothesized that development of mitochondrial dysfunction (MD) after statin therapy might be linked to endothelial dysfunction and thus limiting its beneficial effects. We studied the effect of MD on endothelial function in 119 patients with CAD on long-term statins (> 1 year). Brachial artery flow-mediated dilation (FMD) was assessed by high-resolution ultrasonography and blood levels of lactate, pyruvate, fasting glucose, and lipids were measured. MD (defined by a lactate/pyruvate ratio >75th percentile of the age- and sex-matched normal controls, i.e., ≥18) was observed in 43/119(36%) patients. There were no significant differences in age, gender, and clinical characteristics between patients with or without MD (all P > 0.05). Patients with MD received higher dose of statin (23.5 ± 19.3 vs. 17.1 ± 10.5 mg simvastatin-equivalent dose, P = 0.05) and had lower FMD (2.69 ± 2.94 vs. 4.33 ± 2.80%, P = 0.003) than those without MD. Multivariate analysis showed that statin dosage was independently associated with MD (OR:1.03, P = 0.03), and MD significantly predicted an absolute 1.36% decrease in FMD (P = 0.01). In conclusion, a significant proportion of patients with CAD on statin developed MD, which was associated with high-dose statin and with impaired FMD, suggesting that increased statin dosage may induce MD and contribute to endothelial dysfunction in patients with CAD. © Springer Science+Business Media, LLC 2010.en_HK
dc.languageengen_HK
dc.publisherHumana Press, Inc. The Journal's web site is located at http://www.cardiotox.comen_HK
dc.relation.ispartofCardiovascular Toxicologyen_HK
dc.rightsThe original publication is available at www.springerlink.com-
dc.subjectEndothelial dysfunctionen_HK
dc.subjectMitochondrial dysfunctionen_HK
dc.subjectStatinen_HK
dc.subject.meshCoronary Artery Disease - drug therapy - physiopathology-
dc.subject.meshEndothelium, Vascular - drug effects - physiopathology-
dc.subject.meshHydroxymethylglutaryl-CoA Reductase Inhibitors - adverse effects-
dc.subject.meshMitochondria, Heart - drug effects - metabolism-
dc.subject.meshMitochondrial Diseases - chemically induced - metabolism-
dc.titleMitochondrial dysfunction induced by statin contributes to endothelial dysfunction in patients with coronary artery diseaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1530-7905&volume=10&issue=2&spage=130&epage=138&date=2010&atitle=Mitochondrial+dysfunction+induced+by+statin+contributes+to+endothelial+dysfunction+in+patients+with+coronary+artery+diseaseen_HK
dc.identifier.emailSiu, CW:cwdsiu@hkucc.hku.hken_HK
dc.identifier.emailYiu, KH:khkyiu@hku.hken_HK
dc.identifier.emailTse, HF:hftse@hkucc.hku.hken_HK
dc.identifier.authoritySiu, CW=rp00534en_HK
dc.identifier.authorityYiu, KH=rp01490en_HK
dc.identifier.authorityTse, HF=rp00428en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s12012-010-9071-1en_HK
dc.identifier.pmid20383667-
dc.identifier.scopuseid_2-s2.0-77956394303en_HK
dc.identifier.hkuros169690en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77956394303&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume10en_HK
dc.identifier.issue2en_HK
dc.identifier.spage130en_HK
dc.identifier.epage138en_HK
dc.identifier.isiWOS:000277709900006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridDai, YL=35168927300en_HK
dc.identifier.scopusauthoridLuk, TH=35170682200en_HK
dc.identifier.scopusauthoridSiu, CW=7006550690en_HK
dc.identifier.scopusauthoridYiu, KH=35172267800en_HK
dc.identifier.scopusauthoridChan, HT=22633582100en_HK
dc.identifier.scopusauthoridLee, SWL=27169452400en_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.scopusauthoridTse, HF=7006070805en_HK
dc.identifier.citeulike7047283-

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