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Article: Mitochondrial dysfunction induced by statin contributes to endothelial dysfunction in patients with coronary artery disease
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TitleMitochondrial dysfunction induced by statin contributes to endothelial dysfunction in patients with coronary artery disease
 
AuthorsDai, YL2
Luk, TH2
Siu, CW2 1
Yiu, KH2
Chan, HT2
Lee, SWL2
Li, SW4
Tam, S3
Fong, B3
Lau, CP2
Tse, HF2 1
 
KeywordsEndothelial dysfunction
Mitochondrial dysfunction
Statin
 
Issue Date2010
 
PublisherHumana Press, Inc. The Journal's web site is located at http://www.cardiotox.com
 
CitationCardiovascular Toxicology, 2010, v. 10 n. 2, p. 130-138 [How to Cite?]
DOI: http://dx.doi.org/10.1007/s12012-010-9071-1
 
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.
 
ISSN1530-7905
2013 Impact Factor: 2.060
2013 SCImago Journal Rankings: 0.749
 
DOIhttp://dx.doi.org/10.1007/s12012-010-9071-1
 
ISI Accession Number IDWOS:000277709900006
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.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorDai, YL
 
dc.contributor.authorLuk, TH
 
dc.contributor.authorSiu, CW
 
dc.contributor.authorYiu, KH
 
dc.contributor.authorChan, HT
 
dc.contributor.authorLee, SWL
 
dc.contributor.authorLi, SW
 
dc.contributor.authorTam, S
 
dc.contributor.authorFong, B
 
dc.contributor.authorLau, CP
 
dc.contributor.authorTse, HF
 
dc.date.accessioned2010-09-06T07:26:49Z
 
dc.date.available2010-09-06T07:26:49Z
 
dc.date.issued2010
 
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.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationCardiovascular Toxicology, 2010, v. 10 n. 2, p. 130-138 [How to Cite?]
DOI: http://dx.doi.org/10.1007/s12012-010-9071-1
 
dc.identifier.citeulike7047283
 
dc.identifier.doihttp://dx.doi.org/10.1007/s12012-010-9071-1
 
dc.identifier.epage138
 
dc.identifier.hkuros169690
 
dc.identifier.isiWOS:000277709900006
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.

 
dc.identifier.issn1530-7905
2013 Impact Factor: 2.060
2013 SCImago Journal Rankings: 0.749
 
dc.identifier.issue2
 
dc.identifier.openurl
 
dc.identifier.pmid20383667
 
dc.identifier.scopuseid_2-s2.0-77956394303
 
dc.identifier.spage130
 
dc.identifier.urihttp://hdl.handle.net/10722/76964
 
dc.identifier.volume10
 
dc.languageeng
 
dc.publisherHumana Press, Inc. The Journal's web site is located at http://www.cardiotox.com
 
dc.publisher.placeUnited States
 
dc.relation.ispartofCardiovascular Toxicology
 
dc.relation.referencesReferences in Scopus
 
dc.rightsThe original publication is available at www.springerlink.com
 
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.subjectEndothelial dysfunction
 
dc.subjectMitochondrial dysfunction
 
dc.subjectStatin
 
dc.titleMitochondrial dysfunction induced by statin contributes to endothelial dysfunction in patients with coronary artery disease
 
dc.typeArticle
 
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<contributor.author>Chan, HT</contributor.author>
<contributor.author>Lee, SWL</contributor.author>
<contributor.author>Li, SW</contributor.author>
<contributor.author>Tam, S</contributor.author>
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<contributor.author>Tse, HF</contributor.author>
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<description.abstract>Despite 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 (&gt; 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 &gt;75th percentile of the age- and sex-matched normal controls, i.e., &#8805;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 &gt; 0.05). Patients with MD received higher dose of statin (23.5 &#177; 19.3 vs. 17.1 &#177; 10.5 mg simvastatin-equivalent dose, P = 0.05) and had lower FMD (2.69 &#177; 2.94 vs. 4.33 &#177; 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. &#169; Springer Science+Business Media, LLC 2010.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. The University of Hong Kong
  3. Queen Mary Hospital Hong Kong
  4. Tung Wah Hospital