Article: Mitochondrial dysfunction induced by statin contributes to endothelial dysfunction in patients with coronary artery disease
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- Publisher Website: 10.1007/s12012-010-9071-1
- Scopus: eid_2-s2.0-77956394303
- PMID: 20383667
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| Title | Mitochondrial dysfunction induced by statin contributes to endothelial dysfunction in patients with coronary artery disease | ||||||
|---|---|---|---|---|---|---|---|
| Authors | Dai, YL2 Luk, TH2 Siu, CW1 2 Yiu, KH2 Chan, HT2 Lee, SWL2 Li, SW4 Tam, S3 Fong, B3 Lau, CP2 Tse, HF1 2 | ||||||
| Keywords | Endothelial dysfunction Mitochondrial dysfunction Statin | ||||||
| Issue Date | 2010 | ||||||
| Publisher | Humana 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?] DOI: http://dx.doi.org/10.1007/s12012-010-9071-1 | ||||||
| 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 (> 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. | ||||||
| ISSN | 1530-7905 2011 Impact Factor: 2.067 2011 SCImago Journal Rankings: 0.160 | ||||||
| DOI | http://dx.doi.org/10.1007/s12012-010-9071-1 | ||||||
| ISI Accession Number ID | WOS:000277709900006
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 | References in Scopus | ||||||
| Grants | Relationship between mitochondrial dysfunction and vascular function in patients with cardiovascular diseases |
| dc.contributor.author | Dai, YL | ||||||
|---|---|---|---|---|---|---|---|
| dc.contributor.author | Luk, TH | ||||||
| dc.contributor.author | Siu, CW | ||||||
| dc.contributor.author | Yiu, KH | ||||||
| dc.contributor.author | Chan, HT | ||||||
| dc.contributor.author | Lee, SWL | ||||||
| dc.contributor.author | Li, SW | ||||||
| dc.contributor.author | Tam, S | ||||||
| dc.contributor.author | Fong, B | ||||||
| dc.contributor.author | Lau, CP | ||||||
| dc.contributor.author | Tse, HF | ||||||
| dc.date.accessioned | 2010-09-06T07:26:49Z | ||||||
| dc.date.available | 2010-09-06T07:26:49Z | ||||||
| dc.date.issued | 2010 | ||||||
| dc.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 (> 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.grant | Relationship between mitochondrial dysfunction and vascular function in patients with cardiovascular diseases | ||||||
| dc.description.grantcode | 101363 | ||||||
| dc.description.nature | Link_to_subscribed_fulltext | ||||||
| dc.identifier.citation | Cardiovascular 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.citeulike | 7047283 | ||||||
| dc.identifier.doi | http://dx.doi.org/10.1007/s12012-010-9071-1 | ||||||
| dc.identifier.epage | 138 | ||||||
| dc.identifier.hkuros | 169690 | ||||||
| dc.identifier.isi | WOS:000277709900006
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.issn | 1530-7905 2011 Impact Factor: 2.067 2011 SCImago Journal Rankings: 0.160 | ||||||
| dc.identifier.issue | 2 | ||||||
| dc.identifier.openurl | | ||||||
| dc.identifier.pmid | 20383667 | ||||||
| dc.identifier.scopus | eid_2-s2.0-77956394303 | ||||||
| dc.identifier.spage | 130 | ||||||
| dc.identifier.uri | http://hdl.handle.net/10722/76964 | ||||||
| dc.identifier.volume | 10 | ||||||
| dc.language | eng | ||||||
| dc.publisher | Humana Press, Inc. The Journal's web site is located at http://www.cardiotox.com | ||||||
| dc.publisher.place | United States | ||||||
| dc.relation.ispartof | Cardiovascular Toxicology | ||||||
| dc.relation.references | References in Scopus | ||||||
| dc.rights | The original publication is available at www.springerlink.com | ||||||
| dc.subject.mesh | Coronary Artery Disease - drug therapy - physiopathology | ||||||
| dc.subject.mesh | Endothelium, Vascular - drug effects - physiopathology | ||||||
| dc.subject.mesh | Hydroxymethylglutaryl-CoA Reductase Inhibitors - adverse effects | ||||||
| dc.subject.mesh | Mitochondria, Heart - drug effects - metabolism | ||||||
| dc.subject.mesh | Mitochondrial Diseases - chemically induced - metabolism | ||||||
| dc.subject | Endothelial dysfunction | ||||||
| dc.subject | Mitochondrial dysfunction | ||||||
| dc.subject | Statin | ||||||
| dc.title | Mitochondrial dysfunction induced by statin contributes to endothelial dysfunction in patients with coronary artery disease | ||||||
| dc.type | Article |
Author Affiliations
- The University of Hong Kong Li Ka Shing Faculty of Medicine
- The University of Hong Kong
- Queen Mary Hospital Hong Kong
- Tung Wah Hospital