| Role of aldehyde dehydrogenase 2 Glu504lys polymorphism in acute coronary syndrome. | |
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MedLine Citation:
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PMID: 21958412 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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This study aimed to investigate the association of the aldehyde dehydrogenase 2 (ALDH2) Glu504Lys polymorphism, which exists in 30-50% of East Asians, and risk of acute coronary syndrome (ACS). We enrolled 1092 unrelated Han Chinese, including 546 with ACS and 546 age- and sex-matched controls. Subjects with ALDH2 mutant genotypes showed significantly higher ACS than did controls (46.7% versus 31.9%, P < 0.001). Logistic regression analysis revealed the ALDH2 mutant independently associated with ACS (odds ratio [OR] 1.95, 95% confidence interval [CI]: 1.31-2.92, P = 0.001), but the association was weaker on adjusting for alcohol consumption (OR 1.82, 95% CI: 1.23-2.70, P = 0.003). Similar results were found in a subgroup analysis of patients with primary ST-segment elevation myocardial infarction (STEMI). The ALDH2 mutant was significantly associated with level of high-sensitivity C-reactive protein (hs-CRP) in patients with ACS (P = 0.002) and in controls (P = 0.009) and number of circulating endothelial progenitor cells (EPCs) (P = 0.032); furthermore, inclusion of hs-CRP level and EPCs number as independent variables in regression analysis reduced the importance of ALDH2 polymorphism in ACS or primary STEMI. However, ALDH2 polymorphism was not associated with number of coronary arteries with significant stenosis, Gensini score or flow-mediated dilation of the brachial artery. Our results suggest that ALDH2 mutation is a genetic risk marker for ACS, which is explained in part by alcohol consumption, inflammation and number of circulating EPCs. |
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Authors:
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Feng Xu; Yu Guo Chen; Li Xue; Rui Jian Li; He Zhang; Yuan Bian; Cheng Zhang; Rui Juan Lv; Jin Bo Feng; Yun Zhang |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of cellular and molecular medicine Volume: 15 ISSN: 1582-4934 ISO Abbreviation: J. Cell. Mol. Med. Publication Date: 2011 Sep |
Date Detail:
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Created Date: 2011-09-30 Completed Date: 2012-01-05 Revised Date: 2012-06-11 |
Medline Journal Info:
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Nlm Unique ID: 101083777 Medline TA: J Cell Mol Med Country: England |
Other Details:
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Languages: eng Pagination: 1955-62 Citation Subset: IM |
Copyright Information:
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© 2011 The Authors Journal compilation © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd. |
Affiliation:
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The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of Shandong University, Ji'nan, [corrected] China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute Coronary Syndrome
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enzymology*,
genetics*,
physiopathology,
ultrasonography Aldehyde Dehydrogenase / genetics* Amino Acid Substitution / genetics* Brachial Artery / physiopathology C-Reactive Protein / metabolism Case-Control Studies Cell Count Cell Movement Demography Endothelial Cells / cytology, metabolism Female Genetic Predisposition to Disease* Humans Male Middle Aged Myocardial Infarction / enzymology, genetics, physiopathology, ultrasonography Polymorphism, Single Nucleotide / genetics* Stem Cells / cytology, metabolism Vasodilation / physiology |
| Chemical | |
Reg. No./Substance:
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9007-41-4/C-Reactive Protein; EC 1.2.1.3/ALDH2 protein, human; EC 1.2.1.3/Aldehyde Dehydrogenase |
| Comments/Corrections | |
Erratum In:
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J Cell Mol Med. 2012 May;16(5):1155 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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