Document Detail


Role of aldehyde dehydrogenase 2 Glu504lys polymorphism in acute coronary syndrome.
MedLine Citation:
PMID:  21958412     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular and molecular medicine     Volume:  15     ISSN:  1582-4934     ISO Abbreviation:  J. Cell. Mol. Med.     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-09-30     Completed Date:  2012-01-05     Revised Date:  2012-06-11    
Medline Journal Info:
Nlm Unique ID:  101083777     Medline TA:  J Cell Mol Med     Country:  England    
Other Details:
Languages:  eng     Pagination:  1955-62     Citation Subset:  IM    
Copyright Information:
© 2011 The Authors Journal compilation © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
Affiliation:
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:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Acute Coronary Syndrome / 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:
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:
J Cell Mol Med. 2012 May;16(5):1155

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Dissolution Parameters Reveal Role of Structure and Solvent in Molecular Gelation.
Next Document:  Tris(triazolyl) Calix[6]arene-Based Zinc and Copper Funnel Complexes: Imidazole-like or Pyridine-lik...