title: Role of aldehyde dehydrogenase 2 Glu504lys polymorphism in acute coronary syndrome.
abstract: 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.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.
authors.forename: Feng
authors.initials: F
authors.lastname: Xu
authors.forename: Yu Guo
authors.initials: YG
authors.lastname: Chen
authors.forename: Li
authors.initials: L
authors.lastname: Xue
authors.forename: Rui Jian
authors.initials: RJ
authors.lastname: Li
authors.forename: He
authors.initials: H
authors.lastname: Zhang
authors.forename: Yuan
authors.initials: Y
authors.lastname: Bian
authors.forename: Cheng
authors.initials: C
authors.lastname: Zhang
authors.forename: Rui Juan
authors.initials: RJ
authors.lastname: Lv
authors.forename: Jin Bo
authors.initials: JB
authors.lastname: Feng
authors.forename: Yun
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D054058:Acute Coronary Syndrome / Q000000981:diagnostic imaging / Q000201:enzymology* / Q000235:genetics* / Q000503:physiopathology; D000444:Aldehyde Dehydrogenase / Q000235:genetics*; D000071396:Aldehyde Dehydrogenase, Mitochondrial; D019943:Amino Acid Substitution / Q000235:genetics*; D001916:Brachial Artery / Q000503:physiopathology; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D002452:Cell Count; D002465:Cell Movement; D003710:Demography; D042783:Endothelial Cells / Q000166:cytology / Q000378:metabolism; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000201:enzymology / Q000235:genetics / Q000503:physiopathology; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism; D014463:Ultrasonography; D014664:Vasodilation / Q000502:physiology
chemical_list: D002097:C-Reactive Protein; C096127:ALDH2 protein, human; D000444:Aldehyde Dehydrogenase; D000071396:Aldehyde Dehydrogenase, Mitochondrial