title: Platelet-activating factor-acetylhydrolase A379V (exon 11) gene polymorphism is an independent and functional risk factor for premature myocardial infarction.
abstract: BACKGROUND
  Oxidation of low density lipoproteins is an initial step of atherogenesis that generates pro-inflammatory phospholipids, including platelet-activating factor (PAF). PAF is degraded by PAF-acetylhydrolase (PAF-AH), which has been postulated to be a risk factor for myocardial infarction (MI). The role of PAF-AH for the onset of premature MI is unclear.
  
  
  METHODS
  Polymorphisms located in putatively functional regions were investigated in a cohort of patients having premature MI onset prior to 46 years of age (n = 200) and a sex-age-matched control group (n = 200). The activity of PAF-AH and coronary angiograms were evaluated for the severity of coronary atherosclerosis.
  
  
  RESULTS
  The V allele of A379V (exon 11) polymorphism on PAF-AH gene was more frequent in patients with premature MI (P = 0.001). This V allele polymorphism was also associated with a lower activity of plasma PAF-AH and a more complex coronary atherosclerosis (p Trends <0.05). Multiple logistic regression analysis showed that this polymorphism was an independent risk factor (Odds Ratio [OR] 1.66, 95% CI 1.14.1 to 5.80, P = 0.008) as well as smoking (OR 3.72, 95% CI 1.77 to 9.28, P = 0.001), diabetes mellitus (OR 2.25, 95% CI 1.40 to 5.32, P = 0.007) and hypertension (OR 1.88, 95% CI 1.25 to 5.36, P = 0.003) for the onset of premature MI.
  
  
  CONCLUSIONS
  We conclude that a functional and significant association between the A379V polymorphism on exon 11 of PAF-AH gene and premature MI exists in this Taiwanese population. This polymorphism is significantly associated with the PAF-AH activity and the severity of coronary atherosclerosis.
authors.affiliation: Division of Cardiology, Departments of Internal Medicine, National Cheng-Kung University Medical Center, 138 Sheng-Li Road, Tainan 704, Taiwan.
authors.forename: P-Y
authors.initials: PY
authors.lastname: Liu
authors.forename: Y-H
authors.initials: YH
authors.lastname: Li
authors.forename: H-L
authors.initials: HL
authors.lastname: Wu
authors.forename: T-H
authors.initials: TH
authors.lastname: Chao
authors.forename: L-M
authors.initials: LM
authors.lastname: Tsai
authors.forename: L-J
authors.initials: LJ
authors.lastname: Lin
authors.forename: G-Y
authors.initials: GY
authors.lastname: Shi
authors.forename: J-H
authors.initials: JH
authors.lastname: Chen
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase / Q000235:genetics*; D000328:Adult; D017668:Age of Onset; D015331:Cohort Studies; D005091:Exons; D005260:Female; D005838:Genotype; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000201:enzymology / Q000235:genetics*; D010741:Phospholipases A / Q000378:metabolism; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: D010741:Phospholipases A; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase