title: Polymorphism of the apolipoprotein E and angiotensin I converting enzyme genes in Japanese patients with myocardial infarction.
abstract: OBJECTIVE
  To investigate the genetic contribution for myocardial infarction.
  
  
  METHODS
  We investigated common polymorphisms of apolipoprotein E gene and angiotensin converting enzyme (ACE) gene in Japanese population. Subjects were 422 healthy people and 254 patients with myocardial infarction. We evaluated the 287 base pair (bp) insertion (I)/deletion (D) polymorphism in intron 16 of the ACE gene and a polymorphism in the apolipoprotein E gene by using the polymerase chain reaction.
  
  
  RESULTS
  The ACE genotype prevalences for II, ID, and DD were 36.2, 46.1, and 17.7%, respectively, among the myocardial infarction patients. The prevalence of the D allele of the ACE gene among the myocardial infarction patients (0.593) exceeded that among the healthy controls (0.407). The prevalences of the epsilon 2, epsilon 3, and epsilon 4 alleles of the apolipoprotein E genotype among healthy controls were 0.024, 0.882, and 0.094, and those among survivors of myocardial infarction were 0.024, 0.834, and 0.142, respectively. Myocardial infarction patients had an excessive prevalence of the apolipoprotein E epsilon 4 allele (P < 0.05). Multiple regression analysis demonstrated that the independent risk factors for developing myocardial infarction were age, DD genotype of ACE gene, and apolipoprotein E epsilon 4 allele. Stenotic coronary vessels in myocardial infarction patients did not differ significantly among the patients with various ACE and apolipoprotein E genotypes in the present study.
  
  
  CONCLUSIONS
  Among the Japanese, apolipoprotein E epsilon 4 carriers and subjects with ACE DD genotype are at an increased risk of myocardial infarction.
authors.affiliation: Second Department of Internal Medicine, Iwate Medical University, Morioka, Japan. knakai@iwate-med.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Nakai
authors.forename: T
authors.initials: T
authors.lastname: Fusazaki
authors.forename: T
authors.initials: T
authors.lastname: Zhang
authors.forename: T
authors.initials: T
authors.lastname: Shiroto
authors.forename: M
authors.initials: M
authors.lastname: Osawa
authors.forename: J
authors.initials: J
authors.lastname: Kamata
authors.forename: M
authors.initials: M
authors.lastname: Itoh
authors.forename: K
authors.initials: K
authors.lastname: Nakai
authors.forename: W
authors.initials: W
authors.lastname: Habano
authors.forename: T
authors.initials: T
authors.lastname: Kiuchi
authors.forename: S
authors.initials: S
authors.lastname: Yamamori
authors.forename: K
authors.initials: K
authors.lastname: Hiramori
mesh_terms: D000368:Aged; D000483:Alleles; D001057:Apolipoproteins E / Q000235:genetics*; D001483:Base Sequence; D005260:Female; D005838:Genotype; D006801:Humans; D007438:Introns / Q000235:genetics; D007564:Japan; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D009203:Myocardial Infarction / Q000201:enzymology / Q000208:ethnology / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D016133:Polymerase Chain Reaction / Q000379:methods; D011110:Polymorphism, Genetic / Q000235:genetics*; D012307:Risk Factors
chemical_list: D001057:Apolipoproteins E; D007703:Peptidyl-Dipeptidase A