title: Arg389Gly polymorphism of the human beta1-adrenergic receptor in patients with nonfatal acute myocardial infarction.
abstract: BACKGROUND
  We sought to investigate the relation between the Arg389Gly polymorphism in the human beta1-adrenergic receptor (ADRB1) gene and acute myocardial infarction (AMI). It was previously reported that augmented sympathetic activity might play an important role as a trigger of AMI by enhanced hemodynamic or mechanical forces through ADRB1 activation. Recently, a common polymorphism has been identified at amino acid position 389 (Arg or Gly) of the human ADRB1, within a region important for receptor-Gs protein coupling and subsequent agonist-stimulated adenylyl cyclase activation.
  
  
  METHODS
  To investigate the relation between the Arg389Gly polymorphism in the ADRB1 gene and AMI, we genotyped 354 patients with AMI and 354 age- and sex-matched control subjects by use of polymerase chain reaction amplification and the restriction fragment length polymorphism analysis.
  
  
  RESULTS
  The prevalence of the Arg389 homozygote (CC) genotype was significantly more frequent in patients with AMI than in control subjects (68.1% vs 47.2%, P <.0001). In logistic regression models, the odds ratio (OR) of Arg389 homozygote (CC) versus Arg389Gly heterozygote (CG) + Gly389 homozygote (GG) genotypes between control subjects and patients with AMI was 2.86 (95% CI 1.92-4.26, P =.0001). The association of the Arg389Gly polymorphism of ADRB1 with AMI was statistically significant and independent of other risk factors.
  
  
  CONCLUSIONS
  Our findings suggest that the genotype of Arg389Gly polymorphism in the human ADRB1 gene is associated with AMI.
authors.affiliation: Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
authors.forename: Chikao
authors.initials: C
authors.lastname: Iwai
authors.forename: Hozuka
authors.initials: H
authors.lastname: Akita
authors.forename: Kenji
authors.initials: K
authors.lastname: Kanazawa
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Shiga
authors.forename: Masahiro
authors.initials: M
authors.lastname: Terashima
authors.forename: Yasuaki
authors.initials: Y
authors.lastname: Matsuda
authors.forename: Eiji
authors.initials: E
authors.lastname: Takai
authors.forename: Yoshitomo
authors.initials: Y
authors.lastname: Miyamoto
authors.forename: Masakatsu
authors.initials: M
authors.lastname: Shimizu
authors.forename: Teishi
authors.initials: T
authors.lastname: Kajiya
authors.forename: Takatoshi
authors.initials: T
authors.lastname: Hayashi
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Yokoyama
mesh_terms: D000368:Aged; D000483:Alleles; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics*; D011110:Polymorphism, Genetic; D018342:Receptors, Adrenergic, beta-1 / Q000235:genetics*; D013223:Statistics as Topic
chemical_list: D018342:Receptors, Adrenergic, beta-1