title: Plasminogen activator inhibitor-1 promoter 4G/5G genotype is not a risk factor for myocardial infarction in a Japanese population.
abstract: There is little question that the blood clotting process is triggered and causes the vascular occlusion associated with myocardial infarction. Although it is less clear what part blood coagulation events might play in the etiology of coronary artery disease, impaired regulation of anticoagulation or fibrinolysis might be involved. Among anticoagulant and fibrinolytic factors, an elevated plasma plasminogen activator inhibitor-1 (PAI-1) concentration has been identified as a risk factor for the development of myocardial infarction. An association between one polymorphism of the PAI-1 promoter (4G/5G single nucleotide deletion/ insertion at position -675) and plasma PAI-1 levels was described in 1995. However, most recent studies seem to point to the lack of such an association. This is the first report on the frequency of this polymorphism in the Japanese population with respect to the risk of myocardial infarction. Sixty-six patients with myocardial infarction and sixty-two healthy control patients were chosen for the analysis of the PAI-1 promoter 4G/5G genotype with polymerase chain reaction-single strand conformation polymorphism. Five myocardial infarction patients and six in the control group were homozygous for the 4G/4G genotype. Twenty-eight and 27 4G/5G and 33 and 29 5G/5G genotypes were found in myocardial infarction and control groups, respectively. The total frequencies of the 4G and 5G alleles were approximately 30% and 70% in both control and myocardial infarction groups. In conclusion, the PAI-1 promoter genotype is not a risk factor for myocardial infarction in the Japanese population. This is in contrast to the first report in Caucasians, suggesting an interaction with other genetic or environmental factors which influences the risk of myocardial infarction.
authors.affiliation: The Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Sugano
authors.forename: H
authors.initials: H
authors.lastname: Tsuji
authors.forename: H
authors.initials: H
authors.lastname: Masuda
authors.forename: K
authors.initials: K
authors.lastname: Nakagawa
authors.forename: H
authors.initials: H
authors.lastname: Nishimura
authors.forename: T
authors.initials: T
authors.lastname: Kasahara
authors.forename: M
authors.initials: M
authors.lastname: Yoshizumi
authors.forename: Y
authors.initials: Y
authors.lastname: Nakahara
authors.forename: H
authors.initials: H
authors.lastname: Kitamura
authors.forename: K
authors.initials: K
authors.lastname: Yamada
authors.forename: M
authors.initials: M
authors.lastname: Yoneda
authors.forename: K
authors.initials: K
authors.lastname: Maki
authors.forename: T
authors.initials: T
authors.lastname: Tatsumi
authors.forename: A
authors.initials: A
authors.lastname: Azuma
authors.forename: M
authors.initials: M
authors.lastname: Nakagawa
mesh_terms: D000368:Aged; D044466:Asian People / Q000235:genetics*; D005260:Female; D005838:Genotype; D006801:Humans; D015994:Incidence; D007564:Japan / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology / Q000235:genetics*; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics*; D016133:Polymerase Chain Reaction / Q000379:methods; D018807:Polymorphism, Single-Stranded Conformational; D011401:Promoter Regions, Genetic; D012307:Risk Factors
chemical_list: D017395:Plasminogen Activator Inhibitor 1