title: Polymorphism of the apolipoprotein E and angiotensin-converting enzyme genes in Japanese subjects with silent myocardial ischemia.
abstract: The apolipoprotein epsilon4 allele and homozygous deletion allele (DD) of the angiotensin-converting enzyme gene are reported to be associated with an increase in the incidence of ischemic heart disease. In this study, we examined whether the apolipoprotein epsilon4 genotype and angiotensin-converting enzyme/DD allele are associated with silent myocardial ischemia. We screened 3920 subjects undergoing general checkups who no symptoms of ischemic heart disease. Seventy subjects (2 percent) showed ischemic ST-segment depression during the double two-step exercise test. One hundred and twenty control subjects without ischemic ST-segment depression were recruited from the same population and matched for sex, age, and blood pressure. We performed genotyping of the apolipoprotein E gene (epsilon2, epsilon3, and epsilon4) and angiotensin-converting enzyme gene (I and D) using polymerase chain reaction-restriction fragment length polymorphism and polymerase chain reaction, respectively. Allele frequently of epsilon4 of the apolipoprotein E gene was higher in the ischemic group (11 percent) than the nonischemic group (5 percent) (chi2 = 5.35, P < .05), but there was no significant association between the allele or the genotype frequency of the angiotensin-converting enzyme gene and the incidence of ischemic ST-segment depression. Furthermore, stepwise multiple regression analysis also revealed that total cholesterol level and epsilon4 genotype were predictors of ischemic change in the exercise tolerance test (chi2 = 12.8, P < .005, R(2) = .051). These results suggest that the apolipoprotein epsilon4 allele is an independent genetic risk factor for silent myocardial ischemia in Japanese subjects.
authors.affiliation: Department of Geriatric Medicine, Osaka University Medical School, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Nakata
authors.forename: T
authors.initials: T
authors.lastname: Katsuya
authors.forename: H
authors.initials: H
authors.lastname: Rakugi
authors.forename: S
authors.initials: S
authors.lastname: Takami
authors.forename: M
authors.initials: M
authors.lastname: Ohishi
authors.forename: K
authors.initials: K
authors.lastname: Kamino
authors.forename: J
authors.initials: J
authors.lastname: Higaki
authors.forename: Y
authors.initials: Y
authors.lastname: Tabuchi
authors.forename: Y
authors.initials: Y
authors.lastname: Kumahara
authors.forename: T
authors.initials: T
authors.lastname: Miki
authors.forename: T
authors.initials: T
authors.lastname: Ogihara
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D001057:Apolipoproteins E / Q000235:genetics*; D002784:Cholesterol / Q000097:blood; D005080:Exercise Test; D005260:Female; D005838:Genotype; D006801:Humans; D007564:Japan; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000208:ethnology / Q000235:genetics*; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: D001057:Apolipoproteins E; D002784:Cholesterol; D007703:Peptidyl-Dipeptidase A