title: Relation of genetic polymorphisms of apolipoprotein E, angiotensin converting enzyme, apolipoprotein B-100, and glycoprotein IIIa and early-onset coronary heart disease.
abstract: OBJECTIVE
  Apolipoprotein E (APOE) E4, apolipoprotein B-100 (APOB) Q3611 allele, the angiotensin converting enzyme (ACE) deletion (D) allele and glycoprotein IIIa (GP3A) P33 mutant allele are reported to predispose to early-onset coronary heart disease (CHD). These associations were not all confirmed in more recent studies. To determine the impact of these alleles on CHD, we examined the prevalence of these mutations in patients presenting with early-onset CHD and compared them to those manifesting CHD later in life. The delayed-onset was considered a sign of longevity and would serve as a comparative group to assess prevalence of the biochemical and genetic risk factors.
  
  
  METHODS
  300 patients with a history of myocardial infarction or angina pectoris and angiographically documented CHD were studied. Patients were divided into two groups: group 1 (G1 = 150 patients) presenting with these findings under the age of 50 years; while group 2 (G2 = 150 patients) were patients presenting for the first time over the age of 65 years. Prevalence of the alleles of APOE, APOB, ACE and GP3A was assessed by molecular analysis. An association of any of these genotypes with early onset CHD could lead to a higher prevalence in the younger age group.
  
  
  CONCLUSIONS
  None of the suspected alleles namely APOB Q3611 [G1: 10.7% vs. G2: 9.0%, p = 0.57], ACE D (G1: 52.0% vs. G2: 49.7%, p = 0.57), or the GP3A P33 (G1: 17.3% vs. G2: 15.7%; p = 0.58) showed any significant difference between the two groups. Subjects with APOE E4 were more frequent in the younger age group (G1: 18.3% vs. G2: 13.7%; p = 0.047), while APOE E2 was more frequent in G2 (G2: 10.0% vs. G1: 2.7%; p = 0.0002). Multivariate analysis showed an odds ratio of APOE E2 allele in G1 of 0.27 with a confidence interval of 0.10-0.73.
authors.affiliation: Department of Pathology, Dalhousie University Faculty of Medicine, Nova Scotia, Canada.
authors.forename: B A
authors.initials: BA
authors.lastname: Nassar
authors.forename: J
authors.initials: J
authors.lastname: Dunn
authors.forename: L M
authors.initials: LM
authors.lastname: Title
authors.forename: B J
authors.initials: BJ
authors.lastname: O'Neill
authors.forename: S A
authors.initials: SA
authors.lastname: Kirkland
authors.forename: E
authors.initials: E
authors.lastname: Zayed
authors.forename: I R
authors.initials: IR
authors.lastname: Bata
authors.forename: R C
authors.initials: RC
authors.lastname: Cantrill
authors.forename: J
authors.initials: J
authors.lastname: Johnstone
authors.forename: G I
authors.initials: GI
authors.lastname: Dempsey
authors.forename: M H
authors.initials: MH
authors.lastname: Tan
authors.forename: W C
authors.initials: WC
authors.lastname: Breckenridge
authors.forename: D E
authors.initials: DE
authors.lastname: Johnstone
mesh_terms: D000328:Adult; D017668:Age of Onset; D000368:Aged; D000704:Analysis of Variance; D053299:Apolipoprotein B-100; D001055:Apolipoproteins B / Q000235:genetics*; D001057:Apolipoproteins E / Q000235:genetics*; D003327:Coronary Disease / Q000235:genetics* / Q000401:mortality; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008136:Longevity; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000235:genetics*; D011110:Polymorphism, Genetic; D012307:Risk Factors; D015996:Survival Rate
chemical_list: D053299:Apolipoprotein B-100; D001055:Apolipoproteins B; D001057:Apolipoproteins E; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D007703:Peptidyl-Dipeptidase A