Relation of genetic polymorphisms of apolipoprotein E, angiotensin converting enzyme, apolipoprotein B-100, and glycoprotein IIIa and early-onset coronary heart disease

Citation
Ba. Nassar et al., Relation of genetic polymorphisms of apolipoprotein E, angiotensin converting enzyme, apolipoprotein B-100, and glycoprotein IIIa and early-onset coronary heart disease, CLIN BIOCH, 32(4), 1999, pp. 275-282
Citations number
71
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
CLINICAL BIOCHEMISTRY
ISSN journal
00099120 → ACNP
Volume
32
Issue
4
Year of publication
1999
Pages
275 - 282
Database
ISI
SICI code
0009-9120(199906)32:4<275:ROGPOA>2.0.ZU;2-5
Abstract
Objective: Apolipoprotein E (APOE) E4, apolipoprotein 8-100 (APOB) Q3611 al lele, the angiotensin converting enzyme (ACE) deletion (D) allele and glyco protein IIIa (GP3A) P33 mutant allele are reported to predispose to early-o nset coronary heart disease (CHD). These associations were not all confirme d in more recent studies. To determine the impact of these alleles on CHD, we examined the prevalence of these mutations in patients presenting with e arly-onset CHD and compared them to those manifesting CHD rater in rife. Th e delayed-onset was considered a sign of longevity and would serve as a com parative group to assess prevalence of the biochemical and genetic risk fac tors. Methods: 300 patients with a history of myocardial infarction or angina pec toris and angiographically documented CHD were studied. Patients were divid ed into two groups: group 1 (G1 = 150 patients) presenting with these findi ngs under the age of 50 years; while group 2 (G2 = 150 patients) were patie nts presenting for the first time over the age of 65 years. Prevalence of t he 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. Results and Conclusions: None of the suspected alleles namely APOB Q3611 [G 1: 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 significan t difference between the two groups. Subjects with APOE E4 were more freque nt in the younger age group (G1. 18.3% vs. G2: 13.7%; p = 0.047), while APO E E2 was more frequent in G2 (G2: 10.0% vs. G1: 2.7%; p = 0.0002). Multivar iate analysis showed an odds ratio of APOE E2 allele in G1 of 0.27 with a c onfidence interval of 0.10-0.73. Copyright (C) 1999 The Canadian Society of Clinical Chemists.