title: The apolipoprotein epsilon2 allele and the severity of coronary artery disease in Type 2 diabetic patients.
abstract: OBJECTIVE
  To examine the hypothesis that apolipoprotein E2 is associated with more severe coronary disease in Type 2 diabetic patients.
  
  
  METHODS
  In this retrospective cohort study, 491 patients with angiographically assessed coronary disease were recruited from those attending a university hospital cardiology department. Participants completed detailed questionnaires, from which the presence or absence of diabetes was determined. Fasting blood samples were obtained for apolipoprotein E genotype and measurement of blood lipid parameters.
  
  
  RESULTS
  The prevalence of triple vessel disease was significantly lower in non-diabetic, epsilon2 allele carriers (39.3% vs. 16.2%; odds ratio (OR) 0.30 (0.12-0.71), P < 0.03) compared with E3/3 carriers. In Type 2 diabetic patients, epsilon2 allele carriers had an excess of triple vessel disease compared with E3/3 genotypes (43.3 vs. 68.8%; OR 2.8 (1.07-7.30), P < 0.05). The differences were independent of other variables. The apo E4 subgroup showed no significant differences in the frequency of triple vessel disease.
  
  
  CONCLUSIONS
  Diabetic epsilon2 allele carriers had more severe coronary artery disease than diabetic patients with other apo E isoforms. In non-diabetic patients the epsilon2 allele appeared to protect against severe coronary disease. We hypothesize that interaction between the diabetic milieu and the epsilon2 allele accelerates plaque progression. It suggests that diabetic patients who are carriers of the epsilon2 allele, even in the heterozygous form, should be the focus of particular therapeutic attention. Diabet. Med. 18, 445-450 (2001)
authors.affiliation: Clinical Diabetes Unit, Division of Endocrinology and Diabetology, University Hospital, 1211 Geneva 4, Switzerland.
authors.forename: B
authors.initials: B
authors.lastname: Kalix
authors.forename: M C
authors.initials: MC
authors.lastname: Meynet
authors.forename: M C
authors.initials: MC
authors.lastname: Garin
authors.forename: R W
authors.initials: RW
authors.lastname: James
mesh_terms: D016632:Apolipoprotein A-I / Q000097:blood; D053329:Apolipoprotein E2; D001055:Apolipoproteins B / Q000097:blood; D001057:Apolipoproteins E / Q000235:genetics*; D001786:Blood Glucose / Q000032:analysis; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D015243:Cholesterol, VLDL / Q000097:blood; D015331:Cohort Studies; D003327:Coronary Disease / Q000097:blood / Q000453:epidemiology / Q000235:genetics / Q000503:physiopathology*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000235:genetics* / Q000503:physiopathology*; D005260:Female; D006580:Genetic Carrier Screening; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D015995:Prevalence; D012189:Retrospective Studies; D011795:Surveys and Questionnaires; D013557:Switzerland; D014280:Triglycerides / Q000097:blood
chemical_list: D016632:Apolipoprotein A-I; D053329:Apolipoprotein E2; D001055:Apolipoproteins B; D001057:Apolipoproteins E; D001786:Blood Glucose; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D015243:Cholesterol, VLDL; D014280:Triglycerides; D002784:Cholesterol