The apolipoprotein epsilon 2 allele and the severity of coronary artery disease in Type 2 diabetic patients

Citation
B. Kalix et al., The apolipoprotein epsilon 2 allele and the severity of coronary artery disease in Type 2 diabetic patients, DIABET MED, 18(6), 2001, pp. 445-450
Citations number
26
Categorie Soggetti
Endocrynology, Metabolism & Nutrition
Journal title
DIABETIC MEDICINE
ISSN journal
07423071 → ACNP
Volume
18
Issue
6
Year of publication
2001
Pages
445 - 450
Database
ISI
SICI code
0742-3071(200106)18:6<445:TAE2AA>2.0.ZU;2-8
Abstract
Aims To examine the hypothesis that apolipoprotein E2 is associated with mo re severe coronary disease in Type 2 diabetic patients. Research design and methods In this retrospective cohort study, 491 patient s with angiographically assessed coronary disease were recruited from those attending a university hospital cardiology department. Participants comple ted detailed questionnaires, from which the presence or absence of diabetes was determined. Fasting blood samples were obtained for apolipoprotein E g enotype 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 p atients, epsilon2 allele carriers had an excess of triple vessel disease co mpared 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 sh owed no significant differences in the frequency of triple vessel disease. Conclusions Diabetic epsilon2 allele carriers had more severe coronary arte ry disease than diabetic patients with other apo E isoforms. In non-diabeti c patients the epsilon2 allele appeared to protect against severe coronary disease. We hypothesize that interaction between the diabetic milieu and th e 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.