Relationship between severity of coronary artery disease and apolipoprotein E gene polymorphism.

OBJECTIVE: To explore the possible contribution of the apolipoprotein (apo) E polymorphisms to the extent and severity of coronary artery disease (CAD) related to lipid metabolism. METHODS: Overall, 53 Turkish patients, aged 54+/-11 years defined by coronary angiography were included in this cross-sectional study. Reardon's coronary artery scoring was used. Serum lipids were measured with enzymatic colorimetric methods. Apolipoproteins were measured with nephelometry. Apolipoprotein E gene polymorphisms were determined by the reverse hybridization method. Statistical analyses were performed using one-way ANOVA, Kruskal-Wallis and Chi- square tests. RESULTS: The genotype frequencies were 7.5% for E2/E3, 77.4% for E3/E3 and 15.1% for E3/E4. The E2 allele frequency was slightly lower than E4 allele. There were no significant differences between apo E2/E3, E3/E3 and E3/E4 genotypes for severity scorings (26, 41 and 32 respectively, p=0.30) and extent scorings (3.2, 5.5, 4.5, p=0.17). It was found that the most of patients who had E2/3 and E3/4 alleles had low severity scores. On the other hand, there were no significant score difference for patients who had E3/3 alleles. Lipids were not significantly different among the different genotypes. The E3 allele was associated with high apo B levels compared with E2 and E4 genotypes. It was found that severity and extent of disease were not related with lipid metabolism. CONCLUSION: We concluded that there were no statistically significant differences between genotypes for extent and severity scorings, but the apo E3 allele is associated with more severe disease than E2 allele. These associations with severity were mediated not only by changes in lipid metabolism but may be also by other mechanisms in CAD patients.

Evaluation of insulin resistance in normoglycemic patients with coronary artery disease.

BACKGROUND: Insulin resistance is clearly associated with coronary artery disease (CAD) in diabetics. Insulin resistance may also be present in normoglycemic individuals, and some of these patients can be diagnosed as having metabolic syndrome (MS) according to various definitions. However, the relationship between hyperinsulinemia and CAD is obscure in normoglycemic individuals, especially in patients who do not meet the criteria for MS. HYPOTHESIS: This study evaluated insulin resistance in normoglycemic patients with CAD, and investigated the association of insulin resistance with inflammation and lipid levels. METHODS: Fifty-six CAD patients, and 57 age- and sex-matched controls with normal coronary arteries confirmed by conventional coronary arteries angiography were included in the study. Participants were considered for the diagnosis of MS according to criteria of the National Cholesterol Education Program (NCEPATP III) and the International Diabetes Federation (IDF). Fasting plasma glucose, insulin, lipids, and c-reactive protein (CRP) levels were studied. The homeostasis model assessment insulin resistance index (HOMA IR) was calculated. RESULTS: The ratio of subjects with MS was similar in the 2 groups. Insulin, CRP, low-density lipoprotein (LDL) cholesterol, and HOMA IR were higher in the study group than in the controls. The HOMA IR, LDL cholesterol, and serum CRP levels were determined as predictors of CAD. CONCLUSION: Our data revealed that insulin resistance and subclinical inflammation are present in normoglycemic patients with CAD. As the proportion of patients with MS was similar in the 2 groups, we suggest that HOMA IR values may provide more sensitive information than MS definitions about the association between insulin resistance and CAD in normoglycemic patients.