The E-selectin S128R polymorphism is not a risk factor for coronary artery disease in patients with diabetes mellitus type 2

Abstract

Aim/hypothesis: E-selectin is thought to play a key role in the early stages of vascular disease by facilitating the attachment of leukocytes to the endothelium. Recently, a polymorphism in the E-selectin gene (S128R) has been associated with higher E-selectin levels in patients with diabetes mellitus and with premature coronary artery disease. The impact of the S128R polymorphism on the development of diabetic coronary artery disease has not been investigated yet.

Patients and methods: A total of 254 patients recruited from the Division of Cardiology, University of Vienna with diabetes mellitus type 2 was assessed for the E-selectin S128R polymorphism by a novel mutagenic separated PCR, allowing fast and reliable genotyping without restriction enzyme digest. Ninety-five patients had a history of myocardial infarction, 90 were admitted with stable coronary artery disease whereas in 69 the presence of CAD could be excluded.

Results: Of all 254 individuals tested, 197 (77.6%) exhibited wildtype E-selectin 128S genotype, 54 (21.3%) were heterozygous S128R and 3 (1.1%) were homozygous for the 128R allele. In all groups the genotype frequencies did not differ significantly. No associations were found between E-selectin genotype and coronary artery disease or myocardial infarction.

Conclusion/interpretation: In subjects suffering from diabetes mellitus type 2 the E-selectin S128R polymorphism is not associated with coronary artery disease nor with an increased risk for myocardial infarction. Thus, screening for this polymorphism is not indicated for risk assessment of CAD in patients with diabetes mellitus.