Gene polymorphisms and acute coronary syndrome
Abstract
Background: Genetic variants in factors that modulate inflammation, endothelial function, lipid metabolism and thrombosis could influence individual susceptibility to coronary artery disease. The aim of our study was to investigate the effect of interleukin-6 (IL-6), endothelial nitric oxide synthase (eNOS), apolipoprotein E (apoE), platelet glycoprotein receptor IIIa (GPIIIa), tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) gene polymorphisms on risk of developing acute coronary syndrome (ACS) in a group of Slovenian individuals.
Methods: We examined 180 subjects, 100 patients with ACS as a first clinical manifestation of obstructive coronary artery disease and 80 age- and gender-matched healthy individuals. Polymorphic sites of the IL-6, eNOS, apoE, GPIIIa, t-PA and PAI-1 genes were determined by polymerase chain reaction.
Results: The IL-6 -174C allele (CC+GC genotypes) and the eNOS TT genotype occurred significantly more frequently in ACS patients then in controls (66 % vs. 51 % and 20 % vs. 9 %, respectively; both p < 0.05). There was no significant difference in the distribution of the eNOS 4a/b, apoE ε 2/ ε 3/ ε 4, GPIIIa PIA1/PIA2, t-PA I/D and PAI-1 4G/5G genotypes between the two groups. By multivariate regression analysis adjusting for traditional risk predictors, the -174C IL-6 allele conferred a 3.0-fold increased risk for ACS (95 % CI 1.2–7.2; p < 0.05) in our study population.
Conclusions: In the present study, the IL-6 -174G/C polymorphism emerged as an independent factor for ACS risk. The eNOS G/T genotype distribution differed significantly between the two groups, but in adjusted analyses its effect was blunted by traditional risk factors. No association between the eNOS 4a/b, apoE ε 2/ ε 3/ ε 4, GPIIIa PIA1/PIA2, t-PA I/D and PAI-1 4G/5G gene polymorphisms and ACS was established.
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References
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