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Title: Glycoprotein IIIa gene polymorphism and coronary artery disease
Author(s): A. Aydinalp , I. Atar , F.B. Atac , A.C. Yazici , M. Cicek , M. Yilmaz , A. Ozgul , A. Atar , M.E. Korkmaz , B. Özin , H. Müderrisoglu
Journal: Acta Cardiologica
Volume: 65    Issue: 2   Date: 2010   
Pages: 225-230
DOI: 10.2143/AC.65.2.2047058

Abstract :
Objective — Prevalence of glycoprotein IIIa gene polymorphisms (PlA2) has been reported to be elevated in persons who die of sudden death. PlA2 has been suggested as contributing to the development of atherosclerosis via coronary plaque rupture and thrombus formation. In this prospective study, we investigated the correlation between the PlA2 polymorphism, atherosclerotic plaque burden, and its prognostic significance.
Methods and results — One hundred and seventy-eight patients (mean age 51 ± 9.6 years) suspected to have atherosclerotic coronary artery disease underwent a coronary angiography and were evaluated for gene polymorphisms. Patients were followed up for 4 years for major adverse cardiac events (MACE). Thirty-eight patients (21%) had the PlA2 polymorphism. There was no statistically significant correlation between presence of atherosclerotic plaque burden, severity of coronary artery stenosis, and glycoprotein genotype. During the follow-up there were no significant differences between the 2 groups with regard to MACE. Any cause of death and cardiovascular death were higher in patients with PlA2 polymorphism but these differences were not significant. On univariate analysis, smoking, presence of severe coronary artery disease, and presence of myocardial infarction were correlated with elevated risk of MACE; presence of atypical angina was correlated with fewer MACE. On multivariate analysis, smoking was an independent risk factor for a MACE. On univariate or multivariate analysis, there was no relation between the PlA2 polymorphism and a MACE.
Conclusions — The glycoprotein IIb/IIIa genotype was not shown to indicate the presence of atherosclerotic plaque. There was no correlation between the genotype and plaque vulnerability.

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