title: Glycoprotein IIIa gene polymorphism and coronary artery disease.
abstract: OBJECTIVE
  Prevalence of glycoprotein IIIa gene polymorphisms (PIA2) has been reported to be elevated in persons who die of sudden death. PIA2 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 PIA2 polymorphism, atherosclerotic plaque burden, and its prognostic significance.
  
  
  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 PIA2 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 PIA2 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 PIA2 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.
authors.affiliation: Dept. of Cardiology Baskent University, Faculty of Medicine, Ankara Hospital, Ankara, Turkey. alpaydinalp@superonline.com
authors.forename: Alp
authors.initials: A
authors.lastname: Aydinalp
authors.forename: Ilyas
authors.initials: I
authors.lastname: Atar
authors.forename: Fatma Belgin
authors.initials: FB
authors.lastname: Atac
authors.forename: Ayse Canan
authors.initials: AC
authors.lastname: Yazici
authors.forename: Mutlu
authors.initials: M
authors.lastname: Cicek
authors.forename: Mustafa
authors.initials: M
authors.lastname: Yilmaz
authors.forename: Aliseydi
authors.initials: A
authors.lastname: Ozgul
authors.forename: Ash
authors.initials: A
authors.lastname: Atar
authors.forename: Mehmet Emin
authors.initials: ME
authors.lastname: Korkmaz
authors.forename: Bülent
authors.initials: B
authors.lastname: Ozin
authors.forename: Haldun
authors.initials: H
authors.lastname: Muderrisoglu
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000378:metabolism; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000235:genetics*; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D006801:Humans; D039661:Integrin beta3 / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011110:Polymorphism, Genetic; D011237:Predictive Value of Tests; D015995:Prevalence; D011379:Prognosis; D011446:Prospective Studies; D011859:Radiography; D012307:Risk Factors; D014421:Turkey / Q000453:epidemiology
chemical_list: D015415:Biomarkers; D039661:Integrin beta3