R J Pegoraro1, N Ranjith. 1. Department of Chemical Pathology, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa.
Abstract
BACKGROUND: The relationship between polymorphisms in the genes for plasminogen activator inhibitor type 1(PAI-1) and platelet glycoprotein IIIa (PGIIIa), clinical and environmental features, and the risk of premature coronary heart disease (CHD) in Asian Indian subjects living in South Africa, has been investigated. METHODS: The prevalence of the PAI-1 promoter 4G/5G and the PGIIIa PI A1A2 polymorphisms was examined in 195 unrelated Asian Indian patients ( <or= 45 years) who presented with myocardial infarction (MI). Results were compared with those from 107 unaffected siblings (18-45 years) and 300 healthy age- and race-matched control subjects. RESULTS: Overall, neither the PAI-1 4G/5G nor the PGIIIa PI A1A2 polymorphism demonstrated an independent risk for MI. No synergistic effect was observed between these two polymorphisms when analysed together. There was a marginal association between the 4G allele of the PAI-1 gene and the risk of MI in individuals who smoked compared with non-smokers (26 vs 11%; p = 0.028; OR 2.74; 95% CI 1.04-8.47). The PGIIIa PI A2 allele was, however, strongly associated with a previous history of MI (17 vs 6%; p = 0.004; OR 3.00; 95% CI 1.38-6.46), as well as the severity of disease as determined by angiography (single/double- vs triple-vessel disease: 3% vs 15%; p = 0.020; OR 0.19; 95% CI 0.02-0.92). CONCLUSION: In young Asian Indians who smoke, the PAI-1 4G allele is a mild risk factor for the development of MI. The PGIIIa PI A2 allele constitutes a significant risk for individuals who have a previous history of MI, as well as serving as an indicator for the severity of CHD.
BACKGROUND: The relationship between polymorphisms in the genes for plasminogen activator inhibitor type 1(PAI-1) and platelet glycoprotein IIIa (PGIIIa), clinical and environmental features, and the risk of premature coronary heart disease (CHD) in Asian Indian subjects living in South Africa, has been investigated. METHODS: The prevalence of the PAI-1 promoter 4G/5G and the PGIIIa PI A1A2 polymorphisms was examined in 195 unrelated Asian Indian patients ( <or= 45 years) who presented with myocardial infarction (MI). Results were compared with those from 107 unaffected siblings (18-45 years) and 300 healthy age- and race-matched control subjects. RESULTS: Overall, neither the PAI-1 4G/5G nor the PGIIIa PI A1A2 polymorphism demonstrated an independent risk for MI. No synergistic effect was observed between these two polymorphisms when analysed together. There was a marginal association between the 4G allele of the PAI-1 gene and the risk of MI in individuals who smoked compared with non-smokers (26 vs 11%; p = 0.028; OR 2.74; 95% CI 1.04-8.47). The PGIIIa PI A2 allele was, however, strongly associated with a previous history of MI (17 vs 6%; p = 0.004; OR 3.00; 95% CI 1.38-6.46), as well as the severity of disease as determined by angiography (single/double- vs triple-vessel disease: 3% vs 15%; p = 0.020; OR 0.19; 95% CI 0.02-0.92). CONCLUSION: In young Asian Indians who smoke, the PAI-1 4G allele is a mild risk factor for the development of MI. The PGIIIa PI A2 allele constitutes a significant risk for individuals who have a previous history of MI, as well as serving as an indicator for the severity of CHD.
Authors: Elizabeth M Kiefer; Qiuhu Shi; Donald R Hoover; Robert Kaplan; Russell Tracy; Michael Augenbraun; Chenglong Liu; Marek Nowicki; Phyllis C Tien; Mardge Cohen; Elizabeth T Golub; Kathryn Anastos Journal: J Acquir Immune Defic Syndr Date: 2013-03-01 Impact factor: 3.731