Interaction Between Endothelial Nitric Oxide Synthase Gene Polymorphisms (−786T>C, 894G>T and Intron 4 a/b) and Cardiovascular Risk Factors in Acute Coronary Syndromes

Background and Aims Endothelial rupture of coronary plaque can represent the pathomorphological substratum of acute coronary syndrome (ACS). Polymorphisms in the NOS3 gene (eNOS) –786T>C, 894G>T and intron 4 a/b VNTR can be associated with a higher susceptibility for ACS. The present study is...

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Published in:Archives of medical research Vol. 43; no. 3; pp. 205 - 211
Main Authors: da Costa Escobar Piccoli, Jacqueline, Manfredini, Vanusa, Hamester, Fernanda Irma, Bandinelli, Josiane Bettim, Turkienicz, Ilan Maltz, Chies, José Artur Bogo, Peres, Alessandra, Bodanese, Luiz Carlos, Bogo, Maurício Reis
Format: Journal Article
Language:English
Published: United States Elsevier Inc 01-04-2012
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Summary:Background and Aims Endothelial rupture of coronary plaque can represent the pathomorphological substratum of acute coronary syndrome (ACS). Polymorphisms in the NOS3 gene (eNOS) –786T>C, 894G>T and intron 4 a/b VNTR can be associated with a higher susceptibility for ACS. The present study is focused on the investigation of the interaction of these polymorphisms and cardiovascular risk factors in 135 patients with ACS and 115 control subjects. Methods Case–control study where the allele and genotype frequencies of the polymorphisms –786T> C, 894G> T and intron 4 VNTR of the gene encoding eNOS were determined by PCR-RFLP associated with cardiovascular risk factors. Results An association of the 894TT genotype and 894GT+GG (OR 1.4; 95% CI 1.0–1.8) in ACS has been observed. Subjects without dyslipidemia and intron 4 a/b genotype present a lower chance for ACS development, whereas subjects without diabetes and 894TT genotype show a higher risk for ACS (OR 1.7; 95% CI 1.2–2.3). In patients without dyslipidemia, the 894GG genotype presented a tendency to behave as a protector factor against ACS. Also, the 894GG genotype has been a protective factor for ACS in females (OR 0.5; CI 95% 0.2–0.9). Conclusions Our results suggest that eNOS polymorphisms may be an additional risk factor in development of ACS.
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ISSN:0188-4409
1873-5487
DOI:10.1016/j.arcmed.2012.03.011