Association of a novel single nucleotide polymorphism of the prostacyclin synthase gene with myocardial infarction

2002 ◽  
Vol 143 (5) ◽  
pp. 797-801 ◽  
Author(s):  
Tomohiro Nakayama ◽  
Masayoshi Soma ◽  
Satoshi Saito ◽  
Junko Honye ◽  
Junji Yajima ◽  
...  
2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
O Petyunina ◽  
M P Kopytsya ◽  
A E Berezin ◽  
A A Berezin

Abstract Introduction Endothelial NO-synthase (eNOS) is constitutive enzyme, which is expressed in mature endothelial cells and promotes direct vascular dilatation. Single nucleotide polymorphism (SNP) of T786C in eNOS gene may influence on adverse cardiac remodeling after ST-elevation myocardial infarction (STEMI). Purpose To investigate possible associations between SNP T786C in eNOS gene and adverse cardiac remodeling after STEMI Methods 177 acute STEMI patients treated with primary and facilitate percutaneous coronary intervention that were admitted to intensive care unit of a Therapy National Institute were enrolled in the study. Anthropometry, cardiovascular risk assay, coronary angiography, echocardiography and biomarkers' measure were performed at baseline. The DNA extraction was performed with a commercial kit using real-time polymerase chain reaction PCR. All procedures performed in the study involving human participants were in accordance with the ethical standards and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards and approved by the local ethics committee (Protocol No. 8, 29.08.2016). Written informed consent was obtained from each patient. Results There were correlations between 786CC polymorphism in eNOs gene and adverse cardiac remodeling (r=0.48; p=0.001), LDL cholesterol (r=0.32; p=0.012), type 2 diabetes mellitus (r=0.30; p=0.042), diastolic BP (r=−0.26; p=0.048), unstable angina prior to STEMI (r=0.25; p=0.047) and total quantity of complicated STEMI (r=0.23; p=0.042). Additionally, there were not significant relations between 786CC polymorphism in eNOs gene and multiple coronary vessel injury, STEMI localization, levels of circulating biomarkers of myocardial injury, and amount of damaged coronary arteries. Using univariate and multivariate regressive logistic analysis we found that 786CC genotype of eNOS was independent predictor for late adverse LV remodeling (β-coefficient = 1.57342; odds ratio = 4.8231; 95% confidence interval = 1.5349–15.1552; p=0.0071). Conclusions The polymorphism 786CC in eNOs gene was found as an independent predictor for late adverse cardiac remodeling after STEMI. Acknowledgement/Funding None


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