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Background: In recent years more attention is paid to the methods of interventional treatment of coronary artery disease. However, despite the numerous clinical studies the problem of stent restenosis after interventional procedures remains an important one. The studies of the molecular mechanisms of restenosis of coronary arteries and findings for new genetically determined predictors of restenosis after stenting become vital and essential. The NO-synthase influence on the development of endothelial dysfunction is practically assured, but the studies on the NOS genes' polymorphism effect on the incidence rate of in-stent restenosis are isolated and based on a limited number of clinical observations. The determined facts demonstrate the relevance of the conducted study, the results of which formed a new understanding of the role of NO-synthase genes in the predisposition to hyper-proliferative stents in patients with coronary artery disease. Aims: Set association between the eNOS gene polymorphisms and the risk of restenosis in patients with coronary artery disease hospitalized for coronary restenosis.

Materials and methods: We examined 484 patients with the verified diagnosis of the ischemic heart disease who underwent treatment at the unit of atherosclerosis and chronic coronary heart disease of «Cardiology Research Institute». Stenting of coronary arteries was performed in 210 people. The group of a restenosis enrolled 60 patients and the group without restenosis — 150. Genotyping was performed by non-enzymatic technique for isolation of genomic DNA from the venous blood of the surveyed, NOS genes' polymorphisms were detected by polymerase chain reaction (PCR).

Results: The established development of in-stent restenosis was associated with the following eNOS gene polymorphisms: VNTR ― in homozygotes for the minor allele (genotype aa) and heterozygotes (genotype ab); 894G/T ― in heterozygotes (the GT genotype) and homozygotes (TT genotype).

Conclusions: VNTR and 894G/T polymorphisms of eNOS gene are associated with risk for restenosis and can serve as additional markers for risk of restenosis after coronary stenting.

About the authors

L. M. Ogorodova

Siberian State Medical University

Author for correspondence.
ORCID iD: 0000-0002-2962-1076


Russian Federation

K. Y. Rukin

LLC «Management company «United clinical diagnostic laboratory»

ORCID iD: 0000-0002-4894-6909


Russian Federation

S. I. Vintizenko

Tomsk National Research Medical Center of the Russian Academy of Sciences

ORCID iD: 0000-0002-9566-4787


Russian Federation

I. V. Petrova

LLC «Management company «United clinical diagnostic laboratory»

ORCID iD: 0000-0001-9034-4226


Russian Federation


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