Gene polymorphisms role of blood coagulation in myocardial infarction development in patients with malignant tumors of thoracoabdominal localization

Aim. To evaluate the role of polymorphic variants blood coagulation genes (F2, F5, F7, F13, FGB, ITGA2, ITGB3, PAI-1) in development myocardial infarction patients with malignant tumors thoracoabdominal localization.
 Materials and methods. The study included 143 operated oncological Department surgical methods treatment No.11 (thoracic Oncology) Blokhin National Medical Research Center Oncology 20182019. group (n=62) consisted a history or perioperative period. control (n=81) who did not have severe concomitant cardiovascular diseases, including family history. Molecular genetic to determine gene polymorphisms were performed laboratory clinical oncogenetic use reagents Cardiogenetic Thrombophilia (LLC DNA-Technology, Russia, RU No. FSR 2010/08414 from 22.11.2016).
 Results. In group, 90.3% (n=56) cases showed polymorphism -675 5G4G PAI-1 (SERPINE1, plasminogen activator inhibitor) associated decrease activity fibrinolytic system an increased risk thrombosis. this mutation was observed significantly less frequently 67.9% (n=55) (p0.001). infarction, 807 CT ITGA2 (integrin a2) responsible for platelet aggregation detected 66.1% (n=41) compared 19.8% (n=16) (p0.0001). Polymorphism 1565 TC ITGB3 (platelet-derived fibrinogen receptor) fibrinogen-induced 25.8% 12.4% (n=10) without pathology (p0.05). 48.4% (n=30) disorders FGB (fibrinogen, missense -455GA) also registered, which resulted dysfibrinogenemia, leading thrombogenicity; 2 times common 25.9% (n=21) (p0.01). 1691 GA F5 (coagulation factor V, Leiden factor), is considered one most significant factors thrombosis Caucasians, 4.8% (n=3) while found group. 20210 F2 II prothrombin), key protein cascade levels prothrombin, 3.2% (n=2) after infarction; carrier any case. Disorders that promote hypocoagulation noted. Among had 10976 F7 VII) 17.7% (n=11) cases, 103 GT F13 XIII) 41.9% (n=26) cases. these aberrations found: 18.5% (n=15) (p0.05) 45.7% (n=37) (p0.05), respectively.
 Conclusion. Based on results molecular thrombogenic risk, statistically difference frequency occurrence involved process (polymorphisms: -455 gene, gene) diseases. thrombosis, reached 4.8%. obtained data markers thrombophilia localization allow us identify high developing take additional measures prevention thrombotic complications.