135 patients with STEMI, 109 (80.7%) men and 26 (19.3%) women, mean age (59.21±8.92) years were examined. The control group consisted of 30 healthy individuals. The level of VEGF-A in the main group - 247.94 [107,22-486,50] pg/ml, in the control - 80,76 [56,20-149,51] pg/ml, (p=0,011). 2 groups were created: GG-genotype (n=70) and GC+CC-genotype (n=65). The level of VEGF-A was significantly higher GG carriers -314.01 [159,94-627,66] pg/ml compared with GC+CC 221,28 [77,58-440,82] pg/ml, (p=0.045).In the GC+CC genotype was a significantly higher incidence of the combined endpoint (p=0.020), also there was an increase in EDV LV (р=0.044), ESV LV (р=0.039) compared with GG carriers. A logistic analysis showed that the level of VEGF-A (β=0.0015896, p=0.02), the genotype GC+CC (β=1.72, p=0.011), the level of troponin I (β=-0.013, p=0.023) and complicated course of the acute period of MI (β=2.23, p=0.001) were predictors of adverse course during 12 months follow-up (p<0.0001). The threshold level of VEGF-A≤255.72 pg/ml was established (AUC-0.630; 95% confidence interval 0.534-0.719; p=0.0472). The concentration of the biomarker below this level with a sensitivity of 72% and a specificity of 58% predicts an adverse course within 12 months. A multivariate logistic analysis of the influence of endpoint factors was found that the unfavorable course of the disease depends on the level of VEGF-A (β=-0.0016; p=0.035), LDL-C (β=-1.62064; p=0.034) and the complications in the acute period of the disease (β=1, 89998; p=0.023). A model for predicting the development of adverse events after STEMI for 12 months has been developed. The sufficient efficiency of this model is evidenced by the shape of the ROC-curve and the AUC-0.75 (p=0.0001), with the sensitivity 80% and the specificity 67.8%. Patients in each subgroup received 2 variants of dual antiplatelet therapy: acetylsalicylic acid 100 mg once daily and clopidogrel 75 mg once daily or ticagrelor 90 mg twice daily. Carriers of the C allele (GC+CC) receiving clopidogrel had a significantly lower concentration of VEGF-A 115.02 [63,84-422,72] ng/ml than patients receiving ticagrelor 241,36 [156,84 -440.82] ng/ml (p=0.044). Patients with GG genotype taking ticagrelor had a significant reduction in NT-proBNP and better exercise tolerance (p=0.059). The GG genotype under ticagrelor, the number of adverse events was 4 (10.8%), and in those who received clopidogrel - 5 (15.2%), with no significant differences (p=0.588). In carriers of the C allele (GC+CC) who received ticagrelor 6 (15.4%) endpoints were recorded, of which 4 cases (10.5%) - rehospitalizations and 2 deaths (5.26%). In the subgroup of patients receiving clopidogrel, the number of adverse events was 14 (51.8%) (p=0.005): 9 (33.3%) hospitalizations for heart failure, 1 (3.7%) recurrent MI and 4 (7%) deaths from all causes. Multivariate regression logistic analysis showed that the genotype GC+CC gene VEGF-A (p=0,0465), reduced LV ejection fraction (<50,60%) (p=0,0096) and the clopidogrel tretment (p=0.044) in patients are predictors of adverse disease. The scientific novelty of the dissertation is that the prevalence of the G634C polymorphism of the VEGF-A gene in patients with STEMI has been studied, the association between the VEGF-A levels and carriers of polymorphic genotypes has been established. It is shown that patients with the GG genotype have a significantly higher concentration of the biomarker in the acute period of the disease compared with GC+CC. It was studied that carriers of the C allele (GC+CC) are a high-risk group and have significantly higher endpoints during the year of observation. Scientific data on the prognostic role of VEGF-A for the postinfarction period have been expanded. The concentration of VEGF-A≤255,72 pg/ml is a predictor of adverse events during 12 months of follow-up. The GC+CC genotype of the VEGF-A gene in combination with a reduced concentration are a risk group for reaching endpoints. In patients of GC+CC genotype, the appointment of ticagrelor as an alternative to clopidogrel effectively improves the course of the post-infarction period. The practical significance of the obtained results is that it is advisable to use the suggested model with determination of VEGF-A levels, LDL-C and the complications in the acute period to improve the accuracy of prediction and prevention of adverse events in patients with STEMI. To identify the high-risk patients with STEMI it is recommended to determine the genotype of the G634C polymorphic of the VEGF-A gene. Very high risk groups are carriers of the C allele (GC+CC). When performing dual antiplatelet therapy, it is advisable to prefer ticagrelor 90 mg twice daily to reduce the incidence of cardiovascular complications after STEMI in patients with the GC+CC genotype whereas for the GG genotype the administration of ticagrelor or clopidogrel is equally effective, and this is of high socio-economic importance.
