Abstract

The aim — to determine the discriminative potency of new original scale of prognosis of poor clinical outcomes after ST segment elevation myocardial infarction (STEMI) in patients with complete revascularization.Materials and methods. From entire population of STEMI patients (n = 268) we enrolled 177 individuals who underwent complete revascularization with the use of primary percutaneous coronary intervention (PCI). Blood flow through the culprit artery was restored at TIMI III level. During hospital admission, patients underwent clinical evaluation, coronary angiography, echocardiography and Dopplerography, the degree of risk was determined using TIMI, SYNTAX and GRACE scales, and the level of biomarkers (circulating and genetic) were assessed. Combined clinical end point, which included CV death, recurrent angina/ myocardial infarction, newly diagnosed heart failure and hospitalization for cardiovascular reasons were determined for 6 months of follow‑up.Results and discussion. Combined end point was determined in 75 (40.6 %) patients: newly onset of heart failure was reported in 46 patients (26.0 %), CV death occurred in 12 (6.8 %) patients, major adverse cardiac events (MACEs) were determined in 58 (32.8 %) patients, recurrent hospitalization due to CV reasons was fixed in 17 (9.6 %) patients. Multivariate log‑regression analysis corrected for the severity of coronary atherosclerosis showed that C786C genotype of eNOS gene, Val66Met + Met66Met genotype of the brain‑derived neurotrophic factor (BDNF), A1166C + C1166C genotype of angiotensin‑II receptor type 1 (ATІІR1), macrophage inhibitory factor (MIF), vascular endothelial growth factor‑A (VEGF‑A), soluble tumorigenesis‑2 suppressor (sST2) showed more significant predictive value compared to the standard model. Models based on the use of 4 — 6 biomarkers had advantages over those based on the use of 1 — 3 biomarkers in the prediction of a combined endpoint (Log‑rank test = 0.0341; odds ratio 0.4796; 95 % confidence interval 0.2430 — 0.9465). A model for predicting adverse events was developed based on the presence of C786C genotype of eNOS gene, (А1166С + С1166С) of ATІІR1 gene, serum sST2 ≥ 35 pg/ml, VEGF‑A ≤ 172 pg/ml and MIF ≥ 2792.7 pg/ml. Patients with STEMI who had a score higher than the median (> 5 points) had a statistically significantly worse prognosis than individuals with a lower score.Conclusions. The proposed predictive model of adverse endpoints after STEMI had better discriminative ability than the standard model.

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