Distribution of genotypes polymorphisms of genes markers of systemic inflammatory response among patients with STEMI

Abstract

One of the important problems of modern medicine is the continuous increase of cardiovascular disease. An urgent problem at the present stage is the treatment of patients with acute forms of coronary heart disease, since vascular accidents are the leading causative factors of mortality from cardiovascular disease. Recently, an increasing number of studies have determined the role of genetic markers for predicting the adverse course of various cardiovascular diseases, including acute myocardial infarction. The distribution of genes markers of systemic inflammatory responses was determined in patients with STEMI. There are riteria for inclusion in the study: male and female patients from 46 to 75 years old; for postmenopausal women, more than 1 year; the presence of STEMI in the first 12 hours of the onset of the disease; informed consent of the patient to participate in the study. DNA was isolated from leukocytes from whole blood using the Express DNA Blood Kit (Litech). In the process of DNA extraction, the recommendations given in the kit instructions were followed. SNP polymorphisms of C-reactive protein genes were determined G-3014>A, tumor necrosis factor-α G-308>A, interleukin-10 G-1082>A by real-time polymerase chain reaction using a Rotor-Gene 6000 thermocycler (Corbett Research, Australia). The structure of the primers from the standard SNP-express-PB sets (Litech) was used. It was determined, that in patients with STEMI, an increase in the proportion of homozygotes (GG) and a decrease in heterozygotes (GA) of the genotypes of the G-3014>A polymorphism of the C-reactive protein gene are determined in comparison with the Hardy–Weinberg distribution. Polymorphism G-308>A of the tumor necrosis factor-α gene among patients with STEMI had a significant discrepancy with Hardy–Weinberg equilibrium, with an increase in the proportion of homozygotes (GG) and a decrease in heterozygotes (GA) and homozygotes (AA). The distribution of G-1082>A polymorphism of the interleukin-10 gene was characterized by an increase in the proportion of homozygotes (GG) and a decrease in heterozygotes (GA) in patients with STEMI compared to the Hardy–Weinberg distribution.