BACKGROUND: Atrial fibrillation (AF) is the most common persistent heart rhythm disorder. AIM: Assessment of clinical predictors of atrial fibrillation in the Kazakh population. METHODS: An analytical clinical and epidemiological study of 75 patients with AF of Kazakh nationality. Descriptive analysis of medical records was carried out and the results of laboratory and instrumental research methods. Statistical analysis was carried out using the Statistica 6.0 Software package from StatSoft Inc. (USA) and MS Excel. RESULTS: In the majority of the studied patients (86.7%), atrial fibrillation was associated with hypertension, in 49.3% of patients was diagnosed with coronary artery disease. A permanent form of atrial fibrillation was observed in 63%, in 20% AF manifested itself in the form of paroxysms, in 17% AF was persistent. AF, which arose against the background of CHF, was established in 41.3% of the patients studied by us, while a decrease in LVEF below 40% was observed in 21.3% of the examined patients. In our study, diabetes mellitus was diagnosed as a comorbid pathology in 24% of patients and diabetes mellitus correlated with permanent AF in 66.7%. Thyroid pathology was observed in 9.3% cases. CRHD as a concomitant disease occurred in 12% of cases. In 5.7% of cases, AF was registered as idiopathic (primary) without a history of cardiovascular and concomitant pathology. Smoking as a risk factor was observed in 16%, alcohol consumption, was noted by 8 patients (10.7%). In 40% of cases, patients with AF were obese, 45.3% of the patients were overweight (BMI ≥25).

One of the most important achievements of medical science is the development and implementation of endovascular methods for treating ischemic heart disease, the volume of which is progressively increasing in relation to other methods of myocardial revascularization. As a result of data from various researchers, the mechanism for the development of coronary artery restenosis in patients with coronary artery disease undergoing endovascular interventions can be an inflammatory reaction, smooth muscle hyperplasia, formation of a wall clot and its organization, as well as the effect of an angiotensin-converting enzyme that activates angiotensin-II, an inducer and inhibits the activity of bradykinin, which inhibits cell growth.Recent studies of molecular and cellular mechanisms of restenosis in models of vascular damage in animals, as well as histological studies of human coronary arteries, have shown that the basis for the development of restenosis is the activation of migration and proliferation of vascular cells under the influence of growth factors caused by damage, which is a manifestation of angiogenesis and leads to neointima hyperplasia and neoadvention, narrowing the lumen of arteries.However, today there is no single point of view regarding the role of vascular growth factors in the development of the restenotic process, the number of studies highlighting the dynamics of the concentration of vascular growth factors in response to balloon expansion or implantation of coronary stents, and their possible role in the neointima formation and the restenosis development.

BACKGROUND: There is a reason to believe that the polymorphism of genes encoding some enzymes and receptors plays a role in increasing of restenosis development risk. It is common knowledge that ethnicity affects the frequency of heterozygous genotypes occurrence. There is the evidence that polymorphism of the FGB gene (rs1800790) and THBD gene was determined in the ethnic group of Kazakhs with restenosis of the coronary arteries, which can be considered as genetic predictors of restenosis development. Today, the questions of the role of the genetic component in the development of coronary heart disease (CHD) remain open. AIM: Evaluation of gene polymorphism in patients with restenosis of coronary arteries after stent installation. MATERIALS AND METHODS: The group consisted of Kazakh population of the age category from 45 to 65 years of both sexes: Group I (50 persons) patients with a diagnosis of CHD, with a fixed stent and the development of restenosis during the year; Group 2 (58 persons) – with a fixed stent and no restenosis during the year. The association of genetic polymorphisms was evaluated in accordance with the case–control design based on the generalized linear model assuming a log-additive inheritance model. RESULTS: Thus, when comparing two groups using five patterns of inheritance, the following SNP were revealed: Codominant inheritance pattern – rs1045642 (p = 0.0427), dominant inheritance pattern – rs12041331 (p = 0.036088), rs13431554 (p = 0.025461), and rs1045642 (p = 0.012774), and overdominant inheritance pattern – rs12041331 (p = 0.051736), rs5918 (p = 0.057652), and rs13431554 (р = 0.036006). Thus, three SNPs associated with stenting were identified: rs7543130 (p = 0.009324), rs6785930 (p = 0.016858), and rs7819412 (p = 0.061325) and two SNPs associated with the development of restenosis after stent placement: rs1061781 (p = 0.063184) and rs342293 (p = 0.061636). CONCLUSION: The polymorphisms associated with the risk of developing restenosis after stenting were determined: Codominant inheritance pattern – one polymorphism (rs1045642, p = 0.0427); dominant inheritance pattern – three polymorphisms (rs12041331, p = 0.036088; rs13431554, p = 0.025461; rs1045642, p = 0.012774), and overdominant inheritance pattern – one polymorphism (rs13431554, p = 0.036006). Based on the hybrid machine learning approach (RuleFit), four rules were obtained for assessing the empirical risk of restenosis developing after stenting – from 20% to 40%.

Due to the fact that there are scientific discussions about the significance of gene polymorphisms in the risk of developing cardiovascular complications after a percutaneous coronary intervention, it is of interest to evaluate the genetic predictors of the development of cardiovascular events. This study is a molecular genetic study. Association with the genes of biomarkers for inflammation and immune response increases the risk of cardiovascular events: rs1234313 (TNFSF4): (A/G, OR-4.57 (2.35–8.87), p ≤ 0.0001), (A/G-A/A, OR-3.14 (1.75–5.63), p ≤ 0.0001), and (A/G, OR = 4.01 (2.19–7.36), p ≤ 0.0001); rs3184504 (SH2D3); ATXN2: (C/T, OR-2.53 (1.28–5.01), T/T, OR-2.99 (1.13–7.92), p = 0.017)), (C/T-T/T, OR-2.61 (1.35–5.07), p = 0.000), and (OR-1.89 (1.15–3.09), p = 0.009)). According to the lipid metabolism biomarker genes, rs2943634: (A/C OR-2.57 (1.18–5.62), p = 0.013); according to the endothelial biomarker genes, rs2713604: (DNAJB8-AS1; GATA2): (C/T, OR-4.27 (2.35–7.76), p ≤ 0.0001), (C/T-C/C, OR-4.13 (2.31–7.40), p ≤ 0.0001), (OR-4.05 (2.24–7.30), p ≤ 0.0001), and (C/T, OR-3.46 (1.99–6.00), p ≤ 0.0001). The regression analysis found that in the presence of the rs2943634 gene polymorphism, the risk of late cardiovascular events increases by 4.007 times with 95% CI (1.502:10.692), p = 0.006. The genes of biomarkers for the risk of cardiovascular events are rs1234313(TNFSF4), rs3184504 (SH2D3; ATXN2), rs2943634, and rs2713604 (DNAJB8-AS1; GATA2). The only predictor of the development of new cardiovascular events was rs2943634, which belongs to the group of lipid metabolism biomarkers.