The aim of the study is to evaluate the association of some molecular genetic markers with progressive atherosclerosis. 
Material and methods. In total, the study included 202 patients (147 men and 55 women), who were divided into 2 groups. The 1st (main) group included patients with coronary artery disease (100 people) who had a combination of two or more cardiovascular events during the last 2 years before inclusion: myocardial infarction or unstable angina pectoris, arterial stenting for urgent indications (coronary and peripheral), stroke; acute ischemia, thrombosis or amputation of the lower extremities. The 2nd group (comparisons) included 102 patients with coronary artery disease who did not have any of the above cardiovascular events during the last 2 years before inclusion. DNA was isolated from peripheral blood samples by phenol-chloroform extraction. 
Results. According to the frequencies of genotypes of the I/D polymorphism (rs36232792) of the SOD1 gene, no statistically significant differences were obtained between the group with progressive atherosclerosis and the control, neither in general, nor when divided by sex and age. The odds ratio of developing progressive atherosclerosis in carriers of the rare homozygous DD genotype of the rs3834129 polymorphism of the CASP8 gene is 2.3 ne is 2.3 times higher compared to carriers of the other two genotypes (DD vs II + ID, 95 % CI 1.1–5.1; p = 0.037). In men, the odds ratio is higher than in the general group – 4.4, p = 0.015. Women also tend to accumulate carriers of the DD genotype in the group with progressive atherosclerosis (26.7 % vs 16.0 %), but the differences do not reach the level of statistical significance. 
Conclusions. The carriage of the DD genotype of the rs3834129 polymorphism of the CASP8 gene is associated with progressive atherosclerosis in patients with CAD. No association of I/D polymorphism (rs36232792) of the SOD1 gene with progressive atherosclerosis was found. Acknowledgments. The molecular genetic fragment of the study was supported by State Budget theme no. 122031700094-5.

The aim of the study was to investigate the relationship between the level of risk factors (RF) of cardiovascular diseases (CVD) and chronic non-communicable diseases (NCD) and their changes over 9 years with the dynamics of indicators of cognitive function (CF) in an ageing population.
Material and methods. The study was based on a random population sample of men and women aged 45–69 years old examined at baseline in 2003–2005 (n = 9360, Novosibirsk, HAPIEE project). Present analysis included a subsample of persons with repeated CF measurements (n = 3153). The average follow-up period was 9.2 ± 0.7 years (from 47–74 to 55–84 years). Repeated measurements of RF, history and treatment of CVD and NCDs, indicators of CF (memory, semantic verbal fluency, attention and processing speed) were done. The associations between 9-year regression of CF and the baseline level of RF and their 9-year dynamics were evaluated in linear and logistic regression.
Results. In the studied population sample the extent of 9-year regress of CFs was associated with baseline high level of systolic blood pressure (p = 0.005) and fasting blood glucose (FG) (p = 0.003), low body mass index (BMI) (p = 0.011) in men and smoking (p = 0.037) in women aged 47–74 years old. Regarding the difference between baseline and prospective level of RF in 9 years, the regress of CF was associated with decrease of total cholesterol value (p = 0.027), continued smoking (p = 0.032) in men, decrease of BMI (p = 0.024 and p = 0.012) in women decrease of the average dose of alcohol per session (p = 0.005 and p = 0.014) in women, and increase of the average dose of alcohol in men (p = 0.049). Independent predictors of low prospective value of different CF scores at age of 55–84, were the baseline level of FG above 5.95 mmol/l (p = 0.013 and p = 0.044), the level of BMI equal or lower 24.2 kg/m²  (p = 0.016 and p = 0.023), former smoking (p = 0.007) in men, and non-drinking status in women (p = 0.005 and p = 0.004). 
Conclusions. In studied population we identified the associations between modifiable risk factors of CVD and chronic NCD and their changes during 9-year follow-up, and the extent of age-related regress of CF. These findings might have an implication in prevention of cognitive impairment.

The effect of blood lipid profile levels on the service life of autovenous femoral-popliteal bypass has not been fully studied. The aim of the study was to assess the effect of lipid metabolism disorders on the long-term results of autovenous femoral-popliteal bypass surgery. 
Material and methods. Results of treatment of 648 patients who underwent autovenous femoral-popliteal bypass grafting were analyzed. In accordance with the outcome of surgical treatment, the patients were divided into 2 clinical groups: the first group (290 patients) included patients who, according to the instrumental methods of research in the long-term period, had occlusion of the autovenous femoral-popliteal bypass, the second group (358 people) included patients whose autovenous conduit was passable. The average service life of the autovenous femoral-popliteal bypass in patients of the first group was 78 ± 18 months. Patients in the first and second groups aged 64.5 ± 7.9 and 64.9 ± 8.6 years, respectively, p = 0.58, males prevailed (n = 503, 77.62 %). 
Results. Analysis of lipidogram data showed higher content of total cholesterol, low density lipoprotein, triacylglycerol, atherogenic coefficient in patients of the first clinical group. Dyslipidemia was recorded in 256 (88.3 %) patients of the first group and 190 patients of the second group (53.1 %), p = 0.001. The patency time of the autovenous conduit in patients of the first group, who was diagnosed with dyslipidemia, was 68.15 months, without this complication – 105.84 months. 
Conclusions. Dyslipidemia and hyperlipidemia significantly reduce the lifespan of the autovenous femoral-popliteal bypass. The work has no funding

Single nucleotide polymorphisms rs1008832 of the CACNA1C gene, rs4027402 of the SYNE2 gene, rs2340917 of the TMEM43 gene, rs58225473 of the CACNB2 gene were found by sequencing the clinical exome of a group of men who died of sudden cardiac death (SCD) at the age of 45 years. The aim of the study is to study the association of single nucleotide polymorphisms rs1008832 of the CACNA1C gene, rs4027402 of the SYNE2 gene, rs2340917 of the TMEM43 gene, rs58225473 of the CACNB2 gene with SCD in a case-control study using routine molecular genetic analysis. 
Material and methods. SCD group (n = 400, mean age 53.2 ± 8.7 years, 70.9 % men, 29.1 % women) was formed using the SCD criteria of the European Society of Cardiology from the anonymous DNA bank of the deceased sudden death (1999–2019). The control group (n = 400, mean age 53.1 ± 8.3 years, 68.3 % men, 31.7 % women) was matched by sex and age to the SCD group from DNA banks of international projects MONICA and HAPIEE of living at the time of researches participants. Genotyping was carried out using the polymerase chain reaction followed by analysis of restriction fragment length polymorphism. 
Results. There were no statistically significant differences in the frequencies of genotypes and alleles of single nucleotide polymorphisms rs1008832 of the CACNA1C gene, rs4027402 of the SYNE2 gene, rs2340917 of the TMEM43 gene, rs58225473 of the CACNB2 gene between the SCD group and the control group (p > 0.05). 
Conclusions. The association of single nucleotide rs1008832 of the CACNA1C gene, rs4027402 of the SYNE2 gene, rs2340917 of the TMEM43 gene, rs58225473 of the CACNB2 gene with SCD has not been confirmed. 

Aim of the study was to evaluate of the effect of intravenous metoprolol tartrate administered before percutaneous coronary intervention (PCI), in combination with long-term use of high-dose atorvastatin, on dynamic changes in biochemical and ultrasound markers, as well as on the outcomes of early myocardial remodeling in patients with ST-segment elevation acute myocardial infarction (MI). 
Material and methods. A prospective randomized clinical trial included 136 patients with MI. The terms of the study were 35 ± 5 (from 30 to 40) days from the moment of admission to the hospital. The first group (control) included patients who received standard interventional and drug treatment at the hospital and outpatient post-infarction stages. The second group (exposure) included individuals who received a single intravenous injection of metoprolol tartrate before PCI, followed by a switch to oral metoprolol succinate on a systemic basis. These patients, as well as in the first group, regularly received all components of the basic drug therapy, including atorvastatin at a dose of 80 mg per day for one month from the onset of MI. On the 1st-2nd day of MI and a month later, plasma levels of biochemical biomarkers were assessed in patients; on the 1st, 10th day and one month later, ultrasound markers were evaluated using echocardiography. Upon the follow-up clinical outcomes of post-infarction myocardial remodeling were analyzed. 
Results. We confirmed that the use of a single intravenous injection of metoprolol tartrate (5–15 mg) in acute myocardial infarction before PCI against the background of high-dose atorvastatin (80 mg/day) for one month from the onset of myocardial infarction demonstrated convincing efficacy in relation to the prevention of early myocardial remodeling, which we assessed by the dynamics of ultrasound markers, as well as by the plasma activity of all three key biochemical markers in comparison with the control group of patients. 
Conclusions. The use of a single intravenous injection of metoprolol tartrate in the acute phase of MI against the background of high-dose atorvastatin for one month from the onset of MI is a highly effective pharmacological method for preventing the formation of early postinfarction myocardial remodeling.

Aim of the study was to assess the composition of blood microbiome in patients with atherosclerosis, to compare it with microflora and microbiome of atherosclerotic plaques, to identify common taxons for microbiomes of blood and atherosclerotic plaques, as well as to perform a correlation analysis of various blood and urine parameters in the examined patients with the structure of «core» of the blood bacterial community. 
Material and methods. 19 men and 5 women aged 33–81 years (mean age 64.1 ± 9.8 years) with common carotid artery atherosclerosis confirmed by Doppler ultrasonography of vessels were examined. The microbial diversity of 24 blood samples from patients with vascular atherosclerosis was examined using 16S ribosomal RNA (16S rRNA) gene sequencing. 16 samples of atherosclerotic carotid artery plaques were examined by а bacteriological method. Correlation analysis of the results was performed by methods of nonparametric statistics. 
Results. Most of the sequences obtained were classified as Proteobacteria (73.9 %), Actinobacteria (11.4 %), Bacteroidetes (2.8 %), Cyanobacteria (1.3 %), Firmicutes (1.1 %), Fusobacteria (0.7 %). Genes of 16S rRNA of Propionibacterium acnes, undifferentiated species of the families Micrococcaceae, Caulobacteraceae, Bradyrhizobiaceae, genera Bradyrhizobium and Sphingomonas were found in all the examined blood samples of patients with atherosclerosis and comprised from 67.7 to 87.5 % of the microbial community taxons. 75 % of biopsy samples from atherosclerotic plaques showed growth of the bacteria: Propionibacterium acnes (43.8 %), Staphylococcus epidermidis (18.8 %), Staphylococcus capitis (6.3 %), Staphylococcus saccharolyticus (6.3 %). The common taxons for blood microbiomes and atherosclerotic plaques are Propionibacterium acnes and Bradyrhizobiaceae. 
Discussion. The present study is the first to report the blood microbiome of patients with atherosclerosis and to detect viable cultures of Propionibacterium acnes and Staphylococcus in biopsy samples of atherosclerotic plaques, providing a mechanistic link between microorganisms and cardiovascular disease. Propionibacterium acnes and Bradyrhizobiaceae are common taxons for blood microbiomes and atherosclerotic plaques. It can be assumed that Propionibacterium acnes species is a specific taxon both of atherosclerotic carotid artery plaques and blood of patients with carotid atherosclerosis; additional studies on the etiological significance of the microbial factor in the formation of atherosclerotic plaques are required.

Purpose of the study. Based on the assessment of endothelial and hemostasiological parameters, to study the possibilities of early diagnosis of vascular disorders in case of vibration disease in combination with arterial hypertension. 
Material and methods. 253 patients with vibration disease in combination with arterial hypertension were examined in the conditions of the regional center of occupational pathology based on a specialized department of occupational pathology. The indicators of systemic, vascular-platelet, plasma-coagulation hemostasis, the state of markers of endothelial cell hemostasis are considered; platelet aggregation activity was determined; the study of adhesion molecules, the functional state of the endothelium. 
Results. Endothelial dysfunction in vibration disease in combination with arterial hypertension is characterized by increase of content of signaling molecules sPECAM-1, sVCAM-1 and sP-selektin, level of endothelin-1 in combination with increased production of vascular endothelial growth factor and transforming growth factor; endothelial markers are associated with the frequency of unfavorable polymorphic variants of genes; systemic hemostasis is characterized by an increase in the level of thrombospondin and thrombomodulin, platelet growth factor in conditions of a decrease in plasminogen activity, an increase in the concentration of α2-macroglobulin and fibrin decay products; identified early endothelial-hemostasiological markers of vascular disorders. 
Conclusions. As an early diagnosis of vascular disorders in vibration disease in combination with arterial hypertension, it is advisable to use early endothelial-hemostasiological markers of vascular disorders: content of inducible NO synthase, vascular endothelial growth factor, transforming growth factor β1, adhesive molecule, platelet growth factor BB, thrombospondin and fibrinopeptide A index, plasminogen activity, polymorphism of plasminogen, endothelial NO synthase, endothelin-1 and transforming growth factor β1 genes.

Patients with familial hypercholesterolemia should be monitored throughout life, starting at an early age, since high levels of low-density lipoprotein cholesterol from birth and its cumulative effect play a significant role in the early development of complications of the atherosclerotic process. A clinical case of familial heterozygous hypercholesterolemia, first diagnosed in a patient at the age of 16, is described. As part of the cascade screening, the patient’s parents were examined. A molecular genetic study of DNA revealed the substitution rs879254721 NM_000527.5(LDLR):c.922G>A (p.Glu308Lys) in the LDLR gene in the proband and in the proband’s mother in the heterozygous variant. Regardless of the availability of molecular genetic testing, all families with familial hypercholesterolemia require ongoing lifelong follow-up and focused clinical evaluation.

This article describes a clinical case of management of a patient with myocardial infarction (MI) who underwent orthopic heart transplantation. The main cause of myocardial infarction in a transplanted heart is cardiac allograft vasculopathy (ICA), a rapidly progressive form of atherosclerosis. The process involves concentric narrowing of the lumen of the coronary arteries, usually occurring from several months to several years after transplantation. Currently, ICA is the limiting factor in the long-term survival of the allograft. According to the registry of the International Society for Heart and Lung Transplantation (ISHLT), angiographic signs of ICA are found in 8–10 % of patients after 1 year, in 20 % after 3 years, in 30 % after 5 years, in 45 % after 8 years, and more than in 50 % after 10 years. This article presents the latest available pathophysiological data on ICA, methods of diagnosis, prevention, management, treatment and further prognosis of myocardial infarction in patients with heart transplants. In addition, a clinical case of a patient with myocardial infarction without ST-segment elevation after orthotopic heart transplantation is described. The authors participated in the development of the concept and design of the article. The manuscript is grounded and verified for the importance of intellectual content. The manuscript was finally approved by the authors for publication. The authors agree to be responsible for all parts of the work.