The aim of the study is to investigate the possibilities of using fatty acids of erythrocyte membranes and blood serum to differentiate steatosis and steatohepatitis in patients with fatty liver disease (FLD) of various origins. Material and methods. The study included 84 men with FLD of various origins (alcoholic, non-alcoholic, mixed, i.e. alcoholic + metabolic), average age 48.4 ± 13.9 years, fibrosis degree 0-1 (FibroScan® 502 Echosens, France). Using serum tests NashTest, AshTest as part of FibroMax, ActiTest as part of FibroTest (BioPredictive, France), 44 patients showed minimal necroinflammatory activity in the liver tissue (steatosis), and 40 patients showed pronounced necro- inflammatory activity (considered as steatohepatitis). The study of the composition of fatty acids of erythrocyte membrane, blood serum was carried out using gas chromatography/mass spectrometry – a system based on three Agilent 7000B quadrupoles (USA). Results. Fatty acids of erythrocyte membranes, significant for differentiation of steatohepatitis and steatosis in patients with FLD of various genesis, were established: levels of docosatetraenoic C22:4n-6 (p = 0.0001), arachidic C20:0 (p = 0.034) were significantly higher, and the content of pentadecanoic C15:0 (p=0.0006), 7-palmitoleic C16:1;7 (p = 0.0093), myristic C14:0 (p = 0.025), eicosapentaenoic C20:5n-3 (p = 0.032), hexadecadienoic acid C16:2 n-6 (p = 0.042) – lower in steatohepatitis than those in patients with liver steatosis. The greatest potential in distinguishing the degree of necroinflammatory activity in the liver was demonstrated by pentadecanoic acid C15:0 – AUC 0.736 (95 % CI 0.63–0.843), sensitivity 68.3 %, specificity 75.9 %. The created diagnostic panel of a combination of erythrocyte membrane fatty acids (C15:0, C14:0, C16:1;7) showed the highest sensitivity – 76.5 % with low specificity of 67.1 %. Conclusions. The identified features of the fatty acid profile of erythrocyte membranes and blood serum should be considered as promising biomarkers for the detection of steatohepatitis from the point of view of further research in this area.

This study aimed to compare the prevalence of psychosocial risk factors for cardiovascular disease (CVD) among adults aged 25–64 in the largest metropolis (Novosibirsk) and a large city (Tyumen) in Western Siberia. Material and methods Representative samples of adults aged 25–64 from Novosibirsk (metropolis) and Tyumen (large city) were examined between 2010–2013 and 2015–2017. Psychosocial factors, including personal anxiety (PA), vital exhaustion (VE), and depression (D), were assessed using standardized methods from the WHO MONICA-psychosocial program protocol. Results. In the Siberian metropolis, higher prevalence rates of elevated PA and D were observed compared to the large city: in men in younger age groups (25–34 years for D; 35–44 years for PA and D); in women in extreme age groups (25–34 and 55–64 years for D). Conversely, the large city showed higher prevalence rates for certain psychosocial factors: in men in older age group (55–64 years for D). and in women in younger (25–34 years for VE) and middle-aged (45–54 years for PA) groups. Conclusions. Significant differences in the prevalence of psychosocial CVD risk factors were identified across age categories in urban populations of Western Siberia. These findings underscore the importance of tailoring preventive programs to address age- and location-specific risk profiles in Siberian cities.

Objective. The study aims to investigate the relationship between the severity of COVID-19 and the course of stable coronary heart disease (CHD), as well as to evaluate the role of lipoprotein(a) [LP(a)] as a predictor of multifocal atherosclerosis in patients during the post-COVID period. Material and methods. 431 patients with stable coronary heart disease (CHD) who had confirmed COVID-19 infections lasting between 3 to 18 months were examined. Patients were divided into two groups according to the severity of COVID-19: Group 1 included 203 patients with mild COVID-19 and Group 2 included 228 patients with moderate COVID-19 in the acute period. Clinical, laboratory and instrumental diagnostic methods including lipid profile indices (apolipoprotein A1 (apoA1), B (apoB), lipoprotein (a) (Lp(a)) and coronary angiography to assess the extent of atherosclerosis were used in the study. Logistic regression method was used to identify predictors of multifocal atherosclerosis (MFA) based on comprehensive analysis of clinical data. Results. CHD patients with a moderately severe course of acute COVID-19 in the post-COVID period were characterised by more pronounced altered indices of lipid and carbohydrate metabolism, as well as a higher frequency of hemodynamically significant coronary artery lesions, leading to a worsening of the course of the CHD and an increased risk of complications. They were significantly more likely have uncontrolled arterial hypertension (p < 0.001), atrial fibrillation (p = 0.035) and type 2 diabetes (p = 0.007), and higher levels of such biomarkers as the terminal fragment of brain natriuretic peptide precursor (p < 0.001), glycated haemoglobin (HbA1c) (p = 0.005), apoA1 (p < 0.001), lower apoB/A1 ratio (p = 0.04) and higher Lp(a) concentration (p < 0.001). Construction of multivariate logistic regression model found that in patients with stable CHD in the post-COVID period, Lp(a) level > 317.56 μg/ml increased the risk of MFA by 2.74 times, apoA1 level > 199.4 mg/dl – by 5.27 times, level, HbA1c > 5.85 % – by 8 times, left ventricular mass index > 122.23 in g/m² – by 1.92 times, male sex – by 2.92 times. Conclusions. The obtained data suggest that patients with stable CHD who underwent COVID-19 of medium severity in the acute stage of the infectious process represent a risk group of subsequent more severe course of the underlying disease.

The aim of the study was to analyze the associations of rs2305948 KDR (VEGFR2) genotypes, the state of collateral coronary blood flow, as well as the intensity of statin therapy with the development of structural and functional remodeling of the left ventricle and the onset of ischemic cardiovascular events during long-term observation in patients with myocardial infarction (MI). Material and methods. The prospective observational study included 51 patients with acute MI with ST-segment elevation. All patients underwent coronary angiography and angioplasty with stenting of the coronary arteries, as well as echocardiography and laboratory diagnostics with biomarker assessment at the hospital stage and over time (36 months). Also, the rs2305948 genotypes of the KDR (VEGFR2) gene were determined using real-time polymerase chain reaction. Two groups were allocated for further observation: 1 – with poor coronary collaterals (n = 25), 2 – with good coronary collaterals (n = 26). The duration of outpatient observation and treatment of both groups of patients with registration of ischemic cardiovascular events after MI was 108 months. Results and discussion. In group 1, compared with group 2, there was a higher incidence of severe left ventricular structural and functional remodeling (LVSFR) over 36 months (p = 0.0380), the combined end point (CEP) over 108 months (p = 0.0001), carriage of genotypes C/T and T/T rs2305948 KDR (VEGFR2) (p = 0.0002), as well as the size of the acute and past MI zone (according to the value of the LV local contractility impairment index) (p = 0.0107 and p = 0.0443, respectively); at the post-infarction stage – all echocardiographic parameters of LVSFR (p < 0.05). According to the logistic regression analysis, the development of LVSFR was directly affected by hypertension (p = 0.037) and inversely by the presence of good coronary collaterals in the MI zone (p = 0.024); the onset of CEP was directly determined by the comorbidity index (p = 0.041) and inversely by the presence of good coronary collaterals (p < 0.0001), as well as long-term treatment with high doses of statins (p = 0.043). Conclusions. The development of LVSFR and the onset of CEP are associated with the rs2305948 genotypes of KDR (VEGFR2), the status of coronary collaterals, the size of the MI zone, as well as long-term use of high-dose statin therapy in post-infarction patients.

The aim of the review is the determining of the therapeutic possibilities of local activation of angiogenesis and degradation of atherogenic inflammation during reconstruction of arterial wall layers under conditions of wide implantation of polysaccharide polymers in the para-adventitial zone. The concept of the analytical review is based on the hypothesis of improving the balance between pro-inflammatory and atheroprotective cytokine growth factors when using biopolymers. The analysis of the literature indicates an active direct intervention in the reconstruction of the adventitial layer of the arterial wall using polysaccharide hydrogels with a high affinity for cholesterol, conditions are created for the formation of an additional extracellular matrix outside the intimal and medial zones of the main artery and the reversal of the cholesterol mass from the intimal zone to the para-adventitial space. The creation of productive inflammation in the adventitial zone using biopolymers can be one of the effective ways to degrade early soft atheromatous plaques. Publications indicate the possibility of extracting soft atheromatous plaques from the intimal space of major arteries by wide implantation of polysaccharide hydrogels into the fascial sheath of vessels with the formation of a second-level extracellular matrix. The analysis of literary sources according to the concept was carried out using databases indexed by WoS, Scopus, PubMed, DOAJ, Embase, Ei Compendex mainly for the last 8 years.The literature review allows us to form a modern understanding of the molecular processes occurring in the vessel wall during the development of atherogenic inflammation in an experiment on animals receiving a cholesterol diet, to indicate signs of vascular wall reconstruction with exogenous implantation of biopolymers. In the vascular wall, there is a conjugation of cytokine growth factors with natural or synthetic biomaterials. Immobilized factors will be available to cells that come into contact with the matrix, providing a highly localized signal to control cell fate. Injectable scaffolds are a promising approach for stimulating angiogenesis. Cell migration from the intima and media can be activated by an electrostatic gradient in the presence of a sulfated polymer and lead to the formation of affinity complexes with cholesterol. The high affinity of polysaccharide polymers for cholesterol and LDL, active vascularization of the additional extracellular matrix provoke a gradient of cholesterol translation towards the hydrogel “shirt”. The effect of cholesterol outflow can provide a new therapeutic approach to the pathology of the main vessels.

Arterial thromboembolic complications are rare in cancer patients. Malignant neoplasms and antitumor therapy contribute to an increased risk of arterial thromboembolism, ischemic stroke, and myocardial infarction. The development of arterial thromboembolism in people without a history of cancer may be a harbinger of as yet undetected malignancies. Understanding the process of arterial thromboembolism is an important prerequisite for the proper management of patients with cancer during and after treatment in order to prevent life-threatening complications.