Hyperlipidemia is one of the most common metabolic disorders in humans, leading to the atheros clerosis. It is known that lipid metabolism disorders can be associated with genetic predisposition. However, even in patients with clinically confirmed familial hypercholesterolemia, its genetic cause remains unknown in 30 % of cases. The search for genetic variants associated with primary hyperlipidemias is a promising direction in the development of diagnostics and personalized medicine. Aim of the study was to assess of the association of polymorphic sites rs3813627, rs3135506 and rs3785617 of the apolipoprotein genes APOA2, APOA5 and APOH, respectively, with lipid metabolism and atherogenic index in the population of Novosibirsk. Material and methods. Genotyping by polymerase chain reaction followed by analysis of restriction fragment length polymorphism at the rs3813627, rs3135506 and rs3785617 of the APOA2, APOA5 and APOH genes, respectively, was carried out in 522 people from 9360 a random population sample of Novosibirsk and in 266 people from the same sample with a total cholesterol content more than 300 mg/dl. A one-way ANOVA of the association of genetic variants with serum lipid levels and atherogenicity index was performed. Results. The allele frequencies of all studied polymorphic sites in the Novosibirsk population differed from those previously identified among Europeans. A significant increase (p = 0.02) in average total cholesterol content in AA – AG – GG genotype series for rs3785617 of the APOH was revealed. The frequency of the CC genotype for the rs3135506 of the APOA5 in the group with total cholesterol contentration exceeding 300 mg/dl was lower compared to the control group (p = 0.038, odds ratio 0.66, 95 % confidence interval 0.46–0.97). For rs3813627, there were no differences in genotype frequencies and in lipid metabolism. Conclusions. The rs3135506 and rs3785617 can modify the hyperlipidemia phenotype among the Caucasoid population of Western Siberia.

Discussions continue about the effect of arterial hypertension (AH) on the course and prognosis of COVID-19 infection, while interest in the effect of antihypertensive therapy (AHT), primarily angiotensin converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB), on the course of the disease does not weaken. Aim of the study was to investigate the associations of AH, AHT and the severity of the course of coronavirus infection in Novosibirsk patients. Material and methods. Study design: a single-stage observational study. The study included 268 patients aged 26–84 years (47.5 % men) who underwent COVID-19. All patients underwent anthropometry, echocardiography, and anamnesis data were evaluated. Laboratory studies were carried out using enzyme immunoassay. Results. Patients with AH and moderate/severe COVID-19 had higher values of glucose, body mass index (BMI), waist circumference (WC), and left ventricular mass in terms of height (LVM/height) than patients with mild course. Diastolic blood pressure was significantly less in moderate and severe course than in mild course. The chance of severe COVID-19 in patients with AH is 11 % higher with an increase in BMI by 1 kg/m² (1.110, 95 % CI 1.042–1.182, p = 0.001), by 3.9 % with an increase of 1 cm (1.039, 95 % CI, 1.013–1.066, p = 0.003). Regular use of AHT reduced the chance of severe COVID-19 by 2.3 times. Conclusions. In patients with AH, glucose levels, WC, BMI, and LVL/height are associated with a more severe course of COVID-19. The chance of having a moderate and severe course of COVID-19 in patients with AH is 11% higher with an increase in BMI by 1 kg/m², by 3.9 % with an increase of 1 cm. With regular AHT, the chance of moderate and severe COVID-19 decreased 2.3 times.

The article presents the current state of the problem of atrial fibrillation as the most widespread cardiac rhythm disorder, the occurrence of which significantly worsens the quality of life of patients and reduces their life expectancy. Undoubtedly, a significant number of patients with atrial fibrillation suffer from obesity and heart failure. The review article reviews the understanding of the fundamental pathogenetic mechanisms of atrial fibrillation and the associated changes in the cellular, molecular, electrophysiological, and structural architecture of the atria. Information on the topic from publications based on PubMed, Google Scholar, and eLIBRARY databases was used, with a depth of coverage of 5 years.

The purpose of the review is to highlight the most significant changes in the parameters of red blood cells associated with the development of thrombosis in patients with coronavirus infection. A search was carried out using keywords in the databases Scopus, Web of Science, PubMed according to literary sources of the last 3 years on changes in erythrocyte indices associated with thrombosis against the background of COVID-19 infection. Information is presented on the main shifts in red blood indicators during SARS-CoV-2 infection associated with the development of thrombosis: virus attachment and amplification of viral proteins in erythropoiesis progenitor cells; activation of stress erythropoiesis with an increase in nuclear erythrocyte cell content up to 45 %; activation of band 3 protein oxidation with its excessive cleavage, oxidation and cleavage of alpha-chains of spectrin, ankyrin; changes in the lipid architecture of the membrane and a decrease in the activity of erythrocyte antioxidant activity, which mediate violations of cell deformability and impaired release of ATP; a decrease in the ability of erythrocytes to secrete nitric oxide; a decrease in the level of sphingolipids of the erythrocyte membrane; excessive production of microvesicles with tissue factor; an increase in the rigidity of erythrocytes with impaired release of intra-erythrocyte nitric oxide due to an attack by the SARS-CoV-2 virus 1-hemoglobin beta chain and porphyrin capture with potential heme inhibition; an increase in activated complement components C3b and C4d, immunoglobulin IgG expression on erythrocyte surface, which worsens cell deformability; attachment of erythrocytes through Toll-like receptor 9 to neutrophil extracellular traps, which promotes thrombosis; increased presentation of phosphatidylcholine on erythrocyte membranes, which facilitates the assembly of the tenase complex and prothrombinase complex, contributing to the production of thrombin, an increase in intracellular calcium levels with stimulation of the formation of microvesicles with prothrombotic potential; activation of oxidative stress in erythrocytes under conditions of hypoxia with generation of reactive oxygen species, hemoglobin autooxidation. Conclusions. The data obtained indicate the active role of erythrocytes in the development of intravascular disorders and microcirculation disorders with the risk of cardiovascular complications in patients with COVID-19. Probably, the involvement of red blood cells causes the development of systemic hypoxia in those patients. A detailed study of the identified shifts makes it possible to identify new targets for therapy and improve the prognosis of patients with COVID-19.

Aim of the study was to explore the impact of apolipoprotein E (APOE) gene polymorphisms (GP) on gallstone disease (GSD) and type 2 diabetes mellitus (DM2) and its role in lipid metabolism. APOE4 allele carriers had the highest levels of plasma and bile cholesterol and the lowest levels of bile acids in bile than other alleles. In GSD a higher frequency of APOE4 carriers (2.6 times compared to control) was found. GSD risk was reduced by 12 % in APOE2 carriers compared to APOE3/3. Our 20-year research confirms the association of APOE GP and GSD. The frequency of ε4/ε4 genotype is higher in people aged 18–35 years with a family history of GSD (5.8 %) compared to population of Novosibirsk (1.8 %, p < 0.05). The bile was more lithogenic in APOE4 carriers with GSD: the bile cholesterol level is 8.0 ± 0.5 versus 6.9 ± 0.6 g/l in ε3/ε3 genotype. APOE4 carriers with a family history of GSD had cholate-cholesterol ratio of 6.4 ± 0.7 versus 12.9 ± 0.2 (p < 0.05) in the absence of APOE4. in women with hypertension, the presence of GSD was associated with a combination of low density cholesterol (LDL-C) > 3.5 mmol/l and the APOE4 carriage. DM2 is a recognized risk factor for GSD. The most common opinion is that the ε4 allele is an independent risk of DM2, some authors consider the allele APOE2. Moreover, DM2 patients with the ε3/ε4 genotype have an increase in total cholesterol, LDL-C and non-high-density lipoprotein cholesterol compared to ε3/ε3. Other studies have not found any associations between APOE GP and GSD or DM2. The inconsistency of the data can be explained by the heterogeneity of the included groups and methods of APOE genotyping, which requires further research.