A series of unexplained cases with pneumonia have been reported in China since December 2019. Subsequent studies have found a novel strain of coronavirus, SARS-CoV-2, as the causative agent of acute infectious disease that has been named as coronavirus disease 2019 (COVID-19). COVID-19 has outbroken as a global pandemic affecting over 200 countries. This review focuses on a novel coronovirus disease, reporting all available data on its etiology, epidemiology, pathogenesis, clinical manifestations, principles of diagnosis and treatment. In addition, the impact of COVID on the cardiovascular system is highlighted.

The management of these patients requires healthcare professionals to have specific knowledge on the characteristics of the viral infection, its clinical signs and symptoms combined with cardiovascular diseases, as well as individual and collective prevention measures. The safety of healthcare professionals and favorable prognosis of patients are of the top priority for the modern healthcare system.

The review discusses current challenges associated with the novel coronavirus disease COVID-19 and cardiovascular diseases. The results of few clinical trials and individual case reports have shown the presence of certain problems in treating patients with comorbidity and viral infection. The new data on the drug interactions are reported. Common patterns of typical cardiovascular diseases and COVID-19 are presented. The risk groups with the need for timely diagnosis and intensive cardiac care are identified to prevent adverse outcomes in patients with this comorbidity.

The American College of Cardiology and the World Heart Federation jointly hosted Abt t           the 69th Congress of the American College of Cardiology (АСС) that took place in March 28-30, 2020. It was the first remote annual meeting due to the COVID-19 pandemic. However, it didn’t prevent healthcare professionals from 135 countries to participate in the virtual meeting. The employees of the Research Institute for Complex Issues of Cardiovascular Diseases and the Department of Cardiology and Cardiovascular Surgery of the Kemerovo State Medical University took active part in the virtual live sessions and reports in this article novel evidences from recently completed international clinical trials that were presented at the 69th Congress. The Congress organizers opened a free access to the video, abstracts, slides and workshops in 10 main clinical learning pathways till June 2020.

Aim. To study APOA5 genetic polymorphism in Caucasoid patients with familial hypercholesterolemia.

Methods. Sample of patient with familial hypercholesterolemia (43 unrelated Caucasoid persons) was formed using Dutch Lipid Clinic Network Criteria. Targeted sequencing of genome DNA was performed by NimbleGen SeqCap EZ Choice kit on pyrosequencer Roche Junior GS (Roche, Switzerland).

Results. In patients with familial hypercholesterolemia, 8 substitutions were identified in the APOA5 gene: rs2075291, rs3135506, rs2072560, rs2266788, rs3135507, rs34089864, rs619054, and rs651821, that are known to be associated with dyslipidemia. One novel substitution Ala169Asp was found. It is responsible for changing the charge of a domain for lipid droplets binding in the APOA5 protein. There were no differences in the frequencies of the ApoA5*2 intragenic haplotype, which has been recently reported to be associated with an increased triglyceride levels in patients with familial hypercholesterolemia and the population.

Conclusion. Genetic variants ofAPOA5, common in patients with familial hypercholesterolemia, may be involved in the formation of the pathological phenotype of dyslipidemia. However, a more accurate assessment oftheir contribution is required to differentiate patients with familial hypercholesterolemia according to their triglycerides level.

Aim. To develop a method for measuring circulating monomeric C-reactive protein and to determine the levels of C-reactive protein isoforms (native pentameric C-reactive protein and monomeric C-reactive protein) in patients with stable coronary artery diseases and acute myocardial infarction.

Methods. Plasma and blood serum samples were collected from 22 patients with stable coronary artery disease (CAD), 14 patients with acute myocardial infarction at days 2-3, and 11 healthy volunteers. The analysis was performed using flow cytofluorometry FACS Cantoll and a set of functional particles Cytometric Bead Array (BD Biosciences, USA). Antibodies for CRP (clones 328 and 372 from ImTek, Russia, and clone 8C8 from Sigma-Aldrich, USA), гСКР-GAH (with antibodies for CRP), native CRP (ImTek, Russia) and recombinant monomeric CRP (received as a gift from Dr. L. Potempa) were used in the analysis.

Results. A novel laboratory kit for measuring blood levels of monomeric CRP has been developed. Patients with CAD demonstrated elevated plasma levels of CRP, whereas healthy subjects reported the levels below the lower cut-off. Patients with stable CAD had mCRP concentration of 2.34 (1.42; 3.27) pg/L, whereas patients with acute MI had the highest level of 16.76 (3.65;54.83) pg/L (p = 0.0002, Kruskal-Wallis One Way Annova). There were no any correlations between mCRP levels and nCRP, hs-CRP and IL-6.

Conclusion. The novel laboratory kit allows measuring monomeric C-reactive protein and provides novel data on the role of mCRP in the development and progress of CAD. Obtained data suggest that monomeric C-reactive protein can play no less important role than native C-reactive protein in the diagnosis and progress of cardiovascular diseases as well as other diseases associated with the inflammatory process.

Aim. To study microrheological properties of RBCs and capillary blood flow parameters using optical methods in patients with arterial hypertension (AH) and type 2 diabetes mellitus (DM2).

Methods. RBCs aggregation properties were evaluated in vitro using laser aggregometry and optical trapping. Сapillary nail refill was evaluated in vivo using nailfold digital capillaroscopy.

Results. The aggregation of RBCs in patients suffering from AH was higher compared to healthy subjects who demonstrated a decrease in the aggregation time by 29±9%. A similar trend was observed in patients with AH and DM2. The comparison of the results obtained by different methods showed that patients with AH with a high capillary blood flow velocity measured in vivo reported a decrease in the aggregation index by 14±4% compared to patients with low velocity.

Conclusion. The comparison of microrheological blood properties in patients with AH and AH+DM2 versus the control group showed statistically significant differences in the aggregation index that was higher in AH patients. These differences were more pronounced in patients with AH and DM2. The results obtained by in vitro and in vivo methods were consistent.

Aim. To assess the prevalence of cardiovascular risk factors in young adults aged 25-44 years with early coronary artery disease (CAD) and abdominal obesity (AO) in Novosibirsk.

Methods. A random sample of subjects aged 25-44 years residing Novosibirsk underwent population screening. 1,457 people were examined (653 men and 804 women). The epidemiological diagnosis of CAD was established based on the validated epidemiological (according to the Rose Angina Questionnaire) and clinical (ECG decoded according to the Minnesota code) criteria. Early CAD was detected in 49 people who then were assigned into 4 subgroups: 1) obese subjects with CAD -24 people, 2) non-obese subjects with CAD - 25 people, 3) age- and sex-matched obese controls without CAD - 44 people, 4) age- and sex-matched non-obese controls without CAD - 30 people. The prevalence of the following CVD risk factors was assessed: smoking, increased body mass index (BMI), increased waist circumference (WC), the presence of arterial hypertension (AH), physical inactivity, elevated levels of low-density lipoprotein cholesterol (LDL-C), nonhigh density lipoprotein cholesterol (non-HDL-C), triglycerides (TG) in blood.

Results. BMI, LDL-C and non-HDL-C increase 1.3-fold in obese subjects with CAD along with 1.9-fold increase in TG levels as compared to non-obese subjects with CAD. Obese men with CAD had BMI, non-HDL-C, and TG levels 1.3, 1.5, and 2.6 times higher respectively, compared with non-obese men with CAD. BMI, LDL-C levels, non-HDL-C levels and the presence of AH increased 5.2-, 1.6-, 1.6-, and 4.7-fold, respectively, in obese subjects with CAD compared with non-obese subjects with CAD. Obese men with CAD reported a 4.4- and 6.2-fold increase in the prevalence of increased BMI and the presence of AH, respectively, than non-obese men with CAD. The examined individuals revealed an independent direct association of the relative risk of CAD as a comorbidity of AH (OR = 3.368, CI 1.057-10.728, p = 0.040). In addition, men demonstrated an association with elevated levels of LDL-C (OR = 1.019, CI 1.000-1.039, p = 0.049) and non-HDL-C (OR = 1.019, CI 1.000-1.038, p = 0.049) in blood.

Conclusion. AH, elevated levels of LDL-C, non-HDL-C and TG are considered as significant risk factors in obese people under 45 years of age (mainly in men) with early CAD.

Aim. To compare gene expression profiles of CFEC to human coronary artery endothelial cells, based on the results of whole transcriptome analysis.

Methods. CFEC were isolated from peripheral blood of patients during percutaneous coronary intervention. Human coronary artery endothelial cells were purchased from Cell Applications (300K-05a, USA). Cells were lysed with TRIzol with the following total RNA isolation and DNAse treatment. Then rRNA depletion was performed, followed by DNA library preparation. DNA libraries were then quantified by qPCR (CFX96 Touch, Bio-Rad, USA), pooled in equimolar amounts and sequenced (HiSeq 2000, Illumina) using 2 * 125 bp chemistry.

Results. RNA-seq demonstrated that CFEC were generally similar to human coronary artery endothelial cells, regarding their global gene expression profile. However, CFEC overexpressed specific markers of all endothelial lineages (NRP2, NOTCH4, LYVE1), in particular, lymphatic EC (LYVE1) and had upregulated extracellular matrix and basement membrane genes (COLlAl, COL1A2, COL4A1, COL4A2).

Conclusion. Baseline gene expression in CFEC is close to that of human coronary artery endothelial cells, testifying about their utility for the seeding of tubular scaffolds before the implantation to improve their short- and long-term performance.

Systemic inflammatory response syndrome is a complex multisyndromic, phase-specific pathological process that develops with systemic damage. Outcomes largely depend on the balance of multidirectional sequential stages: hyperinflammatory reaction and compensatory anti-inflammatory response syndrome (CARS). Regulatory T-cells (Tregs) are able to regulate adaptive and innate immune responses and contribute to the various stages ofthe systemic inflammatory response syndrome. At the initial hyperinflammatory stage, Tregs are able to limit self-inflicted damage. At the same time, Tregs contribute to CARS and the formation of induced immunosuppression, predisposing to a high susceptibility to nosocomial and opportunistic infections, with subsequent transition to multiple organ dysfunction syndrome. Regulatory T-cells and their functional changes are considered as predictors and prognostic markers of critical illness.

Disturbance of lipid metabolism can lead to the development of pathological processes. Atherosclerosis is a chronic disease characterized by the development of atherosclerotic lesions as a result of the lipid accumulation in the great arterial walls. As a result of cholesterol accumulation by macrophage within the atherosclerotic lesions, they differentiate into foam cells. Macrophage lipid uptake may occur either though the receptor-dependent pathway by low-density lipoprotein receptors and the SR-A, CD36 and LOX-1 scavenger receptors, or the receptor-independent pathway by pinocytosis and phagocytosis. Various enzymes such as ACAT-1 and Abstract    NCEH, enzymes of the biosynthesis and fatty acid oxidation pathways, as well as various transcription factors - SREBP, Nrf1 and Nrf2 participate in the intracellular regulation of lipids. High-density lipoproteins and transporters such as ABCA1, ABCG1 and SR-BI play a vital role in the regulation of cholesterol efflux from cells. Players of lipid metabolism are regulated by various kinase signaling pathways that activate many transcription factors - LXR, RXR, PPARy, NF-kB, etc. Regulation disturbance of intracellular metabolism and imbalance in uptake and efflux of cholesterol from macrophages lead to their differentiation into foam cells. The aim of this review is to describe the mechanisms underlaying lipid metabolism in macrophages and resulting in the transformation of these cells into foam cells.

Atherosclerotic lesions are characterized by various multiple changes at the gene expression levels. However, there are general trends at the cellular and molecular levels. Extracellular matrix remodeling of blood vessels occurs due to an increase in the mRNA levels of the cathepsin and matalloprotease genes, as well as a decrease in the levels of type I and III collagen transcripts. A change in the transcriptional activity of some genes leads to a disruption in the regulation of the smooth muscle cells cytoskeleton and intercellular interaction, which also contributes to the formation of atherosclerotic lesions. Attraction of leukocytes to the arterial walls by cathepsins, chemokines and other markers associated with signaling systems leads to the infiltration of monocytes into the intima. In addition, there is a change in the ratio of apoprotein expression, the prevalence of the expression of some over others, which leads to the cholesterol accumulation and impaired lipid metabolism.

The genes responsible for the accumulation of oxidized low-density lipoproteinare activated, that induces inflammatory responses through Toll-like receptors. High levels of CD36 and CD68 are observed, signaling the infiltration of lesions by macrophages. This review focuses on the recent studies on the transcriptome of atherosclerotic plaque from the human carotid artery. We examined differentially expressed genes of metalloproteases, cathepsins, chemokines and their receptors, lipid metabolism, extracellular matrix components, receptors associated with signaling systems, macrophage and smooth muscle cells markers. Several studies have overlapping results, as well as new genes that have not previously been reported to be associated with atherosclerosis. Studying of atherosclerotic plaque markers and single signaling pathway genes can provide new insights into the pathways involved in the mechanism of atherogenesis, as well as identify potential biomarkers that characterize the stages of atherosclerotic lesion development.

Preparation of cell suspension from arterial walls is a key issue in planning the research aimed at studying the role of individual cell types in human arteries in vivo, both normal and affected with atherosclerosis. To date, there is a range of approaches for disaggregating arterial tissues. In this review, we report previously published data and techniques for disaggregating arterial tissues. In addition, an algorithm able optimizing the disaggregation of arteries is proposed taking into account emerging problems and probable solutions.