The COVID-19 epidemic has already come to be seen as an emergency of international concern. This relates not only to the wide occurrence of the infection, but also to a fairly high mortality rate, currently more than 6.5 million deaths in the world. The aim of this study was to analyze, generalize and systematize the currently available literary data on the study of the novel coronavirus infection pathogenesis in the human body and to determine key changes that occur after the SARS-CoV-2 penetration into cells. In this way to target physicians primarily based on the pathogenetic processes that occur in the human body, syndromes and symptom complexes that are observed in treatments. Results. The article presents a literature review demonstrating that the specific interaction between the virus and somatic cells is the triggering mechanism for the pathogenesis of coronavirus infection. The main route for SARS-CoV-2 entry into the body is the angiotensin-converting enzyme 2 (ACE2) receptor, which is expressed not only in type 2 alveolar epithelial cells, but also in cells of the kidney, heart, blood vessels and gastrointestinal tract, including endotheliocytes and pericytes. Expression of the ACE2 receptor has also been shown in various structures and parts of the brain, cells of the conjunctiva, limbus, cornea and cells of the substantia propria. A high expression of the ACE2 receptor has been found in the epithelial cells of the oral mucosa, salivary glands, tonsils and tongue. These factors explain a possible involvement of different organs and systems in the development of multiorgan failure. Conclusions. In the development of multiorgan disfunction, two components are important: first, direct cell tropism and viral load, that may be unique in each patient. Secondly, it is the development of immune-mediated reactions to infected cells. Under conditions of hyperimmune inflammation, that is, the development of cytokine storm, acute respiratory distress syndrome progresses, and multiple organ failure develops. Endothelial damage is directly involved in the pathophysiology of this process, that results in the development of endothelial dysfunction, disruption of microcirculation, as well as perivascular inflammation, which aggravates damage to the endothelium and can lead to thrombus formation. The use of modern knowledge about the immunopathogenesis of COVID-19 would help to estimate the risk for severe infection and the possible development of complications, allowing for the timely implementation of effective pathogenetic therapy.

BackgroundPost-COVID-19 syndrome (PCS) has been increasingly recognized as an emerging problem: 50% of patients report ongoing symptoms 1 year after acute infection, with most typical manifestations (fatigue, dyspnea, psychiatric and neurological symptoms) having potentially debilitating effect. Early identification of high-risk candidates for PCS development would facilitate the optimal use of resources directed to rehabilitation of COVID-19 convalescents.ObjectiveTo study the in-hospital clinical characteristics of COVID-19 survivors presenting with self-reported PCS at 3 months and to identify the early predictors of its development.Methods221 hospitalized COVID-19 patients underwent symptoms assessment, 6-min walk test, and echocardiography pre-discharge and at 1 month; presence of PCS was assessed 3 months after discharge. Unsupervised machine learning was used to build a SANN-based binary classification model of PCS development.ResultsPCS at 3 months has been detected in 75% patients. Higher symptoms level in the PCS group was not associated with worse physical functional recovery or significant echocardiographic changes. Despite identification of a set of pre-discharge predictors, inclusion of parameters obtained at 1 month proved necessary to obtain a high accuracy model of PCS development, with inputs list including age, sex, in-hospital levels of CRP, eGFR and need for oxygen supplementation, and level of post-exertional symptoms at 1 month after discharge (fatigue and dyspnea in 6MWT and MRC Dyspnea score).ConclusionHospitalized COVID-19 survivors at 3 months were characterized by 75% prevalence of PCS, the development of which could be predicted with an 89% accuracy using the derived neural network-based classification model.

Over a long period, chronic heart failure was primarily associated with impaired contractility of the left ventricular myocardium, which is a manifestation of systolic dysfunction. Based on modern ideas about the pathophysiology of CHF syndrome, systolic dysfunction is considered as one of the etiological factors along with changes in wall tension and the structure of diastolic filling, i.e. everything that is included in the concept of "LV remodeling". The objective is to present a review of the key parameters of chronic heart failure and left ventricular diastolic dysfunction according to the latest updates. The role and significance of diastolic dysfunction as the cause of chronic heart failure syndrome have only been determined over the past three decades, which can be explained by the difficulty of early diagnostics of diastolic dysfunction. The article describes the historical evolution of heart failure and left ventricular diastolic dysfunction estimation. It is important to note the high prevalence of diastolic dysfunction. The signs of myocardial diastolic dysfunction are detected in people with almost any heart disease. The universal review of the most important parameters which determine this disorder has been presented. It has been shown that Doppler echocardiography is now the noninvasive "gold standard" for estimation of diastolic dysfunction. We have presented methods of treatment for diastolic dysfunction according to the 2017 American College of Cardiology/American Heart Association updated Guidelines for the management of heart failure Conclusions. The experimental studies demonstrate that the survival of HF patients with a preserved EF depends not so much on its indices, but on the severity of DD. DD is a more prognostic marker of mortality rate in patients with HF than EF, which requires further study for better therapeutic efficacy.

Затверджено Вченою радою Харківського національного медичного університету. Протокол № 6 від 18.06. 2018 р.

Obesity is considered as a valid risk factor for cardiovascular disease, due to the fact that the risk of morbidity and mortality from various causes in obese people is signifi cantly higher. Exact mechanisms of metabolic disorders in hypertension with obesity is still discussible. The aim of the study – to determine the peculiarities of carbohydrate, lipid metabolism changes and activity of adipokines and interleukin-22, in patients with hypertension according to nutritional status. Methods: 80 patients (37 males and 43 females) with essential hypertension (EH) of average age 60.17 years were examined. Carbohydrate, lipid profi les, apolipoprotein B (apo B), tumor necrosis factor-α (TNF-α), plasminogen activator inhibitor-1 (PAI-1), adiponectin, interleukin-22 (IL-22) were estimated. Results: In patients with EH and obesity was found carbohydrates metabolism abnormalities, that was manifested as hyperinsulinemia, glucose and HbA1c levels elevation and insulin resistance (according to HOMA index). Lipid metabolism disorders were observed as valid increasing of triglycerides and apo B. Body mass index elevation was associated with progressive increasing of TNF-α and PAI-1 concentration with reducing of adiponectin level in the patients with EH. Positive relationships between TNFand HbA1c, apo B; PAI-1 with glucose levels: negative correlation adiponectin with body mass and waist to hip ratio were detected in the patients with obesity associated (BMI ≥ 30 kg/m2) EH. Positive signifi cant correlations between apo B and insulin levels, HOMA index, and TNF-α concentration were defi ned. IL-22 in overweigh and obese patients was signifi cantly higher, correlates negatively with HDL-C. Conclusion: In patients with EH and obesity the adipokine dysfunction was revealed, that correlates with carbohydrate and lipid parameters that indicate increased proinfl ammatory and prothrombogenic processes. RESUMEN

Practicum in Propedeutics of Internal Medicine. Part 1: “Main methods of the patient’s examination in internal medicine” for 3rd year students of 6th medical faculty

The review article presents the pathogenetic role of atherosclerotic vascular lesions in the development of cardiovascular diseases. The relationship between atherosclerosis and inflammation, which is characterized by the identical mechanism in the early phases, which includes the enhancement of the interaction between the vascular endothelium and circulating leukocytes is shown. The definition of such concepts as dyslipidemia, hyperlipoproteinemia and hyperlipidemia is given. The classification of hyperlipoproteinemia by Fredrickson, the clinical classification of dyslipidemia, proposed by the Ukrainian Scientific Society of Cardiologists, 2011 is considered. The correction of dyslipidemia, by both non-medicamentous measures, and drug treatment according to different variants of dyslipidemia is shown. The main groups of lipid-lowering drugs are listed. Their main mechanisms of action to reduce blood lipid levels are noted, and their side effects are listed. General recommendations are given on the monitoring of lipids and liver enzymes in patients taking lipid-lowering therapy.

Abstract Background and aims: Essential hypertension and type 2 diabetes mellitus possess some common pathogenetic components, in particular, activation of immune inflammatory response, the intercellular mediators of which are cytokines. In our study, hypertensive patients were examined, depending on presence of concomitant prediabetes or type 2 diabetes mellitus, for the level of pro-inflammatory cytokines oncostatin M, interleukin-6 in conjunction with glucometabolic parameters and lipid metabolism parameters. Material and methods: A total of 94 hypertensive patients were examined. Oncostatin M and Interleukin-6 plasma level detected using ELISA (BSM). Results and conclusions: The 1st group consisted of hypertensive patients. The 2nd group included hypertensive patients with prediabetes. The 3rd group were hypertensive patients with type 2 diabetes mellitus. We have revealed the increased circulating level of oncostatin M and interleukin-6 in patients 1st group, which confirms the pathogenetic value of hypertension as a stimulus for hyperproduction of these cytokines. In 2nd group the level of oncostatin M and interleukin-6 decreased, which could probably be explained, on the one hand, by dual effects of the family of interleukin-6 the representatives of which either contribute to the development of insulin resistance or, vice versa, enhance the insulin sensitivity of tissues.

La revisione ha esaminato i metodi esistenti di diagnosi, quando il diabete nei pazienti con ipertensione ed i risultati di una recente ricerca in questo settore. Offerte con i dati di letteratura e analisi delle loro osservazioni, nazionali ed esteri come l'esame, che include la valutazione del metabolismo dei carboidrati, sulla base del livello di glucosio e insulina glucosio nel sangue dopo test di glucosio-tolleranza orale, hlikozilovanoho emoglobina calcolo dell'indice di insulinoresistenza - HOMA .