Adipose tissue (AT) is an endocrine and paracrine organ that synthesizes biologically active adipocytokines, which affect inflammation, fibrosis, and atherogenesis. Epicardial and perivascular fat depots are of great interest to researchers, owing to their potential effects on the myocardium and blood vessels. The aim of the study was to assess the expression and secretion of adipocytokine genes in the AT of patients with coronary artery disease (CAD) and patients with aortic or mitral valve replacement. This study included 84 patients with CAD and 50 patients with aortic or mitral valve replacement. Adipocytes were isolated from subcutaneous, epicardial (EAT), and perivascular AT (PVAT), and were cultured for 24 h. EAT exhibited the lowest level of adiponectin gene expression and secretion, regardless of nosology, and high expression levels of the leptin gene and interleukin-6 (IL-6). However, EAT adipocytes in patients with CAD were characterized by more pronounced changes in comparison with the group with heart defects. High leptin and IL-6 levels resulted in increased pro-inflammatory activity, as observed in both EAT and PVAT adipocytes, especially in individuals with CAD. Therefore, our results revealed the pathogenetic significance of alterations in the adipokine and cytokine status of adipocytes of EAT and PVAT in patients with CAD.

Background: There is growing interest in finding methods to enhance cognitive function and comprehend the neurophysiological mechanisms that underlie these improvements. It is assumed that non-pharmacological interventions have better results in cognitive recovery. The aim of this study was to assess the effect of multi-task cognitive training (MTT) on electroencephalographic (EEG) changes and markers of the neurovascular unit in patients undergoing coronary artery bypass grafting (CABG). Methods: This prospective cohort study involved 62 CABG patients aged 45–75 years, 30 of whom underwent a 5–7-day MTT course. The groups of patients were comparable with respect to baseline clinical and anamnestic characteristics. An EEG study was performed before surgery and 11–12 days after CABG. Markers of the neurovascular unit (S100β, NSE, and BDNF) were examined at three time points: before surgery, within the first 24 h after surgery, and 11–12 days after CABG. Results: Patients without training demonstrated higher relative theta power changes compared to the MTT patients. The course of MTT was associated with low plasma S100β concentration but high BDNF levels at the end of the training course. Conclusions: The theta activity changes and the markers of the neurovascular unit (S100β, BDNF) indicated that the severity of brain damage in cardiac surgery patients after a short course of MTT was slightly reduced. Electrical brain activity indicators and vascular markers can be informative for monitoring the process of cognitive rehabilitation in cardiac surgery patients.

The functional activity of platelets was measured in platelet-rich plasma with inductors: ADP, epinephrine, collagen. Prothrombin activity, international normalized ratio, activated partial thromboplastin time (APTT), thrombin time, fibrinogen concentration, antithrombin III and protein C activity, fibrinolysis were determined in blood plasma. Changes in clot formation and viscoelastic properties of clots were assessed using thromboelastography. Significant differences were found in the hemostasiological profile of sheep and CHD patients. Sheep platelets had increased response to ADP induction and practically no response to epinephrine induction; collagen-induced aggregation was comparable in the study groups. Coagulation hemostasis of sheep was characterized by increased activity of the prothrombin complex, shortened thrombin time, while APTT and fibrinogen values remained comparable. At the same time, sheep exhibited a significant decrease in the activity of anticoagulant and fibrinolytic systems as compared to CHD patients. When assessing dynamic changes in clot formation, it was observed that initiation phase was faster in animals, while clot density exceeded that in patients. The hemostasiological profile of sheep is characterized by the increased speed of thrombus formation, greater strength of the formed clot, and lower lysis ability as compared to CHD patients. The revealed details of the hemostasiological profile of sheep can be potential targets for therapy with antithrombotic drugs that minimize thrombotic risks in preclinical testing of vascular prostheses.

Background/Objectives : The causes and mechanisms underlying the development of leptin resistance (LR) in patients with cardiovascular disease (CVD) remain unknown. Investigating the characteristics of adipose tissue in patients with CVD is a relevant scientific problem that may help to uncover the missing links in the pathogenesis of LR. This study aimed to evaluate systemic and local markers of LR in patients with different forms of CVD, and to determine the prevalence and tissue-specific expression patterns that contribute to LR. Methods: The study included 108 patients with myocardial infarction (MI), 96 patients with chronic coronary heart disease (CHD), and 96 patients with acquired heart disease (AHD). On day 1 of admission to the hospital, leptin and leptin receptor concentrations and the serum-free leptin index (FLI) were measured. Leptin resistance (LR) was defined as a leptin level of >6.45 ng/mL and FLI of >25. In chronic CHD and AHD patients, LEP, LEPR1, LEPR2, LEPR2/2, LEPR3, LEPR3/2, and LEPR4 expression as well as leptin and soluble leptin receptor secretion were assessed in subcutaneous (SAT), epicardial (EAT), and perivascular (PVAT) adipose tissue. Results: MI and chronic CHD patients are characterized by elevated leptin levels and high FLI values in the blood serum, which indicates a high prevalence of LR, in contrast to AHD patients. In chronic CHD, the LR level was highest in EAT and moderate in SAT. Reduced leptin sensitivity in EAT is underlied by decreased expression of LEPR1, LEPR2, LEPR2/2, LEPR3, LEPR3/2, and LEPR4, and increased leptin production by epicardial adipocytes, which contributes to enhancement of leptin resistance at the systemic level. Conclusions: A high LR rate was detected in patients with MI and chronic CHD. The identified changes in EAT lead to the development of leptin resistance in chronic CHD patients.

Aim. To assess the changes of biochemical markers in hospitalization, the relationship with the severity of myocardial fibrosis and the epicardial adipose tissue (EAT) thickness one year after myocardial infarction (MI).Material and methods. A total of 88 patients (65 men and 23 women) with MI were examined. The percentage of cicatricial changes in the myocardium and the EAT thickness were measured using the magnetic resonance imaging (MRI) one year after MI. In the hospitalization (days 1 and 12) and 1 year after MI, the concentrations of N-terminal pro-brain natriuretic peptide (NT-proBNP), stimulating growth factor (ST2), interleukin-33 (IL-33) and type I collagen (COL-1). The data were analyzed using descriptive statistics, correlation and ROC analysis, and logistic regression (Statistica 9.0).Results. One year after MI, cicatricial changes were detected in 68 (77%) patients: 27 people had myocardial fibrosis 15%. We established that myocardial fibrosis after MI is associated with unfavorable medical history, a complicated course during in-hospital period and higher concentrations of ST2, NT-proBNP, COL-1 compared with patients without myocardial fibrosis. High levels of ST2, NT-proBNP increase the risk of myocardial fibrosis by 1,2 and 1,8 times after hospitalization, respectively. In patients with myocardial fibrosis >15%, IL-33 level was significantly lower in the 1st day of MI. It was found that the EAT thickness increases with fibrosis of 5-15%. An increase in the left (LV) and right ventricular (RV) EAT thickness by 1,33 times and 1,34 times, respectively, increases the risk of myocardial fibrosis (LV EAT thickness, mm (OR 1,33; 95% CI (1,08-1,4), AUC 0,75; RV EAT thickness, mm (OR 1,34; 95% CI (1,15-1,43), AUC 0,79). In patients with myocardial fibrosis >15%, EAT thickness decreases and correlates with NT-proBNP increase in the acute period and a one year after MI.Conclusion. The development of myocardial fibrosis one year after MI is associated with an increase in ST2, NT-proBNP, COL-1, both in the hospitalization and 1 year after MI. The decrease in IL-33 concentration during hospitalization with MI is accompanied by the development of fibrosis >15% of the myocardium.

Background. In coronary artery disease, a change in the adipocytokine content of local fat depots of the heart is observed. However, it has not yet been established whether the expression levels of the studied parameters are really related to the degree of atherosclerotic lesion of the spacecraft. Aims to identify the features of the expression of adiponectin, leptin and IL-6 by adipocytes of epicardial, perivascular and subcutaneous adipose tissue depending on the degree of atherosclerotic lesion of the coronary channel in coronary heart disease. Materials and methods. The study conducted at the Research Institute for Complex Issues of Cardiovascular Disease in 20172020, included 84 patients with coronary heart disease (CAD), of which 39 with a moderate degree of atherosclerotic lesion of the coronary artery (CA) ( 22 points on the SYNTAX Score scale), 20 with severe (2331 points) and 25 with extremely severe ( 32 points). Biopsies of subcutaneous (SAT), epicardial (EAT) and perivascular adipose tissue (PVAT) were obtained during elective coronary artery bypass grafting (CABG). The expression of adipocytokine genes was determined using polymerase chain reaction (real-time PCR) using TaqMan probes and the concentration of the studied adipocytokines in adipocyte culture medium by enzyme immunoassay. Statistical analysis was performed using Statistica 9.0, a one-dimensional and multi-dimensional logistic regression analysis. Results. In CAD in adipocytes of the cardiac fat depot, a shift in the balance of adipocytokines is observed towards increased expression and secretion of leptin, IL-6 and a decrease in adiponectin with maximum manifestation in severe and extremely severe coronary lesions. Adipocytes of EAT were characterized by the minimal expression of the adiponectin gene against the background of the maximum leptin and IL-6 in comparison with adipocytes SAT and PVAT. Conclusions. Low expression of the adiponectin in EAT and PVAT against the background of increased expression of leptin and IL-6 is associated with an increase in the degree of atherosclerotic lesion of the coronary channel.