The issue of the prognostic value of obesity in the development of cardiovascular diseases still remains open. Different input of visceral and subcutaneous adipose tissue in the formation of cardiometabolic risk is highlighted in many research works. A range of epidemiological studies provides data confirming relation of the visceral adiposity with abnormal metabolic profile and increased cardiovascular risk, while subcutaneous adipose tissue is attributed with relative protective properties. Pathophysiological mechanisms mediating interconnection of visceral adiposity with the development of atherosclerosis remain studied incompletely. It was stated that sex hormones, estrogens and androgens, participate in the redistribution of adipose tissue, sustenance of energy homeostasis, influence on the secretion of adipokines and immune regulation of adipose tissue. Meanwhile cells of immune system, including cells of the adaptive immunity, widely presented in adipose tissue contribute to the development of the local subclinical inflammation and influence on the features of cardiometabolic effects of adipose tissue. The review discusses possible mechanisms, by which abovementioned relationships are executed and cardiovascular risk in obesity is realized.

Purpose. This work investigates the relations between the production of reactive oxygen species (ROS) by epicardial adipose tissue (EAT) adipocytes and parameters of glucose/insulin metabolism, circulating adipokines levels, and severity of coronary atherosclerosis in patients with coronary artery disease (CAD); establishing significant determinants describing changes in ROS EAT in this category of patients. Material and methods. This study included 19 patients (14 men and 5 women, 53–72 y.o., 6 patients with diabetes mellitus type 2; 5 patients with prediabetes), with CAD, who underwent coronary artery bypass graft surgery. EAT adipocytes were isolated by the enzymatic method from intraoperative explants obtained during coronary artery bypass grafting. The size of EAT adipocytes and ROS level were determined. Results. The production of ROS by EAT adipocytes demonstrated a direct correlation with the level of postprandial glycemia (rs = 0.62, p < 0.05), and an inverse correlation with serum adiponectin (rs = −0.50, p = 0.026), but not with general and abdominal obesity, EAT thickness, and dyslipidemia. Regression analysis demonstrated that the increase in ROS of EAT adipocytes occurs due to the interaction of the following factors: postprandial glycemia (β = 0.95), postprandial insulin (β = 0.24), and reduced serum adiponectin (β = −0.20). EAT adipocytes in patients with diabetes and prediabetes manifested higher ROS production than in patients with normoglycemia. Although there was no correlation between the production of ROS by EAT adipocytes and Gensini score in the total group of patients, higher rates of oxidative stress were observed in EAT adipocytes from patients with a Gensini score greater than median Gensini score values (≥70.55 points, Gr.B), compared to patients with less severe coronary atherosclerosis (<70.55 points, Gr.A). Of note, the frequency of patients with diabetes and prediabetes was higher among the patients with the most severe coronary atherosclerosis (Gr.B) than in the Gr.A. Conclusions. Our data have demonstrated for the first time that systemic impairments of glucose/insulin metabolism and a decrease in serum adiponectin are significant independent determinants of oxidative stress intensity in EAT adipocytes in patients with severe coronary atherosclerosis. The possible input of the interplay between oxidative stress in EAT adipocytes and metabolic disturbances to the severity of coronary atherosclerosis requires further investigation.

The changes of epicardial adipose tissue’s (EAT) morphofunctional characteristics represent an important factor of cardiometabolic impairments development. However, factor data determining the severity of EAT adipocytes’ hypertrophy in patients with coronary atherosclerosis are absent in literature.Aim: To compare the size of the EAT adipocyte and the percentage of hypertrophied adipocytes with the parameters of glucose/insulin metabolism, blood lipid transport function, adipokines’ profile and serum levels of high sensitive C-reactive protein (hsCRP) in patients with chronic coronary artery disease (CAD) undergoing coronary artery bypass grafting (CABG); to establish statistically significant determinants of a pronou ced degree of EAT adipocytes’ hypertrophy.Material and Methods. The study included 42 patients (m/f 28/14) aged 53–72 y.o. with CAD, who underwent CABG. The material for the study was EAT adipocytes obtained by the enzymatic method from intraoperative explants. The basal blood levels of glycemia, insulinemia, C-peptide, blood lipid transport function, adipokines and hsCRP were determined. The median indicators of the size of EAT adipocytes and the proportion of EAT adipocytes over 100 μm were 87.32 μm and 14.64%, respectively. The total sample of patients was divided into two groups: gr. 1 with an average size of EAT adipocytes less than or equal to 87.32 μm and gr. 2 with an average size of EAT adipocytes more than 87.32 μm. Gr. 2 had higher body mass index, waist and hip circumferences, triglycerides, hsCRP, and lower adiponectin levels, while the median proportion of hypertrophied adipocytes was three times higher than in group 1. A model of multiple logistic regression was constructed, according to which statistically significant determinants of the pronounced EAT adipocytes’ hypertrophy are represented by the decreased level of adiponectin, and increased concentrations of hsCRP and C-peptide, which reflects the biosynthesis and secretion of insulin. The predictive accuracy of the model was 82%, sensitivity 85%, specificity 79%, AUC = 0.89.Conclusion. Our results indicate a close correlation between the development of EAT adipocytes hypertrophy, impaired production of adiponectin, insulin, and inflammation processes. Concentrations of adiponectin, hsCRP, and basal C-peptide in the blood are biomarkers that accurately determine the presence of EAT adipocyte hypertrophy.

The aim of the study was to compare the morphological features of epicardial adipose tissue (EAT) adipocyte with the circulating inflammatory biomarkers and parameters of extracellular matrix remodeling in patients with coronary artery disease (CAD). We recruited 42 patients with CAD (m/f 28/14) who were scheduled for coronary artery bypass graft surgery (CABG). EAT adipocytes were obtained by the enzymatic method from intraoperative adipose tissue samples. Concentrations of secreted and lipoprotein-associated phospholipase A2 (sPLA2 and LpPLA2), TNF-α, IL-1β, IL-6, IL-10, high-sensitive C-reactive protein (hsCRP), metalloproteinase-9 (MMP-9), MMP-2, C-terminal cross-linking telopeptide of type I collagen (CTX-I), and tissue inhibitor of metalloproteinase 1 (TIMP-1) were measured in blood serum. Patients were divided into two groups: group 1—with mean EAT adipocytes’ size ≤ 87.32 μm; group 2—with mean EAT adipocytes’ size > 87.32 μm. Patients of group 2 had higher concentrations of triglycerides, hsCRP, TNF-α, and sPLA2 and a lower concentration of CTX-I. A multiple logistic regression model was created (R_N² = 0.43, p = 0.0013). Concentrations of TNF-α, sPLA2 and CTX-I appeared to be independent determinants of the EAT adipocyte hypertrophy. ROC analysis revealed the 78% accuracy, 71% sensitivity, and 85% specificity of the model, AUC = 0.82. According to our results, chronic low-grade inflammation and extracellular matrix remodeling are closely associated with the development of hypertrophy of EAT adipocytes, with serum concentrations of TNF-α, sPLA2 and CTX-I being the key predictors, describing the variability of epicardial adipocytes’ size.

Eurasian clinical practice guidelines for dietary management of cardiovascular diseases include actual healthy diet recommendations and modern dietary approaches for prevention and treatment of cardiovascular diseases. Nutritional assessment and interventions based on pathogenesis of atherosclerosis and cardiovascular diseases are presented.Modern nutritional and dietary recommendations for patients with arterial hypertension, coronary heart disease, chronic heart failure, heart rhythm disorders, dyslipidemia and gout are summarized in present recommendations. Particular attention is paid to the dietary management of cardiovascular patients with obesity and/or diabetes mellitus. This guide would be interesting and intended to a wide range of readers, primarily cardiologists, dietitians and nutritionists, general practitioners, endocrinologists, and medical students.

The aim was to investigate the association of monocyte heterogeneity and presence of circulating endothelial cells with the severity of coronary atherosclerosis in patients with coronary artery disease (CAD) and type 2 diabetes mellitus (T2DM). We recruited 62 patients with CAD, including 22 patients with DM2. The severity of atherosclerosis was evaluated using Gensini Score. Numbers of classical (CD14++CD16–), intermediate (CD14++CD16+), and non-classical (CD14+CD16++) monocyte subsets; circulating endothelial progenitor cells; and the presence of circulating endothelial cells were evaluated. Counts and frequencies of intermediate monocytes, but not glycaemia parameters, were associated with the severity of atherosclerosis in diabetic CAD patients (r_s = 0.689; p = 0.001 and r_s = 0.632; p = 0.002, respectively). Frequency of Tie2+ cells was lower in classical than in non-classical monocytes in CAD patients (p = 0.007), while in patients with association of CAD and T2DM, differences between Tie2+ monocytes subsets disappeared (p = 0.080). Circulating endothelial cells were determined in 100% of CAD+T2DM patients, and counts of CD14++CD16+ monocytes and concentration of TGF-β predicted the presence of circulating endothelial cells (sensitivity 92.3%; specificity 90.9%; AUC = 0.930). Thus, intermediate monocytes represent one of the key determinants of the appearance of circulating endothelial cells in all the patients with CAD, but are associated with the severity of atherosclerosis only in patients with association of CAD and T2DM.