Listeria monocytogenes ST37 Distribution in the Moscow Region and Properties of Clinical and Foodborne Isolates.

Listerias of the phylogenetic lineage II (PLII) are common in the European environment and are hypovirulent. Despite this, they caused more than a third of the sporadic cases of listeriosis and multi-country foodborne outbreaks. L. monocytogenes ST37 is one of them. During the COVID-19 pandemic, ST37 appeared in clinical cases and ranked second in occurrence among food isolates in the Moscow region. The aim of this study was to describe the genomic features of ST37 isolates from different sources. All clinical cases of ST37 were in the cohort of male patients (age, 48-81 years) with meningitis-septicemia manifestation and COVID-19 or Influenza in the anamnesis. The core genomes of the fish isolates were closely related. The clinical and meat isolates revealed a large diversity. Prophages (2-4/genome) were the source of the unique genes. Two clinical isolates displayed pseudolysogeny, and excided prophages were A006-like. In the absence of plasmids, the assortment of virulence factors and resistance determinants in the chromosome corresponded to the hypovirulent characteristics. However, all clinical isolates caused severe disease, with deaths in four cases. Thus, these studies allow us to speculate that a previous viral infection increases human susceptibility to listeriosis.

Expression of Ceramide-Metabolizing Enzymes in the Heart Adipose Tissue of Cardiovascular Disease Patients.

Here, we examined the expression of ceramide metabolism enzymes in the subcutaneous adipose tissue (SAT), epicardial adipose tissue (EAT) and perivascular adipose tissue (PVAT) of 30 patients with coronary artery disease (CAD) and 30 patients with valvular heart disease (VHD) by means of quantitative polymerase chain reaction and fluorescent Western blotting. The EAT of patients with CAD showed higher expression of the genes responsible for ceramide biosynthesis (SPTLC1, SPTLC2, CERS1, 5, 6, DEGS1, and SMPD1) and utilization (ASAH1, SGMS1). PVAT was characterized by higher mRNA levels of CERS3, CERS4, DEGS1, SMPD1, and ceramide utilization enzyme (SGMS2). In patients with VHD, there was a high CERS4, DEGS1, and SGMS2 expression in the EAT and CERS3 and CERS4 expression in the PVAT. Among patients with CAD, the expression of SPTLC1 in SAT and EAT, SPTLC2 in EAT, CERS2 in all studied AT, CERS4 and CERS5 in EAT, DEGS1 in SAT and EAT, ASAH1 in all studied AT, and SGMS1 in EAT was higher than in those with VHD. Protein levels of ceramide-metabolizing enzymes were consistent with gene expression trends. The obtained results indicate an activation of ceramide synthesis de novo and from sphingomyelin in cardiovascular disease, mainly in EAT, that contributes to the accumulation of ceramides in this location.

Cardiovascular and Renal Comorbidities Included into Neural Networks Predict the Outcome in COVID-19 Patients Admitted to an Intensive Care Unit: Three-Center, Cross-Validation, Age- and Sex-Matched Study.

Here, we performed a multicenter, age- and sex-matched study to compare the efficiency of various machine learning algorithms in the prediction of COVID-19 fatal outcomes and to develop sensitive, specific, and robust artificial intelligence tools for the prompt triage of patients with severe COVID-19 in the intensive care unit setting. In a challenge against other established machine learning algorithms (decision trees, random forests, extra trees, neural networks, k-nearest neighbors, and gradient boosting: XGBoost, LightGBM, and CatBoost) and multivariate logistic regression as a reference, neural networks demonstrated the highest sensitivity, sufficient specificity, and excellent robustness. Further, neural networks based on coronary artery disease/chronic heart failure, stage 3-5 chronic kidney disease, blood urea nitrogen, and C-reactive protein as the predictors exceeded 90% sensitivity and 80% specificity, reaching AUROC of 0.866 at primary cross-validation and 0.849 at secondary cross-validation on virtual samples generated by the bootstrapping procedure. These results underscore the impact of cardiovascular and renal comorbidities in the context of thrombotic complications characteristic of severe COVID-19. As aforementioned predictors can be obtained from the case histories or are inexpensive to be measured at admission to the intensive care unit, we suggest this predictor composition is useful for the triage of critically ill COVID-19 patients.

Characteristics of adipocytokine expression by local fat depots of the heart: Relationship with the main risk factors for cardio-vascular diseases.

In our study we investigated the relationships between adipocytokines in adipose tissue (AT) and cardiovascular disease (CVD) risk factors; (2) Methods: fat tissue biopsies were obtained from 134 patients with stable CAD undergoing coronary artery bypass grafting and 120 patients undergoing aortic or mitral valve replacement. Adipocytes were isolated from subcutaneous (SAT), epicardial (EAT), and perivascular AT (PVAT) samples, and cultured for 24 h, after which gene expression of adipocytokines in the culture medium was determined; (3) Results: men showed reduced ADIPOQ expression in EAT and PVAT, LEP expression in PVAT, and LEPR expression in SAT and PVAT compared to women. Men also exhibited higher SAT and lower PVAT IL6 than women. Meanwhile, dyslipidemia associated with decreased ADIPOQ expression in EAT and PVAT, LEPR in EAT, and IL6 in PVAT. Arterial hypertension (AH) associated with low EAT and PVAT ADIPOQ, and high EAT LEP, SAT, as well as PVAT LEPR, and IL6 in SAT and EAT. ADIPOQ expression decreased with increased AH duration over 20 years against an increased LEP background in ATs. Smoking increased ADIPOQ expression in all ATs and increased LEP in SAT and EAT, however, decreased LEPR in PVAT. Patients 51-59 years old exhibited the highest EAT and PVAT LEP, IL-6, and LEPR expression compared to other age groups; (4) Conclusions: decreased EAT ADIPOQ expression against an increased pro-inflammatory IL6 background may increase atherogenesis and contribute to CAD progression in combination with risk factors including male sex, dyslipidemia, and AH.

Effects of Physical Prehabilitation on the Dynamics of the Markers of Endothelial Function in Patients Undergoing Elective Coronary Bypass Surgery.

Our aim in this study was to evaluate the effect of physical training performed before CABG on the perioperative dynamics of the serum levels of asymmetric dimethylarginine (ADMA) and endothelin-1 (ET-1) of patients with stable coronary heart disease (CHD). Patients in the preoperative period were randomized into two groups: the training group (n = 43) underwent high-intensity treadmill training; the patients in the control group (n = 35) received no training before the procedure. The serum concentrations of ADMA and ET-1 were determined in the perioperative period, and the course of the early postoperative period was analyzed. In the training group, we found a significantly lower incidence of postoperative complications during hospital stays (p = 0.013). At the end of the training program, the ADMA levels were 1.8 times higher in the controls than in the training group (p = 0.001). We found that type 2 diabetes increased the probability of complications by 12 times (OR: 12.3; 95% CI: 1.24-121.5; p = 0.03), as well as elevating the concentration of ET-1 on the eve of surgery (OR: 10.7; 95% CI: 1.4-81.3; p = 0.02). Physical prehabilitation reduced the likelihood of complications nine times (OR: 0.11; 95% CI: 0.02-0.83; p = 0.03). The AUC was 0.851 ± 0.07 (95% CI: 0.71-0.98). The obtained results indicate the benefit of physical training during the prehabilitation stage since it can help to preserve endothelial function.

Relationship between Epicardial and Coronary Adipose Tissue and the Expression of Adiponectin, Leptin, and Interleukin 6 in Patients with Coronary Artery Disease.

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.

Assessment of Hygiene Indicators When Using Gloves by Transport Workers in Russia during the COVID-19 Pandemic.

The COVID-19 outbreak represents a global public health emergency. National governments have gradually introduced restrictive measures. Using respiratory protective equipment (face masks) and gloves was essential practice without specific infection control measures or guidelines. This study aimed to assess hygiene indicators when using gloves by transport workers in Russia during the COVID-19 pandemic and to develop integral indicators and recommendations for wearing gloves for workers for whom this is a mandatory requirement. For this purpose, 1103 transport workers were surveyed using a questionnaire. We investigated the hygiene aspects of gloves and evaluated the bacterial contamination of the contact side of the gloves based on the wash results. We assessed the socio-demographic characteristics of the respondents, the duration of the work shift, the frequency of use of types of gloves, skin manifestations, the degree of comfort, and bacterial growth. We carried out the ranking according to comfort, the absence of adverse dermatological reactions when wearing gloves, and bacterial contamination of the inner surface of the gloves. It has been identified that it is necessary to use a comprehensive assessment of gloves to create a register of protective equipment, taking into account the frequency with which it was worn, the severity of the skin condition, comfort, and bacterial contamination.

Adipokine gene expression in adipocytes isolated from different fat depots of coronary artery disease patients.

To compare DPP4, LCN2, NAMPT, ITLN1, APLN mRNA levels in adipocytes isolated from the biopsies of subcutaneous, epicardial and perivascular fat obtained from 25 patients with coronary artery disease. Gene expression signature was determined by RT-qPCR with hydrolysis probes. We found DPP4 and APLN mRNA was higher expressed only in adipocytes isolated from epicardial adipose tissue compared to the subcutaneous fat. The ITLN1 gene was overexpressed in epicardial adipose tissue compared to both subcutaneous and perivascular tissues. APLN mRNA expression was positively correlated with total and LDL cholesterol plasma level, and DPP4 mRNA expression - with VLDL cholesterol concentration. Thus, adipocytes isolated from different adipose depots are characterised by differential gene expression of adipokines. Epicardial adipose tissue is of particular interest in the context of its function, molecular and genetic mechanisms of regulation of the cardiovascular system and as a therapeutic target for correction of adipose tissue-induced effects on health.

Beneficial Effects of a Short Course of Physical Prehabilitation on Neurophysiological Functioning and Neurovascular Biomarkers in Patients Undergoing Coronary Artery Bypass Grafting.

This study aimed to evaluate the effects of a short course of physical prehabilitation on neurophysiological functioning and markers of the neurovascular unit in patients undergoing coronary artery bypass grafting (CABG). We performed a prospective randomized study involving 97 male CABG patients aged 45-70 years, 47 of whom underwent a 5-7-day preoperative course of aerobic physical training (PhT). Both groups of patients were comparable with respect to baseline clinical and anamnestic characteristics. An extended neuropsychological and electroencephalographic (EEG) study was performed before surgery and at 7-10 days after CABG. Markers of the neurovascular unit [S100ß, neuron-specific enolase (NSE), and brain-derived neurotrophic factor (BDNF)] were examined as metabolic correlations of early postoperative cognitive dysfunction (POCD) at three time points: before surgery, within the first 24 h after surgery, and 7-10 days after CABG. POCD developed in 58% of patients who underwent preoperative PhT, and in 79.5% of patients who did not undergo training, 7-10 days after CABG. Patients without prehabilitation demonstrated a higher percentage of theta1 power increase in the relative change values as compared to the PhT patients (p = 0.015). The short preoperative course of PhT was associated with low plasma S100ß concentration, but high BDNF levels in the postoperative period. Patients who underwent a short preoperative course of PhT had better cognitive and electrical cortical activity indicators. Markers of the neurovascular unit indicated lower perioperative brain injury after CABG in those who underwent training. A short course of PhT before CABG can decrease the brain's susceptibility to ischemia and reduce the severity of cognitive impairments in cardiac surgery patients. Electrical brain activity indicators and neurovascular markers, such as S100ß and BDNF, can be informative for the effectiveness of cardiac rehabilitation programs.

Calciprotein Particles Link Disturbed Mineral Homeostasis with Cardiovascular Disease by Causing Endothelial Dysfunction and Vascular Inflammation.

An association between high serum calcium/phosphate and cardiovascular events or death is well-established. However, a mechanistic explanation of this correlation is lacking. Here, we examined the role of calciprotein particles (CPPs), nanoscale bodies forming in the human blood upon its supersaturation with calcium and phosphate, in cardiovascular disease. The serum of patients with coronary artery disease or cerebrovascular disease displayed an increased propensity to form CPPs in combination with elevated ionised calcium as well as reduced albumin levels, altogether indicative of reduced Ca2+-binding capacity. Intravenous administration of CPPs to normolipidemic and normotensive Wistar rats provoked intimal hyperplasia and adventitial/perivascular inflammation in both balloon-injured and intact aortas in the absence of other cardiovascular risk factors. Upon the addition to primary human arterial endothelial cells, CPPs induced lysosome-dependent cell death, promoted the release of pro-inflammatory cytokines, stimulated leukocyte adhesion, and triggered endothelial-to-mesenchymal transition. We concluded that CPPs, which are formed in the blood as a result of altered mineral homeostasis, cause endothelial dysfunction and vascular inflammation, thereby contributing to the development of cardiovascular disease.

Analysis of probable lipotoxic damage and myocardial fibrosis in epicardial obesity.

Myocardial fibrosis is considered a key pathological process in the development of cardiovascular diseases. In epicardial obesity (EO), the main cause of fibrosis development is lipotoxic myocardial damage. It is important to detect myocardial fibrosis at an early stage, using non-invasive diagnostic methods. According to the results of echocardiography (ECG), 110 men with general obesity were divided into the following two groups: Group I with epicardial fat thickness (tEAT) ≥ 7 mm (n = 70) and Group II with tEAT < 7 mm (n = 40) without diastolic dysfunction. The levels of metabolic factors, pro-inflammatory cytokines, adipokines, and free fatty acids (FFA), profibrotic markers were determined in both groups. In Group I, the level of interleukin (IL)-6, C-reactive protein, and tumor necrosis factor (TNF)-α increased and that of leptin and adiponectin decreased compared with those in Group II. There was an increase in the level of all studied profibrotic factors in Group I. The level of TNF-α and IL-6 showed a positive correlation with the level of leptin and FFA and a negative correlation with the level of adiponectin. We also observed a relationship between the level of collagen, transforming growth factor (TGF)-ß, and metalloproteinase (MMP)-3 and EO. Our results showed that confirmed EO correlates with not only disadipocytosis and increased levels of pro-inflammatory cytokines, but also increased levels of profibrotic factors. This suggests that the studied markers of fibrosis may be used to determine preclinical cardiac fibrosis with lipotoxic myocardial damage in patients with EO.

Expression of adipocytokines in heart fat depots depending on the degree of coronary artery atherosclerosis in patients with coronary artery disease.

In coronary artery disease (CAD) the adipocytokine content in the heart fat depot is altered, but it has not been established whether these changes are associated with the degree of atherosclerotic damage to the coronary artery (CA). Were examined 84 patients with CAD, and according to the degree of atherosclerotic state based on the SYNTAX Score scale, were divided: 39 moderate (≤22 points), 20 severe (23-31 points) and 25 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 was determined using real-time PCR. The concentration of the studied adipocytokines in adipocyte culture medium was measured by ELISA. Statistical analysis was performed using logistic regression analysis. In the adipocytes of the cardiac depot of patients with CAD, an increase in the expression and secretion of leptin and IL-6 and a decrease in adiponectin, with a maximum manifestation in severe and extremely severe CA lesions, was observed. EAT adipocytes were characterized by minimal expression of the adiponectin gene maximal gene expression leptin and IL-6 compared to SAT and PVAT adipocytes.

Prognostic potential of cardiac structural and functional parameters and N-terminal propeptide of type III procollagen in predicting cardiac fibrosis one year after myocardial infarction with preserved left ventricular ejection fraction.

The aim of the study were to evaluate the prognostic potential of serum level of N-terminal propeptide procollagen type III (PIIINP) and heart parameters for predicting heart cardiac fibrosis 1 year after ST-segment elevation myocardial infarction (STEMI) with preserved left ventricular ejection fraction (LVEF). 68 patients with STEMI and preserved LVEF with acute heart failure of the I-III degree according to the Killip classification were examined. Echocardiography was performed and PIIINP levels were measured on days 1 and 12, as well as 1 year after STEMI. A year after STEMI, was performed contrast magnetic resonance imaging and patients were assigned into four groups depending on the severity of cardiac fibrosis: cardiac fibrosis 0% (n=49, 57% of 86 patients); ≤5% (n=18, 20.9%); 6-15% (n=10, 11.6%); ≥16% (n=9, 10.5%). Direct correlations between the severity of cardiac fibrosis, PIIINP level and indicators of diastolic function were established. The risk of cardiac fibrosis increases at the level of PIIINP ≥381.4 ng / ml on the 12th day after STEMI with preserved LVEF (p=0.048). Thus, measuring the level of PIIINP in the inpatient period can allow timely identification of patients with a high risk of cardiac fibrosis 1 year after STEMI with preserved LVEF.

Serum and Echocardiographic Markers May Synergistically Predict Adverse Cardiac Remodeling after ST-Segment Elevation Myocardial Infarction in Patients with Preserved Ejection Fraction.

Improvement of risk scoring is particularly important for patients with preserved left ventricular ejection fraction (LVEF) who generally lack efficient monitoring of progressing heart failure. Here, we evaluated whether the combination of serum biomarkers and echocardiographic parameters may be useful to predict the remodeling-related outcomes in patients with ST-segment elevation myocardial infarction (STEMI) and preserved LVEF (HFpEF) as compared to those with reduced LVEF (HFrEF). Echocardiographic assessment and measurement of the serum levels of NT-proBNP, sST2, galectin-3, matrix metalloproteinases, and their inhibitors (MMP-1, MMP-2, MMP-3, TIMP-1) was performed at the time of admission (1st day) and on the 10th-12th day upon STEMI onset. We found a reduction in NT-proBNP, sST2, galectin-3, and TIMP-1 in both patient categories from hospital admission to the discharge, as well as numerous correlations between the indicated biomarkers and echocardiographic parameters, testifying to the ongoing ventricular remodeling. In patients with HFpEF, NT-proBNP, sST2, galectin-3, and MMP-3 correlated with the parameters reflecting the diastolic dysfunction, while in patients with HFrEF, these markers were mainly associated with LVEF and left ventricular end-systolic volume/diameter. Therefore, the combination of the mentioned serum biomarkers and echocardiographic parameters might be useful for the prediction of adverse cardiac remodeling in patients with HFpEF.

Calcium Phosphate Bions Cause Intimal Hyperplasia in Intact Aortas of Normolipidemic Rats through Endothelial Injury.

Calcium phosphate bions (CPBs) are formed under blood supersaturation with calcium and phosphate owing to the mineral chaperone fetuin-A and representing mineralo-organic particles consisting of bioapatite and multiple serum proteins. While protecting the arteries from a rapid medial calcification, CPBs cause endothelial injury and aggravate intimal hyperplasia in balloon-injured rat aortas. Here, we asked whether CPBs induce intimal hyperplasia in intact rat arteries in the absence of cardiovascular risk factors. Normolipidemic Wistar rats were subjected to regular (once/thrice per week over 5 weeks) tail vein injections of either spherical (CPB-S) or needle-shaped CPBs (CPB-N), magnesium phosphate bions (MPBs), or physiological saline (n = 5 per group). Neointima was revealed in 3/10 and 4/10 rats which received CPB-S or CPB-N, respectively, regardless of the injection regimen or blood flow pattern in the aortic segments. In contrast, none of the rats treated with MPBs or physiological saline had intimal hyperplasia. The animals also did not display signs of liver or spleen injury as well as extraskeletal calcium deposits. Serum alanine/aspartate transaminases, interleukin-1ß, MCP-1/CCL2, C-reactive protein, and ceruloplasmin levels did not differ among the groups. Hence, CPBs may provoke intimal hyperplasia via direct endothelial injury regardless of their shape or type of blood flow.

Adipocytes Directly Affect Coronary Artery Disease Pathogenesis via Induction of Adipokine and Cytokine Imbalances.

This study aimed to investigate the adipokine and cytokine profiles of adipocytes from epicardial and subcutaneous adipose tissues in interconnection with the visceral adipose tissue area and the biochemical and clinical characteristics of patients with coronary artery disease. We assessed 84 patients with coronary artery disease (65 men, 19 women) and divided them into two groups based on the presence of visceral obesity. We sampled epicardial and subcutaneous adipose tissues from the patients with visceral obesity. We then cultured the adipocytes and evaluated their adipokine profiles and pro-inflammatory activity. Results show that the mRNA expression of adiponectin in cultures of epicardial adipocytes from patients with and without visceral obesity was lower than that in subcutaneous adipocytes. Moreover, adiponectin mRNA expression in cultures of subcutaneous and epicardial adipocytes from patients with visceral obesity was lower than that in patients without obesity. For leptin, the reverse pattern was observed, with expression higher in cultures of epicardial adipocytes than in subcutaneous adipocytes and higher in epicardial adipocytes from patients with visceral obesity than in those from subjects without visceral obesity. In addition, in epicardial adipocytes, increased expression of proinflammatory cytokine genes (IL6, TNF) was observed compared with that in subcutaneous adipocytes. In contrast, expression of IL10 was higher in cultures of subcutaneous adipocytes than in epicardial adipocytes. The epicardial adipose tissue area was associated with the presence of higher levels of leptin and TNF-α within adipocytes and serum, increased lipid and carbohydrate metabolism. Coronary artery disease, in the context of the status of epicardial adipocytes, can be characterized as "metabolic inflammation," suggesting the direct involvement of adipocytes in pathogenesis through the development of adipokine imbalances and activation of proinflammatory processes.

Increased Serum Parathyroid Hormone, Osteocalcin and Alkaline Phosphatase Are Associated with a Long-Term Adverse Cardiovascular Outcome after Coronary Artery Bypass Graft Surgery.

Despite the fact that an association of osteopoenia/osteoporosis with elevated risk of coronary artery calcification (CAC) and coronary atherosclerosis (CA) is well-established, it remains unclear whether bone turnover markers can be employed in long-term prognostication of such patients. Here we measured serum calcium, phosphate, calcitonin, parathyroid hormone (PTH), osteoprotegerin, osteocalcin, osteopontin, alkaline phosphatase and its bone isoenzyme, subsequently correlating them with an adverse cardiovascular outcome after 3 years of follow-up. The extent of brachiocephalic artery stenosis, CA, or CAC, as well as prevalence of osteopoenia/osteoporosis before the coronary artery bypass graft (CABG) surgery, did not differ between outcome groups, suggesting that subtle molecular mechanisms might be involved in determining the outcome rather than clinical or subclinical disease. After stepwise logistic regression, serum osteocalcin > 26.8 ng/mL and PTH > 49.1 pg/mL were independent predictors of an adverse outcome. Serum ionised calcium correlated with multivessel coronary artery disease; moreover, patients with severe CA (SYNTAX score > 21) had higher serum ionised calcium than those with mild CA. Likewise, serum alkaline phosphatase was associated with severe CA and CAC (Agatston score > 400). In conclusion, serum PTH, osteocalcin, and alkaline phosphatase are associated with an adverse cardiovascular outcome 3 years after CABG surgery regardless of osteopoenia/osteoporosis, coronary/peripheral atherosclerosis, and CAC.

Biological markers and cardiac remodelling following the myocardial infarction.

AIM: To assess growth stimulating factor ST2 and N-terminal pro b-type natriuretic peptide (NT-proBNP) levels in the sera of myocardial infraction (MI) patients, and their correlation with the adaptive and maladaptive variants of cardiac remodelling. METHODS: 87 patients (65 male, 22 females; 67±8.36 years) with ST-elevated MI were included in this study, and 67 patients had an adaptive, physiological, while 20 patients had a maladaptive, pathological variant of myocardium remodelling. RESULTS: On day 1, ST2 and NT-proBNP levels were shown to increase 2.4 and 4.5 folds, respectively, compared with those in the control. ST2 levels in patients with maladaptive remodelling were 1.5-fold higher than those in the adaptive remodelling group. On day 12, a decrease in ST2 levels was observed in both groups. NT-proBNP levels increased 1.8 folds in both groups on day 1, compared with those in the controls. Increased ST2 levels on day 1 after MI were shown to increase the risk of maladaptive remodelling 4.5 folds, while high NT-proBNP levels increased this risk 2.3 times. CONCLUSIONS: ST2 level determination allows us to predict the risk of maladaptive remodelling with a higher sensitivity and specificity than using NT-proBNP levels.

Relationship between epicardial and perivascular fatty tissue and adipokine-cytokine level in coronary artery disease patients.

The aim of this study was to determine the relationship between the thickness of epicardial adipose tissue (EAT) and perivascular adipose tissue (PVAT) and the adipokine-cytokine profile of patients with coronary heart disease, which can be of significant importance for predicting the course of cardiovascular disease (CVD). Eighty-four patients with CVD were assessed and divided into two groups based on the presence of visceral obesity (VO). In patients with VO, the thickness of the epicardial deposits of the left and right ventricles were 1.75 and 1.43 times greater, respectively, than in patients without VO. For patients with VO, the prevalence of the volume of the left anterior descending artery was 10% higher, and the middle third of the envelope artery was 28% higher, when compared to patients without VO. When evaluating inflammatory status, it was established that the concentration of tumor necrosis factor-α, interleukin (IL)-1ß, and leptin in the blood serum of patients with VO exceeded the values of patients without VO. The level of anti-inflammatory IL-10 was 2-times lower in patients with VO. The findings of this study show that increased EAT and PVAT are independent risk factors of CVD, as well as a possible model for the assessment of drug effectiveness for CVD.

Leptin resistance: underlying mechanisms and diagnosis.

Leptin and its receptors have been identified as key regulators of body weight and energy homeostasis. A decrease in tissue sensitivity to leptin leads to the development of obesity and metabolic disorders, such as insulin resistance and dyslipidemia. Mechanisms underlying the development of leptin resistance include mutations in the genes encoding leptin and its receptors, as well as proteins involved in self-regulation of leptin synthesis and blood-brain barrier permeability. Leptin resistance encompasses a complex pathophysiological phenomenon with a number of potential research lines. In this review, we analyze the existing data on the methods used to diagnose leptin resistance.