Dysfunctional changes and remodeling of adipose tissue (АT) are associated with the formation of microcalcifications in the vascular wall. Biologically active substances synthesized by АT (adipocytokines) can act as promoters and inhibitors of vascular calcification development. The few available experimental and clinical studies do not fully explain the possible mechanisms of these effects.Aim. To study the relationships between the adipocytokine profiles of adipocytes in epicardial and perivascular AT with the severity of coronary artery calcification in patients with coronary artery disease (CAD).Material and Methods. A total of 125 patients with CAD aged 59 (53; 66) years were examined. The isolated adipocytes of subcutaneous adipose tissue (SAT), epicardial adipose tissue (EAT), and perivascular adipose tissue (PVAT), obtained during coronary artery bypass grafting, were used to determine gene expression and secretion of adipocytokines (adiponectin, leptin, and IL-6). Expression of adipocytokine genes was assessed using quantitative PCR with detection of products in real time (real-time qPCR); the concentration of adipocytokines in the culture medium was determined by enzyme-linked immunosorbent assay using R&D Systems kits (Canada). Coronary artery (CA) calcification degree was assessed by multislice spiral computed tomography (MSCT) method. The calcium index of CA was determined by the Agatston method using the Syngo Calcium Scoring software package (Siemens AG Medical Solution, Germany).Results. Massive coronary calcification (CC) had the highest prevalence (58.8%) in patients with CAD. The highest level of expression of the ADIPOQ gene in all types of fat stores was observed in patients with moderate/medium CС compared to those with massive CС; the maximum expression of ADIPOQ was observed in the culture of PVAT adipocytes. Expression of the LEP and IL6 genes in massive CC was higher, with the maximum values in the culture of EAT adipocytes relative to SAT and PVAT adipocytes. Decreases in the levels of ADIPOQ mRNA and its secretion, increases in the levels of mRNA of LEP and IL6 and their secretion in adipocytes of the EAT and PVAT were associated with the development of СС in patients with CAD.Conclusion. Proinflammatory adipokines produced by adipocytes of patients with CAD during hypoxia induced vascular calcification by stimulating oxidative stress, osteoblast differentiation, apoptosis, and proliferation of smooth muscle cells. Endothelial cells, when stimulated with proinflammatory adipocytokines, tended to transform into osteoblasts, which further aggravated the degree of vascular inflammation and calcification.

Aim . To study changes in the level of fibrotic scarring marker — the N-terminal propeptide type III procollagen (PIIINP) and structural and functional parameters with the assessment of diastolic function in patients a year after ST segment elevation myocardial infarction (STEMI) and preserved left ventricle (LV) contractility. Material and methods . At first, the study included 120 (100%) STEMI patients. Next, patients with an LV ejection fraction (EF) ≥50% were selected. The final analysis included 86 STEMI patients. Upon hospitalization, the patients underwent routine diagnostic tests, coronary angiography with stenting of culprit artery. Echocardiography and determination of venous blood PIIINP and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels was on the 1 st (time point 1) and 12 th day (time point 2) of disease and after a year (time point 3). To compare the obtained values of fibrotic scarring markers, a control group was formed, including 20 (100%) healthy volunteers, identical in age and sex with the studied sample. Results . On the first day of MI, 25 (29,1%) patients with signs of diastolic dysfunction (DD) were identified among those with preserved LVEF. After 1 year, the number of such patients increased by 10% (n=9). Initially increased (relative to the control group) concentration of PIIINP on the first day (311,2 [220,1; 376,3] ng/ml) decreased by the 12 th day (223,3 [195,3; 312,1] ng/ml) and returned to the initial values a year after the MI (312,6 [228,0; 383,8] ng/ml). The NT-proBNP concentration during the hospitalization period did not exceed the reference values and did not differ between 1 and 2 time points (p=0,127). One year later, the NT-proBNP concentration significantly exceeded the values of the previous determinations and amounted to 124,4 pg/ml (p=0,043). According to the ROC analysis, with a PIIINP ≥387,8 ng/ml on the first day, the risk of DD increases (p=0,050, sensitivity, 84,62%, specificity, 55,56%) within a year after STEMI with preserved LVEF. Conclusion . The threshold of PIIINP (≥387,8 ng/ml) was established for the first day of MI, at which the risk of DD increases one year after the index event. An increase in NT-proBNP concentration one year after STEMI indicates the progression of heart failure.

Aim      To study possible correlations between echocardiography (EchoCG) indexes and markers of myocardial fibrosis, procollagen I C-terminal propeptide (PICP) and procollagen III N-terminal propeptide (PIIINP) during one year following ST-segment elevation myocardial infarction (STEMI).Material and methods  120 patients with STEMI were evaluated. EchoCG was used to assess dimensions and volumes of heart chambers, left ventricular (LV) systolic function, mean pulmonary arterial pressure (mPAP), and indexes of LV diastolic function (Em, early diastolic lateral mitral annular velocity; e', peak early diastolic septal mitral annular velocity; E / e', ratio of peak early diastolic transmitral inflow velocity and mitral annular velocity  -, Е / А, ratio of peak early and late transmitral inflow velocities; DT, deceleration time of LV early diastolic filling). EchoCG indexes and serum concentrations of PICP and PIIINP were determined at 1 (point 1) and 12 (point 2) days of disease and one year after STEMI (point 3). The sample was divided into two groups: group 1 (n=86; 71.7 %) included patients with a LV ejection fraction (EF) ≥50 % and group 2 (n=34; 28.3 %) consisted of patients with LV EF ≤49 %.Results At one year, the number of patients with signs of diastolic dysfunction increased by 10% in group 1 whereas myocardial systolic dysfunction worsened in both groups. LV EF decreased in 15 (17.4%) patients of group 1 and in 4 (11.8%) patients of group 2. Concentrations of PIIINP were correlated with Em, E / e', mPAP, PICP, e', and LV EF.Conclusion      Direct correlations between PIIINP concentrations and Em, E / e', and mPAP were found in the group with LV EF ≥50 %. In the group with LV EF <50 %, correlations were observed between PICP concentrations, LV EF, and e'. Also, in this group, the increase in PIIINP was statistically more significant. These results indicate continuing formation of myocardial fibrosis in a year following MI, which may underlie progression of chronic heart failure.

AIM To comparatively assess formulas for estimating glomerular filtration rate (GFR) in the prediction of poor outcomes in patients with type 2 diabetes mellitus (DM) within one year after myocardial infarction (MI). MATERIALS AND METHODS The investigators examined 89 patients with ST-segment elevation myocardial infarction (STEMI) within 24 hours after the onset of clinical symptoms of the disease. All the patients underwent standard laboratory and instrumental tests. GFR was calculated using the Modified of Diet in Renal Diseases (MDRD) formulas in terms of serum creatinine levels, the Hoek equation: GFR [ml/min/1.73 m2] = (80.35/cystatin C [mg/l]) - 4.3 (CKD-EPI), as well as from cystatin C levels, and the creatinine clearance rate was determined using the Cockcroft and Gault formula (ml/min). During a year after STEMI, the investigators recorded cardiovascular events (CVEs), such as death, recurrent MI, progressive angina pectoris, emergency coronary revascularization, and decompensated chronic heart failure (CHF). The examinees were divided into two groups: 1) 70 (78.6%) patients with MI and no DM; 2) 19 (21.3%) patients with MI and DM. RESULTS Comparative analysis revealed a tendency towards a difference in the detection rate of GFR <60 ml/min/1.73 m2 calculated using the Hoek formula from cystatin C levels: 42.1% in Group 2 and 21.4% in Group 1 (р=0.067). There were no great differences in the GFR estimated using other formulas. Logistic regression analysis was carried out to determine the most sensitive formula for estimating GFR to assess the risk of CVEs in the patients within a year after MI concurrent with and without type 2 DM. A univariate analysis showed that GFR calculations using the CKD-EPI (odds ratio (OR), 13.5; p=0.046) and MDRD (OR, 6.5; р=0.040) formulas and creatinine clearance estimation (OR, 2.4; p=0.025) were most sensitive in selecting MI patients without DM and with poor outcomes. This analysis revealed that GFR estimates using the Hoek formula from cystatin C levels (OR, 6.15; p=0.018) were most sensitive for patients with MI concurrent with type 2 DM. In both models, multivariate analysis included none of the analyzed indicators. CONCLUSION To estimate cardiovascular risk in the long-term post-infarction period, the CKD-EPI formula in the patients without type 2 DM and the Hoek formula from cystatin C levels were noted to be of the greatest prognostic value in patients with DM.

Aims. Our study was aimed to assess the influence of non-specific inflammation and endothelial dysfunction on developmentof cardiovascular events in patients with type 2 diabetes mellitus (T2DM) and progressive angina pectoris. Materials and methods. 140 patients (63 of them were also diabetic) received follow-up for cardiovascular events during12 months after an episode of unstable angina pectoris. Upon hospitalization for acute coronary syndrome analyses wereperformed to assess the degree of systemic inflammation evaluating plasma concentration of pro- and anti-inflammatorymarkers (CRP, fibrinogen, IL-6, -8, -10, TNF-?), as well as blood glucose and glycated haemoglobin HbA1c. Results. TNF-? and IL-6 levels were significantly higher in patients with unfavorable prognosis (p