The content of adipokines, pro- and anti-inflammatory cytokines were studied in adipocytes isolated from epicardial and subcutaneous adipose tissue of 24 coronary heart disease patients. The content of leptin and soluble leptin receptor in adipocytes of epicardial adipose tissue was higher by 28.6 and 56.9% and the level of adiponectin was lower by 33% than in adipocytes of the subcutaneous fat. In culture of epicardial adipocytes, the levels of proinflammatory cytokines TNF-α and IL-1 were higher. Subcutaneous adipose tissue adipocytes were characterized by higher levels of anti-inflammatory cytokines IL-10 and FGF-β. In epicardial adipocytes of coronary heart disease patients, the concentrations of leptin, TNF-α, and IL-1 were higher, while the levels of defense regulatory molecules (adiponectin, IL-10, and FGF-β) were lower than in subcutaneous adipocytes.

BackgroundStudying the role of soluble ST2 (sST2) during hospitalization for myocardial infarction (MI) can be helpful for predicting the course of the hospitalization and development of complications.MethodsWe included 88 patients with MI (median age, 58 yr). Depending on the course of the hospitalization, the patients were divided into two groups: the favorable (n=58) and unfavorable (n=30) outcome groups. On days 1 and 12 after MI, serum sST2 and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured by ELISA.ResultsOn day 1, the concentrations of sST2 and NT-proBNP increased 2.4- and 4.5-fold, compared with the controls. Measurements on day 12 showed a significant decrease in the sST2 level (P=0.001), whereas the NT-proBNP level did not change. On day 1, the sST2 level in the unfavorable outcome group was 2-fold higher than that in the favorable outcome group and 3.7-fold higher than in the controls. On day 12, the marker level decreased in both groups. On day 1, the NT-proBNP level in the unfavorable outcome group was 6.8-fold higher than in the controls and 1.8-fold higher than in the favorable outcome group. On day 12, the level of NT-proBNP remained elevated in both groups. Determining the levels of both sST2 and NT-proBNP increases their diagnostic significance (odds ratio [OR], 1.92; 95% confidence interval [CI], 1.7-3.2; areas under curve [AUC] 0.89; P=0.004).ConclusionsThe level of sST2 is a more sensitive indicator during MI hospitalization than NT-proBNP.

BackgroundDetermination of the impact of visceral obesity and epicardial adipose tissue thickness on stimulating growth factor levels during hospitalization for myocardial infarction is of potential importance for predicting outcomes and assessing the development of cardiofibrotic changes associated with maladaptive myocardial remodeling. In this study, we aimed to investigate the relationships between epicardial adipose tissue thickness, adipokine profiles, and the stimulating growth factor 2/interleukin-33 signaling system during hospitalization for myocardial infarction, and with the cardiac fibrosis extent 1-year post-MI in patients with visceral obesity.MethodsEighty-eight patients with myocardial infarction were grouped based on their visceral obesity. Serum leptin, adiponectin, stimulating growth factor 2, and interleukin-33 levels were measured on days 1 and 12 and at 1 year. The epicardial adipose tissue widths and the cardiac fibrosis areas were measured on day 12 and at 1 year.ResultsVisceral obesity was associated with epicardial adipose tissue thickness increases, adipokine imbalances, elevated leptin levels, and lower adiponectin levels during early hospitalization, and cardiac fibrosis development. Patients without visceral obesity had higher interleukin-33 and stimulating growth factor 2 levels during early hospitalization and lower cardiac fibrosis rates. Epicardial adipose tissue thickness was positively associated with cardiac fibrosis prevalence and interleukin-33 levels and negatively associated with stimulating growth factor 2 levels. The cardiac fibrosis extent was negatively associated with interleukin-33 levels and positively associated with stimulating growth factor 2 levels.ConclusionsIncreases in epicardial adipose tissue thickness are associated with cardiac fibrosis development 1-year post-myocardial infarction and are higher in patients with visceral obesity. The metabolic activity of the epicardial adipose tissue is associated with elevated interleukin-33 and reduced stimulating growth factor 2 levels.

BackgroundThis study aimed to evaluate the markers of insulin resistance and adipokine status in patients with visceral obesity during hospitalization following myocardial infarction (MI) and assess the disturbances of carbohydrate metabolism present 1 year after MI onset.Methods94 male patients with MI were recruited. The exclusion criteria were as follows: age less than 50 or greater than 80 years, the presence of type 2 diabetes mellitus (T2DM), and a prior history of pronounced renal failure.Obesity types were defined according to body mass index (BMI), waist circumference (WC) and visceral adipose tissue (VAT) area. Glucose, insulin, adiponectin, leptin, and insulin resistance (IR) index were measured on days 1 and 12 after the onset of MI. New-onset type 2 diabetes was assessed 1 year after MI onset.ResultsAccording to computed tomography assessments of all study patients, 69 % of patients with MI suffered from visceral obesity. The VAT area was more closely associated with the risk of developing type 2 diabetes compared with the obesity parameters, BMI and WC. Patients with a VAT area greater than 130 cm2 had a 3.6-fold higher risk of developing type 2 diabetes. The presence of IR and hyperleptinemia increased the risk of developing diabetes in the post-MI period 3.5 and 3.7 times, respectively, in patients with visceral obesity compared with patients without visceral obesity.ConclusionVisceral obesity is associated with IR, a 5.7-fold increase in leptin levels and a high risk of developing type 2 diabetes 1 year after MI onset.

BackgroundFree fatty acids (FFA), oxidized low-density lipoprotein (LDL) and its antibodies, lipid profile markers, which are formed under oxidative stress, play an important role in atherosclerotic disease. Assess the levels of these markers in myocardial infarction patients depending on the extent of coronary artery disease (CAD).MethodsST-elevation MI patients with hemodynamically significant stenoses of ≥75% in one, two, three, or more coronary arteries were examined. The patients were divided into three groups according to the severity of coronary lesions. Patients had a ≥75% stenotic lesion in one coronary artery (group 1, n = 135), two coronary arteries (group 2, n = 115), or three or more coronary arteries (group 3, n = 150). The control group comprised healthy subjects (n = 33).ResultsFFA levels on day 1 from MI onset were higher in groups 1, 2, and 3 compared with controls. On day 1 from MI onset, oxidized LDL levels were significantly higher in groups 2 and 3 than those in controls (both р = 0.001). Oxidized LDL levels were significantly higher in patients with multivessel CAD compared with those with single-vessel CAD on days 1 and 12. Antibody levels increased with the number of affected arteries.ConclusionHigh levels FFA, oxidized LDL and its antibody, lipid profile markers, and parameters of the pro/antioxidant systems persist during the subacute phase of MI.

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.

BackgroundPatients with myocardial infarction (MI) have a high mortality. Therefore, new risk markers and predictors of an adverse outcome for MI are required. The role of hyperglycemia in the development of cardiovascular complications in MI patients is still unclear.MethodsA total of 529 consecutive patients with the diagnosis of ST-segment elevation acute coronary syndrome within 24 h of the onset of symptoms were included in the study. All of the patients underwent blood glucose measurement at admission to hospital. The glycemic profile, including measurement of blood glucose levels early in the night and in the morning (3 a.m. and 5 a.m.), was assessed in 77 patients with diabetes on days 6–10 of the course of MI to monitor the efficiency of blood glucose-lowering therapy and to detect hypoglycemic episodes.ResultsIn-hospital mortality showed relationship between the level of blood glucose on admission and in-hospital mortality in patients with MI with ST-segment elevation in combination with diabetes mellitus. There was a direct linear relationship between blood glucose levels and in-hospital mortality in patients without diabetes.ConclusionEpisodes of hypoglycemia recorded in MI patients with diabetes in the hospital stage of treatment do not determine the prognosis, but enable identification of patients with an unfavorable course in the postinfarction period.

Fibrosis is one of the main components in the progression of most cardiovascular diseases, including coronary heart disease, by causing structural changes in the myocardium and vascular wall. The quantitative and qualitative characteristics of fibrosis of the myocardium are responsible for decreasing its elastic properties, developing diastolic dysfunction, impairing myocardial contractility, developing systolic dysfunction and cardiac arrhythmias, and worsening coronary blood flow in patients with heart failure of different etiologies. The important aspect of studying fibrosis is not only its interpretation as a model of the typical pathological process, but also its consideration as a systemic lesion of various organs and tissues. At the same time, the identification of myocardial fibrosis biomarkers that are available for their determination in circulating blood is of particular interest. Since there was evidence for the role of fibrosis in developing dysfunction of various organs and ensuring the systematicity of most diseases, especially at their development stages, the process of fibrosis came to be regarded as a promising therapeutic target. It is relevant to further investigate myocardial fibrosis, which is aimed at increasing the efficiency of its diagnosis and predicting its course and pathogenetically sound therapy.