The relationship of the epicardial fat and adipo-fibrokines in myocardial infarction.

Analysis of the relationship between the epicardial fat with adipokine and system ST2/IL-33 in-hospital period, and also with the extent of fibrosis of the atrial myocardium through the year after myocardial infarction in patients with visceral obesity. Examined 88 patients with myocardial infarction (MI). Visceral obesity (VO) is established by computed tomography. In fact the presence VO the patients divided into two groups. Determined the concentration of leptin, adiponectin, stimulating growth factor (ST-2) and interlekin-33 (IL-33) in serum on 1st, 12-day in-hospital period and 1 year after MI. Thickness epicardial adipose tissue (EAT) and the percentage of cardiovirus of the myocardium was measured by the method MRI, respectively, on the 12th day of hospitalization and a year after MI. The control group consisted of 30 people. Statistical analysis of data was performed using nonparametric tests. Patients with MI is associated with an increase in the thickness of EAT, imbalance of adipokines with increased leptin, decreased adiponectin in early in-hospital period and development of cardiovirus. Higher values of IL-33 and ЅT2 in the early in-hospital period MI patients with no accompanied by a lower prevalence of cardiovirus in the post-hospital period. The thickness of epicardial fat is directly dependent on the prevalence of myocardial fibrosis, the concentrations of IL-33 and in inverse proportion to the concentration of ЅT2. The degree of cardiovirus is in inverse proportion to the concentration of IL-33 and directly dependent on the concentration of ST2. The increase in EAT closely linked to the development of fibrosis of the atrial myocardium after year. The thickness of EAT more patients MI, which is most pronounced imbalance of adipokines. The metabolic activity of EAT correlated with increased IL-33 and ST2 decrease.