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.

[Adiponectin gene expression in local fat depots in patients with coronary heart disease depending on the degree of coronary lesion].

AIM: To determine the dependence of adiponectin gene expression by subcutaneous, epicardial and perivascular adipocytes on the degree of coronary lesion in coronary heart disease. MATERIALS AND METHODS: 84 patients with coronary artery disease were examined. Of these, 39 people showed a moderate degree of atherosclerotic lesion of the coronary bed (less than or equal to 22 points) on the SYNTAX Score scale, 20 severe (2231 points), and 25 extremely severe (more than 32 points). Upon admission to the hospital, all patients underwent an echocardiographic study (Echocardiography, Acuson, Germany) with the calculation of the ejection fraction (EF) of the left ventricle (LV) to assess its systolic function. During a planned surgical intervention (coronary bypass surgery, CABG), adipocytes of subcutaneous, epicardial (EAT) and perivascular adipose tissue (PVAT) were taken. Adiponectin gene expression was evaluated by polymerase chain reaction (real-time PCR) using TaqMan probes. Statistical analysis was performed using Statistica 9.0. RESULTS: The maximum level of adiponectin expression was detected in adipocytes of PVAT, and the minimum EAT. With an increase in the degree of atherosclerotic lesion of the coronary bed, the expression of the adiponectin gene in adipocytes of local depots significantly decreases r=-0.82; p=0.023. Moreover, the low level of gene expression in EAT correlated with a decrease in LV EF by r=0.73; p=0.03. In adipocytes of subcutaneous and especially PVAT, gene expression was the highest in patients with a moderate degree of coronary lesion. CONCLUSIONS: Low adiponectin gene expression in EAT is associated with an increase in the degree of atherosclerotic lesion of the coronary bed and a decrease in LV EF.

[Expression of gene and content of adiponectin in fatty tissue in patients with ischemic heart disease]. / Ékspressiia gena i soderzhanie adiponektina v zhirovoi tkani u patsientov s ishemicheskoi bolezn'iu serdtsa.

The purpose of the study was to investigate the features of expression and adiponectin content in the adipocyte culture of subcutaneous, epicardial, and perivascular adipose tissue and the effect of various doses of rosuvastatin on these processes. 29 patients with coronary artery disease were examined. Adipocytes were isolated from the samples of SAT, EAT and PVAT which were taken during coronary artery bypass surgery, followed by cultivation in the presence of rosuvastatin and evaluation of gene expression and adiponectin concentration. Adipocytes SAT, EAT and PVAT differed in the level of adiponectin secretion and expression of its gene. On day 1 of cultivation the expression of the adiponectin gene in the EAT was 2.3 times lower than in the PVAT. On day 2 of cultivation the expression of the adiponectin gene was reduced both in the EAT and the PVAT as compared to the SAT. When rosuvastatin was added at a concentration of 1 mmol/L, adiponectin gene expression in PVAT was higher than when rosuvastatin was added at a concentration of 5 mmol/L, in the adipocyte culture of SAT effect was opposite. Thus, the adipocytes of EZhT and, to a greater extent, PAS, can be a therapeutic target for statins in the case of the pathological activation of adipose tissue.

[Ghrelin Physiology and Pathophysiology: Focus on the Cardiovascular System].

Ghrelin is a multifunctional peptide hormone, mainly synthesized by P / D1 cells of the stomach fundus mucosa. Its basic effect, which is realized via GHS-R1 α receptor in the arcuate and the ventromedial nucleuses of hypothalamus, is stimulation of the synthesis of pituitary hormones. Ghrelin is involved in control of appetite and energy balance, regulation of carbohydrate and lipid metabolism, cell proliferation and apoptosis, as well as modulation of functioning of gastrointestinal, cardiovascular, pulmonary and immune systems. It was found that cardiomyocytes are able to synthesize ghrelin. High concentrations of GHS-R1α in the heart and major blood vessels evidence for its possible participation in functioning of cardiovascular system. Ghrelin inhibits apoptosis of cardiomyocytes and endothelial cells, and improves the functioning of the left ventricle (LV) after injury of ischemia-reperfusion mechanism. In rats with heart failure (HF) ghrelin improves LV function and attenuates development of cardiac cachexia. In addition, ghrelin exerts vasodilatory effects in humans, improves cardiac function and reduces peripheral vascular resistance in patients with chronic HF. The review contains of the predictive value of ghrelin in the development and prevention of cardiovascular disease.

[The perspectives of application of retinol-binding protein as a biomarker of risk of cardiovascular pathology.]

The fatty tissue is an endocrine organ secreting biologically active factors called adipokines that have systemic and local features. The adipokines play an important role in development of complications caused by obesity. nowadays, retinol-binding protein 4 (RBP4), one of adipokines identified recently, is considered as a connecting link between obesity and its complications. Adipokine participates in development of resistance to insulin and correlated with cardio-metabolic markers at chronic inflammatory diseases, including diabetes mellitus type II, metabolic syndrome and cardio-vascular diseases. It is considered that inflammation, produced by RBP4, induces resistance to insulin and cardio-vascular diseases. It seems that RBP4 is an adipokine that both induces resistance to insulin and participates in pathogenesis of other metabolic complications of obesity. This is confirmed by a tight relationship between RBP4 and atherogenic lipoproteins, atherosclerotic affection of vessels and cardio-vascular diseases. However, an important restriction in certain studies related to RBP4 is that they included patients who received medicinal therapy (sugar lowering and hypo-lipidemic pharmaceuticals) or had renal and hepatic insufficiency. The mentioned factors impact concentration of RBP4 in blood and hence can distort the results. In spite of that, the established potential metabolic role of RBP4 requires a further investigation. Besides further carefully planned studies are required focusing on establishing is RBP4 a molecular participator of molecular alterations or it is only a dynamically volatile "witness". The present review summarizes actual knowledge concerning the role of RBP4 under obesity, in development of dyslipidemia, insulin resistance and cardio-vascular diseases. The purpose of the study is to summarize data of studying of inflammatory and immune effects of RBP4 especially in case of cardio-vascular diseases and also establishment of perspective of applying retinol-binding protein as a potential biomarker of cardiovascular risk.