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Aim. To analyze and compare the clinical, echocardiographic characteristics and serum N-terminal pro-brain natriuretic peptide (NT-proBNP) levels depending on the central cardiometabolic risk factors, with a focus on obesity, in patients with heart failure (HF) with mid-range ejection fraction (HFmrEF).Material and methods. The study included 111 patients with old myocardial infarction and HFmrEF (men, 100%; mean age, 60 years) predominantly of NYHA class II. Echocardiography and blood sampling for NT-proBNP were performed with sinus rhythm. Left atrial volume (LAV) and left ventricular mass (LVM) were indexed to body surface area (BSA) and height raised to a power.Results. Type 2 diabetes, overweight and obesity were diagnosed in 25%, 19%, 38% of cases, respectively, and were associated with greater changes in the morphologic and functional left ventricular parameters. There were no intergroup differences among patients with and without obesity in the LAV and LVM indexed to BSA. However, in patients with a body mass index (BMI) ≥30 kg/m2, the LAV indexed to height squared and LVM indexed to height2,7 were higher (p<0,05 for all). In 11% of obese patients, there were no changes in the criterion LAV or LVM values indexed to BSA, but the values indexed to height raised to a power exceeded the standard values. In 20% of patients with clinical manifestations of stable HFmrEF and structural and functional echocardiographic criteria, NT-proBNP were ≤125 pg/ml. An inverse correlation was found between NT-proBNP and BMI (r=-0,29; p=0,008), and lower values of myocardial stress marker were observed in obese patients (p=0,048).Conclusion. Considering the high incidence of obesity in patients with HFmrEF and its ability to reduce NT-proBNP, an algorithm modification is required for diagnosing HFmrEF as follows: focus on clinical and personalized echocardiography data, taking into account the obesity and, possibly, indexing the threshold natriuretic peptide values in patients with BMI ≥30 kg/m2. The issues of indexation of echocardiographic parameters depending on morphometric parameters in obese patients today remain open, predetermining the limitations in diagnosis of heart failure with left ventricular ejection fraction >40%. This requires the search for optimal standardization and the development of a unified methodological approach.

Objective. To analyze pathogenetic mechanisms underlying the development of endometrial hyperplasia in women of reproductive age. Patients and methods. We have examined 143 women of reproductive age with endometrial hyperplasia (EH). Study participants were divided into three groups: Group I included EH patients without atypia; Group II included patients with atypical hyperplasia of the endometrium; Group III (control group) comprised 56 women with abnormal uterine bleeding, in whom we excluded adenomyosis, uterine fibroids, endometrial hyperplasia, endometrial cancer, and iatrogenic causes of uterine bleeding. Genomic DNA was isolated using phenol-chloroform extraction. Real-time polymerase chain reaction (RT-PCR) was used to detect microRNA-210, -18a, -221, and -222. The detection of tumor pyruvate kinase M2 was performed using the ScheBo® Tumor M2-PK kit designed for quantitative assessment of this metabolic cancer marker in plasma and endometrial tissue samples. Results. Significant risk factors triggering the pathogenetic mechanism of EH development in reproductive age include extragenital disorders (obesity, thyroid diseases, diseases of the urinary system, hypertension) and gynecological diseases (pelvic inflammatory diseases, adenomyosis, benign breast dysplasia, uterine fibroids). Alterations affecting estrogen receptors lead to changes in microRNA messengers, which, in turn, affect target genes and cause changes in the adaptive abilities of the cell. Expression of pyruvate kinase M2 in this chain confirms proapoptotic changes in the cell and the risk of its atypia. Conclusion. The pathogenesis of EH is based on the following factors: polymorphism of the ERS1 and PRG genes, increased expression of miRNA-210, -18a, and -222, decreased expression of miRNA-221, and overexpression of pyruvate kinase M2. Key words: endometrial hyperplasia, miRNA, pyruvate kinase M2, progesterone receptors, estrogen receptors

Purpose To study the impact of genetic variants rs1739843, rs2290149 and rs10838692 in HSPB7 and MADD genes on myocardial remodeling in the patients with postinfarction cardiosclerosis. Methods and Results. The study included 252 men aged 30-65 y.o., who had MI more than 1 year ago. All patients had Q-MI of the anterior wall of the LV. Echocardiography was performed by the standard method (Vivid S6, GE, USA). Arterial hypertension (AH) was registered in more than 60% patients. Myocardial revascularization (CABG/PCI) was performed in more than in 50% of cases. Among 252 cases studies 156 patients had HFrEF (II–IV NYHA) LVEF (Sim)&lt;40% (№1 group) and 96 patients had no clinical signs of HF and LVEF (Sim)&gt;55% (№2 group). The groups were comparable in the AH prevalence and age. Patients all groups were on optimal drug therapy. Polymorphic genetic variants were studies using real-time-PCR. Eccentric types of LV remodeling prevailed in group 1 and concentric types of LV remodeling prevailed in group 2 (p &lt; 0.001). The presence AH combined with CC genotype of rs1739843 in HSPB7 gene and TT genotype of rs2290149 in MADD and simultaneous carriage of the CC genotype of rs1739843 HSPB7 were associated with the presence of non-dilated ventricle (LV volume index ≤75 mL/m2) and relative wall thickness (RWT) &gt;0.42 independently to LV mass index (p = 0.03). The T allele of rs1739843 HSPB7 (p = 0.006) and a combination of T allele of rs1739843 HSPB7 with the TT genotype of rs2290149 of the MADD gene were associated with the presence of dilated ventricles (p = 0.009) with LV hypertrophy (LV mass index &gt;115 g/m2) independently to RWT. Conclusion Our preliminary data demonstrate that the genotype of HSPB7 (rs1739843) can modulated the association of AH and MADD rs2290149 with markers of ventricular hypertrophy and predispose to various types of post-MI remodeling of LV.