Репозиторий Университета

Heart failure is a complex syndrome whose phenotypic presentation and disease progression depends on a complex network of adaptive and maladaptive responses. One of these responses is the endothelial release of NRG (neuregulin)-1-a paracrine growth factor activating ErbB2 (erythroblastic leukemia viral oncogene homolog B2), ErbB3, and ErbB4 receptor tyrosine kinases on various targets cells. NRG-1 features a multitasking profile tuning regenerative, inflammatory, fibrotic, and metabolic processes. Here, we review the activities of NRG-1 on different cell types and organs and their implication for heart failure progression and its comorbidities. Although, in general, effects of NRG-1 in heart failure are compensatory and beneficial, translation into therapies remains unaccomplished both because of the complexity of the underlying pathways and because of the challenges in the development of therapeutics (proteins, peptides, small molecules, and RNA-based therapies) for tyrosine kinase receptors. Here, we give an overview of the complexity to be faced and how it may be tackled.

© 2018 Media Sphera Publishing Group. All rights reserved. Development and use of new anticancer drugs has resulted in the improving of 5-year survival rates in patients with cancer. However, many of the modern chemotherapies are associated with cardiovascular toxicities that increases cardiovascular risk in cancer patients, including hypertension, heart failure, thrombosis and thromboembolism, cardiomyopathy, and arrhythmias. These side effects limitation restrict treatment options and farther perspectives. With increasing use of modern chemotherapies and prolongation of the cancer patients survival, the incidence of cardiovascular disease in this patient population will continue to increase. Accordingly,careful assessment and management of cardiovascular risk factors in cancer patients by oncologists and cardiologists working together is essential for optimal care.

The article describes a clinical case of Descemet's membrane detachment that occurred during cataract phacoemulsification with implantation of intraocular lens. Significant corneal edema developed in the early post-op period. Considering the ability of endothelium to close its own defects even with large injury area, the patient was followed-up for 2 years. Corneal edema was treated during 4 months and concluded with instillations of osmotic and anti-inflammatory drugs. At 1.5-2 months of therapy, the edema was gradually decreasing, and by the 4th month of the follow-up the cornea was practically transparent. Density of endothelial cells in central cornea, where the Descemet's membrane was absent, comprised 1000 cells/mm2. Further observation revealed cornea staying transparent for 2 years after the surgery. Complete optical recovery of patients with Descemet's membrane defect in this case study is supported by similar clinical cases briefly described in the article, and evidence that structural functional recovery of the corneal endothelial layer is possible even when it has large defects (more than 2.5 mm in diameter).

© 2018, Media Sphera Publishing Group. All rights reserved. The paper describes the procedure to prepare endothelial cell monolayer samples from the vascular intima, which is suitable for studying various morphological processes. To obtain high-quality multicellular specimens, it is recommended to preliminarily remove excess tissue from the outside of the vessel and to free the intima; ways to dry the surface and to separate endothelial cells are examined. The paper gives the figures of specimens stained by the Romanowsky-Giemsa method and identifies factor VIII, an endothelial marker, and Chlamydia pneumoniae inclusions in the cytoplasm of endothelial cells.

© 2018 Vserossiiskoe Obshchestvo Kardiologov. All rights reserved. Aim. To evaluate the changes of endothelial function in arterial hypertension (AH) patients with paroxysmal atrial fibrillation (AF) in treatment with propafenone (Propanorm, PRO.MED.CS Praha a.s.) in comparison with bisoprolol. Material and methods. To the study, 62 AH patients included with paroxysmal AH, age 45-63 y.o. (mean age 54,5±3,7 y.o.). Patients were randomized to 2 groups: 32 of group 1 (main) for rhythm-control were taking propafenone (Propanorm, PRO.MED.CS Praha a. s.) 450 mg daily, and 30 of group 2 (comparison) were taking bisoprolol for rate control. The groups were comparable by gender, age, severity of AH and duration of arrhythmia. Changes in endothelium vascular motion function and biochemical markers of endothelial dysfunction were assessed at inclusion and in 12 months of therapy. Results. Sinus rhythm retention in propafenone group facilitated the improvement of vascular motion function of endothelium - endothelium dependent vasodilatation of brachial artery showed tendency to rise significantly from 5,4±0,3% to 6,9±0,1% (р=0,01). In patients taking bisoprolol for pulse reduction during 12 months, there was negative tendency from 4,8±0,2% to 3,6±0,1% (р=0,003), that points on worsening of endothelial function with persistent AF. Repeat measurement of biochemical markers of endothelial dysfunction revealed that in 12 months there is raise of endothelin concentration in both groups. Value of the collagen-binding activeness of von Willebrand factor in 12 months significantly reduced from 131±12 to 118±6 U/dL (р<0,05) in those retaining sinus rhythm with propafenone, and increased from 135±11 U/dL to 147±12 U/dL in those with rate control by bisoprolol. Conclusion. In AH patients with paroxysmal AF retention of sinus rhythm with propafenone facilitated the improvement of vascular motion function of endothelium and decrease of collagen binding activeness of von Willebrand factor.