Updated: 2025-12-17
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0220U102530, 0113U007670 , R & D reports
Endothelial and adipose tissue dysfunctin of and their connection with the liver functional state and cardiovascular remodeling and possibilities of their correction in paitients with cardiovascular pathology
Sierkova Valentyna K, Доктор медичних наук
17-03-2020
Vinnytsia National Pirogov Memorial Medical University
During the research work, new scientific provisions are substantiated and formulated: the role of non-specific systemic inflammation and endothelial dysfunction in the mechanisms of progression of coronary heart disease (CHD) and their interrelation with lipid profile of blood and endocrine function of adipose tissue is determined; predictors of destabilization of the disease, which may contribute to the improvement of diagnosis and prognosis of the course were detected; ways to optimize treatment in patients with different variants of CHD course were proposed. In the structure of comorbidity of stable CHD, type 2 diabetes mellitus (DM) is one of the first places and is found in 18-34% of cases. Potential factors of stable CHD and type 2 DM may be genetically determined and acquired adipokinetic status disorders. The predictive value of the leptin receptor gene polymorphism (LEPR Q223R) and disadipokinemia in post-infarction cardiosclerosis patients with comorbidity with type 2 DM is relevant. Diagnostic of the course and treatment of essential arterial hypertensin with concomitant comorbid non-alcoholic fatty liver disease by determining lipid, carbohydrate, fat metabolism, systemic inflammation activity, arterial rigidity, endothelial dysfunction, systemic hemodynamics and both structural and functional state of the heart and blood vessels was improved.
Ivankova Anatasiia V
Voznyuk Larysa A
Gribenyuk Olena V
Kavatsyuk Oleg O
Kuzminova Nataliia V
Lilevska Anastasiia A
Liamprekht Natalia V
Monastyrskyi Yurii I
Nazarova Maryna S
Osovska Nataliia Yu
Romanova Valentyna O
Sierkova Valentyna K
Suleyman Ayad S
Sheremeta Bogdan V
2020-04-01
Updated: 2025-12-17
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