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High-fat diets combined with the introduction of lincomycin causes the development of steatohepatitis. Introduction antidysbiotic drugs (pro- and prebiotics) has a therapeutic effect.

Modeling of experimental metabolic syndrome in Wistar male rats was accompanied by a sharp increase in neutrophils/lymphocytes ratio and decrease in the numbers of monocytes in the blood, as well as almost 5-fold increase in the urease activity, a 3-fold decrease in the activity of lysozyme, and significant increase in the levels of inflammatory markers (MDA and elastase) in the liver. A 13-fold increase was observed in the level of dysbiosis in the liver and a significant increase in the alkaline phosphatase activity. Using antidysbiotic drugs (Quertulin, Quertgial and lysozyme) normalized the state of liver.

Purpose: We studied the change in serum collagen markers in patients with various forms of atrial fibrillation (AF) Methods: Collagen type C-terminal propeptide (CTPK-I), C-terminal telopeptide of type I collagen (CTTK-I), matrix metalloproteinase I, and tissue inhibitors of matrix metalloproteinase I were used as markers for collagen synthesis. The study group comprised - 70 people, control - 20. Results: The level of CTCP-I and CTTP-I in patients with AF was significantly higher in comparison with the control group (91 +27 ng / ml, 67 + 11 ng / ml, p

Objectives: In this study, the serum level of matrix metalloproteinase-9 was studied as an independent predictor of recurrence after catheter ablation of a persistent form of atrial fibrillation. Methods: The study included 46 patients with a persistent form of atrial fibrillation. In all patients, serum level of matrix metalloproteinase-9 was measured before the procedure of catheter radiofrequency ablation and its association with recurrence of arrhythmia at the end of the postoperative period was estimated. Results: The follow-up period was 12.3+ for 6.4 months, in 16 (34.7%) patients there was a relapse of arrhythmia after the procedure of catheter radiofrequency ablation. The baseline level of matrix metalloproteinase-9 was higher in patients with relapsed arrhythmia (297.73 + 81.28 and 234.41 + 93.36 ng / ml, respectively, p=0.006). Multivariate analysis showed that parameters such as the level of matrix metalloproteinase-9, the history of atrial fibrillation and the diameter of the left atrium were independent predictors of arrhythmia recurrence. Conclusion: The serum level of matrix metalloproteinase-9 is an independent predictor of arrhythmia recurrence after performing the procedure of catheter radiofrequency ablation in patients with persistent form of atrial fibrillation.

Method: TIMP-1 was used as a marker for collagen synthesis. The study group comprised 69 people and the control group 23. Results: Patients with persistent and chronic AF had an elevated level of TIMP-1 in comparison with patients with paroxysmal AF (149.63 + 43.71 ng / ml, 155.90 + 45.86 ng / ml vs 131.51 + 36.92 ng / ml, p

Method: C-terminal telopeptide procollagen type –I (CTTP-I) was used as a marker for collagen synthesis. The study group comprised 69 people and the control group 23. Results: Patients with persistent and chronic AF had an elevated level of CTTP-I in comparison with patients with paroxysmal AF (0.40+0.19 ng/ml, 0.44+0.21 ng/ml vs 0.36+0.17 ng/ml, p=0.016). The level of CTTP-I was significantly lower in the control group compared to patients with paroxysmal, persistent and chronic AF forms (0.36+0.17 ng/ml, 0.40+0.19 ng/ml, 0.44+0.21 ng/ml and 0.27+0.11ng/ml , p=0.016). Conclusions: The level of CTTP-I is significantly different between healthy people and patients with AF. Moreover, these markers also differ depending on the AF form. It can be assumed that the intensity of extracellular synthesis and degradation of type I collagen can be related to the severity and type of AF.

In a study the indicators of cardiac fibrosis at patients with paroxysmal form of atrial fibrillation were investigated. The study group consisted of patients with paroxysmal atrial fibrillation in combination with hypertension and without it. Signs of the left atrium dilation have been identified in comparison to healthy patients. At the same time smaller changes were observed in patients with atrial fibrillation without hypertension. Whereas in the group of patients with arterial hypertension signs of dilatation of the left atrium were most significant. In the study of correlations with indicators of fibrosis echocardiographic parameters found that significant associations observed mainly in index PICP with the parameters of the left atrium. The increase in size of the left atrium PICP associated with increasing concentrations of TIMP-1 and MMP-9.

Atrial fibrillation (AF) is the most common heart rhythm disorder in clinical practice. Today proved that traditional pharmacologic therapies are effective in patients with paroxysmal atrial fibrillation with no structural disorders of the myocardium. Data from clinical and experimental studies have shown the important role of the structural remodeling in the formation of the substrate of atrial fibrillation, producing fibrosis that alters the composition and function of the atrial tissue. The exact mechanism underlying atrial fibrosis is not fully elucidated, but recent experimental and clinical studies have provided important data. It has been shown that in the process of formation and propagation of fibrosis involved number of different signaling systems, including angiotensin-2 and related mediators. This article provides an overview of the current understanding of the formation of atrial fibrillation substrate by fibrosis remodeling. Sum-date data on the mechanisms underlying the fibrosis and progression as well as brightly lit modern therapeutic approaches aimed at reducing structural remodeling to prevent AF.

Atrial fibrillation is one of the most complex cardiac arrhythmias. The pathophysiological mechanisms of this process will probably include the following components: a complex interaction between the focal trigger activity in the area of the pulmonary veins, which is a trigger for arrhythmias and arrhythmogenic substrate contributes to its maintenance. Components of arrhythmogenic process, in its turn, connected to a structural remodelling of the myocardium, in particular with the formation of fibrosis. In recent years, in order to assess the degree of structural remodelling and volume of fibrous tissue changes in patients both before surgery and after, non-invasive imaging techniques are getting more and more widely used, such as cardiac magnetic resonance imaging. Processing and interpretation of data using cardiac magnetic resonance imaging is still an area for discussion. The aim of this article is to summarize data on atrial fibrosis and its evaluation using standard catheter techniques, new non-invasive imaging techniques as well as new approaches in the use of cardiac magnetic resonance imaging developed by our group in patients with atrial fibrillation.

Gozhenko A. I., Bayazitov N. R., Levchenko E. M., Goriachyi V. V., Goriachyi A. V. Патогенетические механизмы фибрилляции предсердий и формирования предсердного фиброза = Pathogenic mechanisms of atrial fibrillation and atrial fibrosis formation. Journal of Education, Health and Sport. 2016;6(10):22-33. eISSN 2391-8306. DOI http://dx.doi.org/10.5281/zenodo.159538 http://ojs.ukw.edu.pl/index.php/johs/article/view/3921 The journal has had 7 points in Ministry of Science and Higher Education parametric evaluation. Part B item 755 (23.12.2015). 755 Journal of Education, Health and Sport eISSN 2391-8306 7 © The Author (s) 2016; This article is published with open access at Licensee Open Journal Systems of Kazimierz Wielki University in Bydgoszcz, Poland Open Access. This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. This is an open access article licensed under the terms of the Creative Commons Attribution Non Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted, non commercial use, distribution and reproduction in any medium, provided the work is properly cited. This is an open access article licensed under the terms of the Creative Commons Attribution Non Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted, non commercial use, distribution and reproduction in any medium, provided the work is properly cited. The authors declare that there is no conflict of interests regarding the publication of this paper. Received: 02.09.2016. Revised 24.09.2016. Accepted: 07.10.2016. УДК: 616.12-008.313.2-036.12-089:615.849 Патогенетические механизмы фибрилляции предсердий и формирования предсердного фиброза А. И. Гоженко, Н. Р. Баязитов, Е. М. Левченко, В. В. Горячий, А. В. Горячий Украинский научно-исследовательский институт медицины транспорта, Одесская Областная клиническая больница Реферат Фибрилляция предсердий (ФП) является наиболее распространенной аритмией в клинической практике. Недавние экспериментальные исследования показали связь фибрилляции предсердий с застойной сердечной недостаточностью (ЗСН). В свою очередь ЗСН коррелирует с предсердным структурным ремоделированием заканчивающимся образование фиброза. Структурное ремоделирование является важным свойством субстрата ФП, продуцируя фиброз, который изменяет состав и функции предсердной ткани. Точные механизмы, лежащие в основе предсердного фиброза до конца не выяснены. Недавние экспериментальные и клинические исследования использующие анализ частотных характеристик показали, что ФП может быть характеризована с помощью отдельных стабильных, высокочастотных областей. Однако точный сигнальный процесс включенный в развитие предсердного фиброза на данный момент неизвестен. Исследования проведенные на животных подтвердили важную роль систем, с участием TGFb1, ангиотензина II и связанных с ним медиаторов в распространении фиброза у пациентов с СН. Исследования проведенные на моделях мышей с гиперэкспрессией TGFb1 показали наличие глубокого предсердного фиброза и фибрилляцию предсердий при наличии нормального желудочкового миокара. Сердечная недостаточность в модели на собаках также продуцировала увеличение в предсердиях экспрессии TGFb1. Ингибирование его предотвращало предсердный фиброз и развитие субстрата для фибрилляции предсердий. В настоящем документе рассматриваются современные представления о том, как предсердный фиброз создает субстрат для ФП, обобщаются имеющиеся данные о механизмах, фиброза и его распространения, и освещаются терапевтические подходы, направленные на уменьшение структурного ремоделирования для предотвращения ФП. Ключевые слова: фибрилляция предсердий, фиброз, катетерная абляция, структурное ремоделирование Pathogenic mechanisms of atrial fibrillation and atrial fibrosis formation A. I. Gozhenko, N. R. Bayazitov, E. M. Levchenko, V. V. Goriachyi, A. V. Goriachyi Ukrainian Scientific Research Institute of Transport Medicine, Odessa Regional Clinical Hospital Abstract Atrial fibrillation (AF) is the most common cardiac arrhythmia in clinical practice. Recent experimental studies have shown an association of atrial fibrillation with congestive heart failure (CHF). In turn, CHF correlates with atrial structural remodeling resulted in the formation of fibrosis. Structural remodelling is an important property of AF substrate, producing fibrosis, which alters the composition and function of the atrial tissue. The exact mechanisms underlying atrial fibrosis has not been fully elucidated. Recent experimental and clinical studies using frequency analysis showed that AF may be characterized by a single stable, high-frequency areas. However, the exact process of the signal included in the development of atrial fibrosis is currently unknown. Studies on animals have confirmed the important role of systems involving TGFb1, angiotensin II and related mediators distributing fibrosis in patients with HF. This paper reviews the current understanding of how atrial fibrosis creates a substrate for AF, summarizes available data on the mechanisms of fibrosis and its distribution, and highlights the therapeutic approaches aimed at reducing the structural remodeling to prevent AF. Key words: atrial fibrillation, fibrosis, catheter ablation, structural remodeling Патогенетичні механізми фібриляції передсердь і формування предсердного фіброзу А. І. Гоженко, М. Р. Баязітов, О. М. Левченко, В. В. Горячий, О. В. Горячий Український науково-дослідницький інститут медицини транспорту, Одеська Обласна клінічна лікарня Фібриляція передсердь (ФП) є найбільш поширеною аритмією в клінічній практиці. Недавні експериментальні дослідження показали зв'язок фібриляції передсердь із застійною серцевою недостатністю (ЗСН). У свою чергу ЗСН корелює з передсердним структурним ремоделюванням що закінчується утворенням фіброзу. Структурне ремоделювання є важливою властивістю субстрату ФП, продукуючи фіброз, який змінює склад і функції передсердної тканини. Точні механізми, що лежать в основі передсердного фіброзу до кінця не з'ясовані. Недавні експериментальні і клінічні дослідження які використовували аналіз частотних характеристик показали, що ФП може бути охарактеризована за допомогою окремих стабільних, високочастотних областей. Однак точний сигнальний процес включений в розвиток предсердного фіброзу на даний момент невідомий. Дослідження проведені на тваринах підтвердили важливу роль систем, за участю TGFb1, ангіотензину II і пов'язаних з ним медіаторів в поширенні фіброзу у пацієнтів з СН. У цьому документі розглядаються сучасні уявлення про те, як передсердний фіброз створює субстрат для ФП, узагальнюються наявні дані про механізми фіброзу і його поширення, і висвітлюються терапевтичні підходи, спрямовані на зменшення структурного ремоделювання для запобігання ФП. Ключові слова: фібриляція передсердь, фіброз, катетерная абляція, структурний ремоделирование

Atrial fibrillation is one of the most complex cardiac arrhythmias. The pathophysiological mechanisms of this process will probably include the following components: a complex interaction between the focal trigger activity in the area of the pulmonary veins, which is a trigger for arrhythmias and arrhythmogenic substrate contributes to its maintenance. Components of arrhythmogenic process, in its turn, connected to a structural remodelling of the myocardium, in particular with the formation of fibrosis. In recent years, in order to assess the degree of structural remodelling and volume of fibrous tissue changes in patients both before surgery and after, non-invasive imaging techniques are getting more and more widely used, such as cardiac magnetic resonance imaging. Processing and interpretation of data using cardiac magnetic resonance imaging is still an area for discussion. The aim of this article is to summarize data on atrial fibrosis and its evaluation using standard catheter techniques, new non-invasive imaging techniques as well as new approaches in the use of cardiac magnetic resonance imaging developed by our group in patients with atrial fibrillation.

Levitsky A. P., Khodakov I. V., Levchenko E. M. Влияние высокожировых рационов с различным жирнокислотным составом на содержание незаменимых жирных кислот в липидах печени = Influence of high fat diets with different composition of fatty acids on the content of essential fatty acids in liver lipids. Journal of Education, Health and Sport. 2015;5(12):598-607. eISSN 2391-8306. DOIhttp://dx.doi.org/10.5281/zenodo.44266 http://ojs.ukw.edu.pl/index.php/johs/article/view/2015%3B5%2812%29%3A598-607 http://pbn.nauka.gov.pl/works/687268 Formerly Journal of Health Sciences. ISSN 1429-9623 / 2300-665X. Archives 2011–2014http://journal.rsw.edu.pl/index.php/JHS/issue/archive The journal has had 7 points in Ministry of Science and Higher Education parametric evaluation. Part B item 755 (23.12.2015). 755 Journal of Education, Health and Sport (null) 2391-8306 7 © The Author (s) 2015; This article is published with open access at Licensee Open Journal Systems of Kazimierz Wielki University in Bydgoszcz, Poland and Radom University in Radom, Poland Open Access. This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. This is an open access article licensed under the terms of the Creative Commons Attribution Non Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non commercial use, distribution and reproduction in any medium, provided the work is properly cited. This is an open access article licensed under the terms of the Creative Commons Attribution Non Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non commercial use, distribution and reproduction in any medium, provided the work is properly cited. The authors declare that there is no conflict of interests regarding the publication of this paper. Received: 10.12.2015. Revised 15.12.2015. Accepted: 29.12.2015. УДК 612.397.23+577.16+613.2 ВЛИЯНИЕ ВЫСОКОЖИРОВЫХ РАЦИОНОВ С РАЗЛИЧНЫМ ЖИРНОКИСЛОТНЫМ СОСТАВОМ НА СОДЕРЖАНИЕ НЕЗАМЕНИМЫХ ЖИРНЫХ КИСЛОТ В ЛИПИДАХ ПЕЧЕНИ INFLUENCE OF HIGH FAT DIETS WITH DIFFERENT COMPOSITION OF FATTY ACIDS ON THE CONTENT OF ESSENTIAL FATTY ACIDS IN LIVER LIPIDS А. П. Левицкий1, И. В. Ходаков1, Е. М. Левченко2 A. P. Levitsky1, I. V. Khodakov1, E. M. Levchenko2 1ГУ «Институт стоматологии НАМН», г. Одесса 2КУ «Одесская областная клиническая больница» 1SE«The Institute of Stomatology of the National acаdemie of medical science of Ukraine», Odessa, Ukraine 2Municipal Institution «Odessa Regional Clinical Hospital» Abstract Aim: To determine the effect of high fat diets with different fatty acid composition on the level of essential fatty acids in the liver. Materials and Methods: We used sunflower, olive, palm oil or butter in the amount of 15% for a high fat diet (HFD). The experiment was carried out in rats for 41 days. In the liver there was determined the content of total lipids (TL), free fatty acids (FFA) and the content of essential fatty acids by the chromatographic method. Results: HFD increases the TL content in the liver (excluding butter) and reduces the level of FFA. HFD reduces the TL content, and it reduces a lot the essential fatty acids’ content in FFA, especially linoleic and eicosapentaenoic acids. Conclusion: Perhaps HFD inhibits lipolysis in the liver and inhibits the synthesis of essential fatty acids. Keywords: fatty food, fatty acids, liver. Резюме Дополнительное введение в базовый комбикорм 15 % подсолнечного, оливкового, пальмового или сливочного масла снижает в печени уровень свободных жирных кислот (СЖК) и содержание незаменимых жирных кислот (особенно, линоленовой и эйкозапентаеновой), причем более существенно во фракции СЖК. Ключевые слова: жировое питание, жирные кислоты, печень.