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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">cardiotomsk</journal-id><journal-title-group><journal-title xml:lang="ru">Сибирский журнал клинической и экспериментальной медицины</journal-title><trans-title-group xml:lang="en"><trans-title>Siberian Journal of Clinical and Experimental Medicine</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2713-2927</issn><issn pub-type="epub">2713-265X</issn><publisher><publisher-name>TSU publishing</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.29001/2073-8552-2015-30-3-13-18</article-id><article-id custom-type="elpub" pub-id-type="custom">cardiotomsk-187</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>КЛИНИЧЕСКИЕ ИССЛЕДОВАНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>CLINICAL STUDIES</subject></subj-group></article-categories><title-group><article-title>ВЛИЯНИЕ ЭНДОКАРДИАЛЬНОЙ ПРОЦЕДУРЫ “ЛАБИРИНТ” У ПАЦИЕНТОВ С ФИБРИЛЛЯЦИЕЙ ПРЕДСЕРДИЙ НА ДИНАМИКУ ПОКАЗАТЕЛЕЙ СИСТЕМЫ ПРОТЕОЛИЗА ВНЕКЛЕТОЧНОГО МАТРИКСА И ФАКТОРОВ РОСТА</article-title><trans-title-group xml:lang="en"><trans-title>EFFECTS OF ENDOCARDIAL MAZE PROCEDURE ON DYNAMICS OF EXTRACELLULAR MATRIX PROTEOLYSIS AND GROWTH FACTOR CONCENTRATIONS IN PATIENTS WITH ATRIAL FIBRILLATION</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Баталов</surname><given-names>Роман Ефимович</given-names></name><name name-style="western" xml:lang="en"><surname>Batalov</surname><given-names>R. E.</given-names></name></name-alternatives><email xlink:type="simple">romancer@cardio.tsu.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Хлынин</surname><given-names>Михаил Сергеевич</given-names></name><name name-style="western" xml:lang="en"><surname>Khlynin</surname><given-names>M. S.</given-names></name></name-alternatives><email xlink:type="simple">mskhlynin@mail.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Усенков</surname><given-names>Станислав Юрьевич</given-names></name><name name-style="western" xml:lang="en"><surname>Usenkov</surname><given-names>S. Yu.</given-names></name></name-alternatives><email xlink:type="simple">sturus@rambler.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Гусакова</surname><given-names>Анна Михайловна</given-names></name><name name-style="western" xml:lang="en"><surname>Gusakova</surname><given-names>A. M.</given-names></name></name-alternatives><email xlink:type="simple">mag_a@mail.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Суслова</surname><given-names>Татьяна Евгеньевна</given-names></name><name name-style="western" xml:lang="en"><surname>Suslova</surname><given-names>T. E.</given-names></name></name-alternatives><email xlink:type="simple">tes@cardio-tomsk.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Попов</surname><given-names>Сергей Валентинович</given-names></name><name name-style="western" xml:lang="en"><surname>Popov</surname><given-names>S. V.</given-names></name></name-alternatives><email xlink:type="simple">psv@cardio-tomsk.ru</email><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Федеральное государственное бюджетное научное учреждение “Научно-исследовательский институт кардиологии”; Федеральное государственное автономное образовательное учреждение высшего образования “Национальный исследовательский Томский государственный университет”</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Federal State Budgetary Scientific Institution “Research Institute for Cardiology”; National Research Tomsk State University</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Федеральное государственное бюджетное научное учреждение “Научно-исследовательский институт кардиологии”</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Federal State Budgetary Scientific Institution “Research Institute for Cardiology”</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2015</year></pub-date><pub-date pub-type="epub"><day>06</day><month>09</month><year>2016</year></pub-date><volume>30</volume><issue>3</issue><fpage>13</fpage><lpage>18</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Баталов Р.Е., Хлынин М.С., Усенков С.Ю., Гусакова А.М., Суслова Т.Е., Попов С.В., 2016</copyright-statement><copyright-year>2016</copyright-year><copyright-holder xml:lang="ru">Баталов Р.Е., Хлынин М.С., Усенков С.Ю., Гусакова А.М., Суслова Т.Е., Попов С.В.</copyright-holder><copyright-holder xml:lang="en">Batalov R.E., Khlynin M.S., Usenkov S.Y., Gusakova A.M., Suslova T.E., Popov S.V.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.sibjcem.ru/jour/article/view/187">https://www.sibjcem.ru/jour/article/view/187</self-uri><abstract><p>Цель: определить влияние интервенционного вмешательства по поводу фибрилляции предсердий (ФП) на динамику протеолиза внеклеточного матрикса. Материал и методы. В исследование вошли 50 пациентов с персистирующей - 27 (18 мужчин), средний возраст 62,1±9,4 лет и длительно-персистирующей - 23 (14 мужчин), средний возраст 64±11 лет формами ФП, с наличием показаний для проведения интервенционного лечения аритмии. Выполнена радиочастотная антральная изоляция легочных вен, задней стенки левого предсердия (ЛП), левого истмуса сердца с использованием системы CARTO (Biosense Webster, США). Определяли динамику показателей системы протеолиза внеклеточного матрикса и факторов роста в сыворотке крови - матриксных металлопротеиназ (ММП) -1, -3, -9, тканевого фактора роста-β1 (TGF-β1), тканевого ингибитора матриксных металлопротеиназ (ТИМП-1), фактора роста фибробластов (FGF), до процедуры “Лабиринт”, непосредственно после нее, через одни сутки, через 3 и 6 мес. Результаты. Концентрация всех матриксных металлопротеиназ непосредственно после процедуры резко снижалась, что, скорее всего, связано со значительным и объемным термическим поражением ЛП. Через сутки концентрация ММП-1 имела тенденцию к восстановлению, в то время как ММП-3 сохранялась на предыдущем уровне, а ММП-9 резко возрастала до уровня, превышающего таковой до вмешательства. По истечению 3 мес. наблюдения концентрация ММП-1 и -3 практически возвращалась к исходной, а ММП-9 резко снижалась до уровня, имеющегося непосредственно после процедуры. Через полгода наблюдения концентрация ММП-1 имела тенденцию к снижению, и была ниже исходного уровня, уровень ММП-3 также не достиг исходного, в то время как концентрация ММП-9 вернулась к исходной точке. Концентрация тканевого фактора роста-β1 также резко снижалась непосредственно сразу после процедуры, с медленным восстановлением к 6-му мес. наблюдения, чего нельзя сказать о факторе роста фибробластов. Так, сразу после процедуры его концентрация снижалась, что можно объяснить массовой гибелью клеток в миокарде предсердий. Через сутки концентрация увеличивалась и достигала исходных значений. Через 3 и 6 мес. концентрация снижалась. Заключение. Снижение активности металлопротеиназ и факторов роста при отсутствии аритмии после РЧА - результат прекращения структурного ремоделирования и, возможно, его регресса.</p></abstract><trans-abstract xml:lang="en"><p>Aim. The aim of the study was to determine the effects of interventional treatment for atrial fibrillation (AF) on the dynamic changes in the system of extracellular matrix proteolysis. Material and methods. A total of 50 patients were included in the study: 27 patients (18 males) had persistent AF (mean age of 62.1±9.4 years); 23 patients (14 males) had long-lasting persistent AF (mean age of 64±11 years). All patients received radiofrequency antral pulmonary veins isolation and linear lesions on the back wall of the left atrium and the mitral isthmus with CARTO system (Biosense Webster, USA). Blood serum changes in the parameters of extracellular matrix proteolysis and concentrations of growth factors including matrix metalloproteinase (MMP)-1, MMP-3, MMP-9, tissue growth factor β1 (TGF-β1), tissue inhibitor of matrix metalloproteinases 1 (TIMP-1), and fibroblast growth factor (FGF) were determined before the Maze procedure, immediately after the procedure, after 1 day, 3 months, and 6 months. Results. The concentrations of all MMPs immediately after the Maze procedure dramatically decreased most likely due to significant thermal damage of the left atrium. On the next day after the procedure, the MMP-1 concentration restored to the initial level, the MMP-3 concentration remained at the same level, whereas the MMP-9 concentration drastically increased to the level exceeding the initial value. After 3 months, the concentrations of MMP-1 and MMP-3 were near the initial levels, whereas MMP-9 concentration dropped to the level recorded immediately after the procedure. After 6 months of observation, the MMP-1 concentration demonstrated downward trend and was lower than the initial value; the MMP-1 level also did not reach the initial level; and the MMP-9 concentration returned to the initial level. The TGF-β1 concentration also dramatically dropped right after the procedure and slowly recovered during 6 months of follow-up. The decrease in the TGF-β1 concentration immediately after the procedure can be explained by massive cell death in the atrial myocardium. One day after the procedure, the TGF-β1 concentration increased and reached the initial level, but it decreased after 3 and 6 months. Conclusion. The reductions in the concentrations of MMPs and growth factors in the absence of AF after the Maze procedure resulted from the arrest and perhaps the reversal of the structural remodeling.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>фибрилляция предсердий</kwd><kwd>радиочастотная аблация</kwd><kwd>фиброз</kwd><kwd>внеклеточный матрикс</kwd><kwd>структурное ремоделирование предсердий</kwd><kwd>atrial fibrillation</kwd><kwd>radiofrequency ablation</kwd><kwd>fibrosis</kwd><kwd>extracellular matrix</kwd><kwd>structural remodeling</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Anyukhovsky E., Sosunov E., Plotnikov A. et al. Cellular electrophysiologic properties of old canine atria provide a substrate for arrhythmogenesis // Cardiovasc. Res. - 2002. - Vol. 54. - P. 462-469.</mixed-citation><mixed-citation xml:lang="en">Anyukhovsky E., Sosunov E., Plotnikov A. et al. Cellular electrophysiologic properties of old canine atria provide a substrate for arrhythmogenesis // Cardiovasc. Res. - 2002. - Vol. 54. - P. 462-469.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Bajpai A., Savelieva I., Camm J. Treatment of atrial fibrillation // Br. Med. Bull. - 2008. - Vol. 88. - P. 75-94.</mixed-citation><mixed-citation xml:lang="en">Bajpai A., Savelieva I., Camm J. Treatment of atrial fibrillation // Br. Med. Bull. - 2008. - Vol. 88. - P. 75-94.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Burstein B., Nattel S. Atrial fibrosis: mechanisms and clinical relevance in atrial fibrillation // J. Am. Coll. Cardiol. - 2008. - Vol. 51. - P. 802-809.</mixed-citation><mixed-citation xml:lang="en">Burstein B., Nattel S. Atrial fibrosis: mechanisms and clinical relevance in atrial fibrillation // J. Am. Coll. Cardiol. - 2008. - Vol. 51. - P. 802-809.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Hanna N., Cardin S., Nattel S. Differences in atrial versus ventricular remodeling in dogs with ventricular tachypacing-induced congestive heart failure // Cardiovasc. Res. - 2004. - Vol. 63. - P. 236-244.</mixed-citation><mixed-citation xml:lang="en">Hanna N., Cardin S., Nattel S. Differences in atrial versus ventricular remodeling in dogs with ventricular tachypacing-induced congestive heart failure // Cardiovasc. Res. - 2004. - Vol. 63. - P. 236-244.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Hinescu M., Gherghiceanu M., Mandache E. Interstitial Cajal-like cells (ICLC) in atrial myocardium: ultrastructural and immunohistochemical characterization // J. Cell. Mol. Med. - 2006. - Vol. 10. - P. 243-257.</mixed-citation><mixed-citation xml:lang="en">Hinescu M., Gherghiceanu M., Mandache E. Interstitial Cajal-like cells (ICLC) in atrial myocardium: ultrastructural and immunohistochemical characterization // J. Cell. Mol. Med. - 2006. - Vol. 10. - P. 243-257.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Choi E.K., Chang P.C., Lee Y.S. et al. Triggered firing and atrial fibrillation in transgenic mice with selective atrial fibrosis induced by overexpression of TGF-β1// Circ. J. - 2012. - Vol. 76 - P. 1354-1362.</mixed-citation><mixed-citation xml:lang="en">Choi E.K., Chang P.C., Lee Y.S. et al. Triggered firing and atrial fibrillation in transgenic mice with selective atrial fibrosis induced by overexpression of TGF-β1// Circ. J. - 2012. - Vol. 76 - P. 1354-1362.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Lee A.A., Dillmann W.H., McCulloch A.D. et al. Angiotensin II stimulates the autocrine production of transforming growth factor-beta 1 in adult rat cardiac fibroblasts // J. Mol. Cell. Cardiol. - 1995. - Vol. 27. - P. 2347-2357.</mixed-citation><mixed-citation xml:lang="en">Lee A.A., Dillmann W.H., McCulloch A.D. et al. Angiotensin II stimulates the autocrine production of transforming growth factor-beta 1 in adult rat cardiac fibroblasts // J. Mol. Cell. Cardiol. - 1995. - Vol. 27. - P. 2347-2357.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Purnomo Y., Piccart Y., Coenen T. et al. Oxidative stress and transforming growth factor-β1-induced cardiac fibrosis // Cardiovasc. Hematol. Disord. Drug Targets. - 2013. - Vol. 13. - P. 165-172.</mixed-citation><mixed-citation xml:lang="en">Purnomo Y., Piccart Y., Coenen T. et al. Oxidative stress and transforming growth factor-β1-induced cardiac fibrosis // Cardiovasc. Hematol. Disord. Drug Targets. - 2013. - Vol. 13. - P. 165-172.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Nattel S., Shiroshita-Takeshita A., Brundel B. Mechanisms of atrial fibrillation: lessons from animal models // Prog. Cardiovasc. Dis. - 2005. - Vol. 48. - P. 9-28.</mixed-citation><mixed-citation xml:lang="en">Nattel S., Shiroshita-Takeshita A., Brundel B. Mechanisms of atrial fibrillation: lessons from animal models // Prog. Cardiovasc. Dis. - 2005. - Vol. 48. - P. 9-28.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Ponten A., Folestad E., Pietras K. Platelet4derived growth factor D induces cardiac fibrosis and proliferation of vascular smooth muscle cells in heart-specific transgenic mice // Circ. Res. - 2005. - Vol. 97. - P. 1036-1045.</mixed-citation><mixed-citation xml:lang="en">Ponten A., Folestad E., Pietras K. Platelet4derived growth factor D induces cardiac fibrosis and proliferation of vascular smooth muscle cells in heart-specific transgenic mice // Circ. Res. - 2005. - Vol. 97. - P. 1036-1045.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Ponten A., Li X., Thoren P. et al. Transgenic overexpression of platelet-derived growth factor4C in the mouse heart induces cardiac fibrosis, hypertrophy, and dilated cardiomyopathy // Am. J. Pathol. - 2003. - Vol. 163. - P. 673-682.</mixed-citation><mixed-citation xml:lang="en">Ponten A., Li X., Thoren P. et al. Transgenic overexpression of platelet-derived growth factor4C in the mouse heart induces cardiac fibrosis, hypertrophy, and dilated cardiomyopathy // Am. J. Pathol. - 2003. - Vol. 163. - P. 673-682.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Schultz J., Witt S., Glascock B. et al. TGF-beta1 mediates the hypertrophic cardiomyocyte growth induced by angiotensin II // J. Clin. Invest. - 2002. - Vol. 109. - P. 787-796.</mixed-citation><mixed-citation xml:lang="en">Schultz J., Witt S., Glascock B. et al. TGF-beta1 mediates the hypertrophic cardiomyocyte growth induced by angiotensin II // J. Clin. Invest. - 2002. - Vol. 109. - P. 787-796.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Lopez B., Gonzalez A., Ravassa S.J. et al. Circulating Biomarkers of Myocardial Fibrosis: The Need for a Reappraisal // Am. Coll. Cardiol. - 2015. - Vol. 65. - P. 2449-2456.</mixed-citation><mixed-citation xml:lang="en">Lopez B., Gonzalez A., Ravassa S.J. et al. Circulating Biomarkers of Myocardial Fibrosis: The Need for a Reappraisal // Am. Coll. Cardiol. - 2015. - Vol. 65. - P. 2449-2456.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Rahmutula D., Marcus G.M., Wilson E.E. et al. Molecular basis of selective atrial fibrosis due to overexpression of transforming growth factor-β1 // Cardiovasc. Res. - 2013. - Vol. 4. - P. 769-779.</mixed-citation><mixed-citation xml:lang="en">Rahmutula D., Marcus G.M., Wilson E.E. et al. Molecular basis of selective atrial fibrosis due to overexpression of transforming growth factor-β1 // Cardiovasc. Res. - 2013. - Vol. 4. - P. 769-779.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">De Jong S., van Veen T.A., de Bakker J.M. et al. Biomarkers of myocardial fibrosis // J. Cardiovasc. Pharmacol. - 2011. - Vol. 57. - P. 522-535.</mixed-citation><mixed-citation xml:lang="en">De Jong S., van Veen T.A., de Bakker J.M. et al. Biomarkers of myocardial fibrosis // J. Cardiovasc. Pharmacol. - 2011. - Vol. 57. - P. 522-535.</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
