<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.3 20210610//EN" "JATS-journalpublishing1-3.dtd">
<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">cardiovascular</journal-id><journal-title-group><journal-title xml:lang="ru">Кардиоваскулярная терапия и профилактика</journal-title><trans-title-group xml:lang="en"><trans-title>Cardiovascular Therapy and Prevention</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1728-8800</issn><issn pub-type="epub">2619-0125</issn><publisher><publisher-name>«SILICEA-POLIGRAF» LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.15829/1728-8800-2018-4-40-45</article-id><article-id custom-type="elpub" pub-id-type="custom">cardiovascular-885</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>АРИТМИИ СЕРДЦА</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ARRHYTHMIAS</subject></subj-group></article-categories><title-group><article-title>Изменение функции эндотелия у пациентов с пароксизмальной формой фибрилляции предсердий  при лечении пропафеноном</article-title><trans-title-group xml:lang="en"><trans-title>Endothelial function changes in paroxysmal atrial fibrillation and treatment with propafenone</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-0758-5609</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Подзолков</surname><given-names>В. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Podzolkov</surname><given-names>V. I.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Профессор, доктор медицинских наук, заведующий кафедрой факультетской терапии № 2 лечебного факультета, директор клиники факультетской терапии.</p><p>Москва, +7 (495) 245-45-32</p></bio><bio xml:lang="en"><p>Moscow</p></bio><email xlink:type="simple">tarzimanova@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-9536-8307</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Тарзиманова</surname><given-names>А. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Tarzimanova</surname><given-names>A. I.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кандидат медицинских наук, доцент кафедры факультетской терапии № 2 лечебного факультета.</p><p>Москва</p></bio><bio xml:lang="en"><p>Moscow</p></bio><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГАОУ ВО Первый МГМУ им. И. М. Сеченова (Сеченовский Университет)</institution></aff><aff xml:lang="en"><institution>First Sechenov Moscow State Medical University of the Ministry of Health (the Sechenov University)</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2018</year></pub-date><pub-date pub-type="epub"><day>20</day><month>08</month><year>2018</year></pub-date><volume>17</volume><issue>4</issue><fpage>40</fpage><lpage>45</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Подзолков В.И., Тарзиманова А.И., 2018</copyright-statement><copyright-year>2018</copyright-year><copyright-holder xml:lang="ru">Подзолков В.И., Тарзиманова А.И.</copyright-holder><copyright-holder xml:lang="en">Podzolkov V.I., Tarzimanova A.I.</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://cardiovascular.elpub.ru/jour/article/view/885">https://cardiovascular.elpub.ru/jour/article/view/885</self-uri><abstract><sec><title>Цель</title><p>Цель. Оценить изменение функции эндотелия у пациентов с артериальной гипертензией (АГ) и пароксизмальной формой фибрилляции предсердий (ФП) при лечении пропафеноном (Пропанормом, ПРО. МЕД. ЦС Прага) в сравнении с терапией бисопрололом.</p></sec><sec><title>Материал и методы</title><p>Материал и методы. В исследование включены 62 больных АГ с пароксизмальной формой ФП в возрасте 45-63 лет (средний возраст 54,5±3,7 лет). Пациенты были рандомизированы в 2 группы: 32 пациента I группы (основная) для сохранения синусового ритма (СР) принимали пропафенон (Пропанормом, ПРО. МЕД. ЦС Прага) в суточной дозе 450 мг, 30 больным II группы (группа сравнения) для контроля частоты желудочковых сокращений был назначен бисопролол. Исследуемые группы были сопоставимы по  возрасту, полу, тяжести АГ и  длительности аритмии. Определение сосудодвигательной функции эндотелия и биохимических маркеров дисфункции эндотелия проводилось при включении больных в исследование и через 12 мес. терапии.</p></sec><sec><title>Результаты</title><p>Результаты. Удержание СР при лечении пропафеноном способствовало улучшению сосудодвигательной функции эндотелия  — показатель эндотелий-зависимой вазодилатации плечевой артерии имел тенденцию к достоверному росту с 5,4±0,3% до 6,9±0,1% (р=0,01). У больных, получавших на протяжении 12 мес. пульсурежающую терапию бисопрололом, была выявлена отрицательная динамика этого показателя с 4,8±0,2% до 3,6±0,1% (р=0,003), что характеризует ухудшение сосудодвигательной функции эндотелия при длительном персистировании ФП. Повторное исследование биохимических маркеров дисфункции эндотелия через 12 мес. лечения выявило повышение концентрации эндотелина в  обеих группах. Значение коллаген-связывающей активности фактора фон Виллебранда через 12 мес. наблюдения достоверно уменьшилось со 131±12 до 118±6 ЕД/дл (р&lt;0,05) у больных, сохранивших СР при приеме пропафенона; и увеличилась с 135±11 ЕД/дл до 147±12 ЕД/ дл у пациентов, принимавших бисопролол.</p></sec><sec><title>Заключение</title><p>Заключение. У больных АГ с пароксизмальной формой ФП сохранение СР при лечении пропафеноном способствовало улучшению сосудодвигательной функции эндотелия и уменьшению уровня коллаген-связывающей активности фактора фон Виллебранда.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Aim</title><p>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.</p></sec><sec><title>Material and methods</title><p>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.</p></sec><sec><title>Results</title><p>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&lt;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.</p></sec><sec><title>Conclusion</title><p>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.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>фибрилляция предсердий</kwd><kwd>пропафенон</kwd><kwd>изменение функции эндотелия</kwd></kwd-group><kwd-group xml:lang="en"><kwd>atrial fibrillation</kwd><kwd>propafenone</kwd><kwd>endothelium function changes</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">Anderson JL, Halperin JL, Albert NM, et al. Management of patients with atrial fibrillation (compilation of 2006 ACCF/AHA/ESC and 2011 ACCF/AHA/HRS recommendations): a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. JACC. 2013;61(18):1935-44. doi:10.1016/j.jacc.2013.02.001.</mixed-citation><mixed-citation xml:lang="en">Anderson JL, Halperin JL, Albert NM, et al. Management of patients with atrial fibrillation (compilation of 2006 ACCF/AHA/ESC and 2011 ACCF/AHA/HRS recommendations): a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. JACC. 2013;61(18):1935-44. doi:10.1016/j.jacc.2013.02.001.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Kaireviciuted D, Lip G, Balakrishnan B, et al. Intracardiac expression of markers of endothelial damage / dysfunction, inflammation, thrombosis, and tissue remodeling, and the development of postoperative atrial fibrillation. J Thromb Haemost. 2011;9:2345–52. doi:10.1111/j.1538-7836.2011.04523.x.</mixed-citation><mixed-citation xml:lang="en">Kaireviciuted D, Lip G, Balakrishnan B, et al. Intracardiac expression of markers of endothelial damage / dysfunction, inflammation, thrombosis, and tissue remodeling, and the development of postoperative atrial fibrillation. J Thromb Haemost. 2011;9:2345–52. doi:10.1111/j.1538-7836.2011.04523.x.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Deanfield J, Halcox J, Rabelink T. Endothelial function and dysfunction. Circulation. 2007;115:85-95. doi:10.1161/CIRCULATIONAHA.106.652859.</mixed-citation><mixed-citation xml:lang="en">Deanfield J, Halcox J, Rabelink T. Endothelial function and dysfunction. Circulation. 2007;115:85-95. doi:10.1161/CIRCULATIONAHA.106.652859.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Komej J, Apostolakis S, Bollmann A, et al. The emerging role of biomarkers in atrial fibrillation. Can J Cardiol. 2013;29(10):1181-93. doi:10.1016/j.cjca.2013.04.016.</mixed-citation><mixed-citation xml:lang="en">Komej J, Apostolakis S, Bollmann A, et al. The emerging role of biomarkers in atrial fibrillation. Can J Cardiol. 2013;29(10):1181-93. doi:10.1016/j.cjca.2013.04.016.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Scridon A, Girerd N, Rugeri L, et al. Progressive endothelial damage revealed by multilevel von Willebrand factor plasma concentration in atrial fibrillation patients. Europace. 2013;15(11):1562-6. doi:10.1093/europace/eut121.</mixed-citation><mixed-citation xml:lang="en">Scridon A, Girerd N, Rugeri L, et al. Progressive endothelial damage revealed by multilevel von Willebrand factor plasma concentration in atrial fibrillation patients. Europace. 2013;15(11):1562-6. doi:10.1093/europace/eut121.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Celermajer D. Non-invasive detection of endothelial disfunction in children and adult at risk of atherosclerosis. Lancet. 1992;340:1111-5.</mixed-citation><mixed-citation xml:lang="en">Celermajer D. Non-invasive detection of endothelial disfunction in children and adult at risk of atherosclerosis. Lancet. 1992;340:1111-5.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Ionescu-Ittu R, Abrahamowicz M, Jack Evicius C, et al. Comparative effectiveness of rhythm control vs rate control drug treatment effect on mortality in patients with atrial fibrillation. Arch Intern Med. 2012;172:997-1004. doi:10.1001/archinternmed.2012.2266.</mixed-citation><mixed-citation xml:lang="en">Ionescu-Ittu R, Abrahamowicz M, Jack Evicius C, et al. Comparative effectiveness of rhythm control vs rate control drug treatment effect on mortality in patients with atrial fibrillation. Arch Intern Med. 2012;172:997-1004. doi:10.1001/archinternmed.2012.2266.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Camm A, Savelieva I. Atrial fibrillation: the rate versus rhythm management controversy. J R Coll Physicians Edinb. 2012;42(18):23-34. doi:10.4997/JRCPE.2012.S03.</mixed-citation><mixed-citation xml:lang="en">Camm A, Savelieva I. Atrial fibrillation: the rate versus rhythm management controversy. J R Coll Physicians Edinb. 2012;42(18):23-34. doi:10.4997/JRCPE.2012.S03.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Yoshino S, Yoshikawa A, Hamasaki S, et al. Atrial fibrillation-induced endothelial dysfunction improves after restoration of sinus rhythm. Int J Cardiol. 2013;168(2):1280-5. doi:10.1016/j.ijcard.2012.12.006.</mixed-citation><mixed-citation xml:lang="en">Yoshino S, Yoshikawa A, Hamasaki S, et al. Atrial fibrillation-induced endothelial dysfunction improves after restoration of sinus rhythm. Int J Cardiol. 2013;168(2):1280-5. doi:10.1016/j.ijcard.2012.12.006.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Freestone B, Chong A, Nuttall S, et al. Impaired flow mediated dilatation as evidence of endothelial dysfunction in chronic atrial fibrillation: relationship to plasma von Willebrand factor and soluble E-selectin levels. Thromb Res. 2008;122(1):85-90. doi:10.1016/j.thromres.2007.09.008.</mixed-citation><mixed-citation xml:lang="en">Freestone B, Chong A, Nuttall S, et al. Impaired flow mediated dilatation as evidence of endothelial dysfunction in chronic atrial fibrillation: relationship to plasma von Willebrand factor and soluble E-selectin levels. Thromb Res. 2008;122(1):85-90. doi:10.1016/j.thromres.2007.09.008.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Ammash N, Konik E, McBane R, et al. Left atrial blood stasis and von Willebrand factor — ADAMTS13 homeostasis in atrial fibrillation. Arterioscler Throm Vasc Biol. 2011;31(11):2760-6. doi:10.1161/ATVBAHA.111.232991.</mixed-citation><mixed-citation xml:lang="en">Ammash N, Konik E, McBane R, et al. Left atrial blood stasis and von Willebrand factor — ADAMTS13 homeostasis in atrial fibrillation. Arterioscler Throm Vasc Biol. 2011;31(11):2760-6. doi:10.1161/ATVBAHA.111.232991.</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>
