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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="en"><front><journal-meta><journal-id journal-id-type="publisher-id">rpcardio</journal-id><journal-title-group><journal-title xml:lang="en">Rational Pharmacotherapy in Cardiology</journal-title><trans-title-group xml:lang="ru"><trans-title>Рациональная Фармакотерапия в Кардиологии</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1819-6446</issn><issn pub-type="epub">2225-3653</issn><publisher><publisher-name>«SILICEA-POLIGRAF» LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.20996/1819-6446-2008-4-5-71-76</article-id><article-id custom-type="elpub" pub-id-type="custom">rpcardio-1162</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="en"><subject>ASSOCIATED PROBLEMS OF CARDIOLOGY</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>СМЕЖНЫЕ ПРОБЛЕМЫ КАРДИОЛОГИИ</subject></subj-group></article-categories><title-group><article-title>CARDIOVASCULAR RISK IN PATIENTS WITH ANKYLOSING SPONDYLITIS: THE ROLE OF SYSTEMIC INFLAMMATION AND ENDOTHELIAL DYSFUNCTION</article-title><trans-title-group xml:lang="ru"><trans-title>КАРДИОВАСКУЛЯРНЫЙ РИСК У БОЛЬНЫХ АНКИЛОЗИРУЮЩИМ СПОНДИЛИТОМ: РОЛЬ СИСТЕМНОГО ВОСПАЛЕНИЯ И ДИСФУНКЦИИ ЭНДОТЕЛИЯ</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>Поддубный</surname><given-names>Д. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Poddubnyy</surname><given-names>D. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кафедра госпитальной терапии</p></bio><bio xml:lang="en"><p>Chair of Hospital Therapy</p></bio><email xlink:type="simple">andreyrebrov@yandex.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>Ребров</surname><given-names>А. П.</given-names></name><name name-style="western" xml:lang="en"><surname>Rebrov</surname><given-names>A. P.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кафедра госпитальной терапии</p></bio><bio xml:lang="en"><p>Chair of Hospital Therapy</p></bio><email xlink:type="simple">andreyrebrov@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Саратовский государственный медицинский университет, 410012 Саратов, Большая Казачья ул., д. 112</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Saratov State Medical University, Bolshaya Kazachya ul. 112, Saratov, 410012 Russia</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2008</year></pub-date><pub-date pub-type="epub"><day>01</day><month>02</month><year>2016</year></pub-date><volume>4</volume><issue>5</issue><fpage>71</fpage><lpage>76</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Poddubnyy D.A., Rebrov A.P., 2016</copyright-statement><copyright-year>2016</copyright-year><copyright-holder xml:lang="ru">Поддубный Д.А., Ребров А.П.</copyright-holder><copyright-holder xml:lang="en">Poddubnyy D.A., Rebrov A.P.</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.rpcardio.online/jour/article/view/1162">https://www.rpcardio.online/jour/article/view/1162</self-uri><abstract><sec><title>Aim</title><p>Aim. To investigate the role of systemic inflammation and endothelial dysfunction as factors of cardiovascular risk in patients with ankylosing spondylitis.</p></sec><sec><title>Material andMethods</title><p>Material andMethods. 100 patients with ankylosing spondylitis were included into the study. Screening for arterial hypertension (HT) and conventional cardiovascular risk factors (smoking, hyper- and dislipoproteinemia, body overweight, heredity and diabetes mellitus) was performed in all patients. 10-year coronary disease risk (Framingham scale) and 10-year risk of fatal cardiovascular event (SCORE scale) was calculated. Additionally the follows cardiovascular risk factors were assessed: C-reactive protein level (CRP), fibrinogen level, platelet count, antithrombin III activity, plasma fibrinolytic activity, vonWillebrand factor (vWF) activity, circulating endothelial cells (CEC) count. Besides, endothelial functionwas evaluated by Doppler-ultrasonography of brachial artery in testswith reactive (endothelium-dependent or flow-mediated dilation) and nitroglycerine (endotheliumindependent dilation) hyperemia. 30 healthy patients were included into control group and were comparable with patients of studied group on sex and age.</p></sec><sec><title>Results</title><p>Results. 10-year coronary disease risk in patients with ankylosing spondylitis was significantly lower than this in patients of control group 4.0%(3,0; 7,5) vs 5.0%(3,0; 11,0), respectively (p&lt;0,05). 10-year risk of fatal cardiovascular event in studied group was relatively low 1.0% (1.0; 2.0). However, analysis of the additional risk factors shown increased thrombogenic potential of blood, which was related to systemic inflammation activity: high platelets count, high fibrinogen activity, increased vWF activity, and decreased fibrinolytic activity. Moreover, signs of endothelial injury (increased level of CEC and vWF activity) and endothelial dysfunction were found in patients with ankylosing spondylitis.</p></sec><sec><title>Conclusion</title><p>Conclusion. Cardiovascular risk in patientswith ankylosing spondylitis estimated on the basis of conventional risk factors is not higher than this in general population. At the same time, these patients have signs of endothelial injure, dysfunction, and increased thrombogenic potential directly related to the systemic inflammation activity.We suppose these factors are responsible for the increased cardiovascular risk in patients with ankylosing spondylitis and, therefore, should be taken into account upon cardiovascular risk assessment.</p></sec></abstract><trans-abstract xml:lang="ru"><sec><title>Цель</title><p>Цель. Исследовать роль системного воспаления и дисфункции эндотелия как факторов кардиоваскулярного риска у больных анкилозирующим спондилитом.</p></sec><sec><title>Материалы и методы</title><p>Материалы и методы. Обследовали 100 больных анкилозирующим спондилитом. У всех пациентов осуществляли скрининг артериальной гипертензии и классическихфакторов риска сердечно-сосудистых заболеваний (курения, гипер- и дислипидемии, избыточной массы тела, наследственности, сахарного диабета).Оценивали 10-летний коронарный риск по Фремингемской шкале и 10-летний риск фатальных сердечно-сосудистых событий по шкале SCORE. В качестве дополнительных факторов риска исследовали уровни С-реактивного белка, фибриногена, тромбоцитов в периферической крови, активность антитромбина III, суммарную фибринолитическую активность плазмы крови, активность фактора Виллебранда, уровень циркулирующих эндотелиальных клеток (ЦЭК), функциональное состояние эндотелия (при допплерографическом исследовании плечевой артерии в пробах с реактивной гиперемией и нитроглицерином). В группу контроля включили 30 практически здоровых человек, сопоставимых по возрасту и полу с основной группой.</p></sec><sec><title>Результаты</title><p>Результаты. (D)31(E)3Десятилетний коронарный риск, рассчитанный с учетом только классическихфакторов риска, у пациентов с анкилозирующим спондилитом составил 4,0% (3,0; 7,5), что существенно ниже соответствующего риска, рассчитанного для сопоставимой популяции без анкилозирующего спондилита – 5,0%(3,0; 11,0), p&lt;0,05. Десятилетний риск фатальных сердечно-сосудистых событий пошкале SCORE у обследованных пациентов составил 1,0%(1,0; 2,0), что может считаться низким уровнем. Однако при анализе дополнительных факторов риска у пациентов с анкилозирующим спондилитом выявлены изменения, указывающие на повышенный протромбогенный потенциал и связанные с активностью системного воспаления: высокие уровни тромбоцитов и фибриногена, повышенная активность фактора Виллебранда и сниженная фибринолитическая активность плазмы. Кроме того, при анкилозирующем спондилите обнаружены признаки повреждения (повышенные уровни ЦЭК и фактора Виллебранда) и дисфункции эндотелия.</p></sec><sec><title>Заключение</title><p>Заключение. Кардиоваскулярный риск у пациентов с анкилозирующим спондилитом, оцениваемый по классическим факторам риска, не превышает среднепопуляционный. В тоже время, у пациентов выявлено наличие признаков повреждения и дисфункции эндотелия и повышения протромбогенного потенциала, что непосредственно связано с активностью системного воспаления. Возможно, что именно эти факторы ответственны за высокий риск сердечно-сосудистых событий при анкилозирующем спондилите и, следовательно, должны учитываться при его оценке.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>анкилозирующий спондилит</kwd><kwd>кардиоваскулярный риск</kwd><kwd>системное воспаление</kwd><kwd>дисфункция эндотелия</kwd></kwd-group><kwd-group xml:lang="en"><kwd>ankylosing spondylitis</kwd><kwd>cardiovascular risk</kwd><kwd>systemic inflammation</kwd><kwd>endothelial dysfunction</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">del Rincon I.D., Williams K., Stern M.P. et al. 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