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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">mrj</journal-id><journal-title-group><journal-title xml:lang="ru">Современная ревматология</journal-title><trans-title-group xml:lang="en"><trans-title>Modern Rheumatology Journal</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1996-7012</issn><issn pub-type="epub">2310-158X</issn><publisher><publisher-name>IMA-PRESS, LLC</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14412/1996-7012-2025-6-35-41</article-id><article-id custom-type="elpub" pub-id-type="custom">mrj-1876</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>ОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ORIGINAL INVESTIGATIONS</subject></subj-group></article-categories><title-group><article-title>Взаимосвязь провоспалительных цитокинов с субклинической дисфункцией миокарда у больных ревматоидным артритом</article-title><trans-title-group xml:lang="en"><trans-title>Relationship between pro-inflammatory cytokines and subclinical myocardial dysfunction in patients with rheumatoid arthritis</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-1003-2087</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Кириллова</surname><given-names>И. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Kirillova</surname><given-names>I. G.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Ирина Геннадьевна Кириллова</p><p>115522, Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>Gennadievna Kirillova</p><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><email xlink:type="simple">dr.i.kirillova@yandex.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/0000-0002-8627-5341</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Потапова</surname><given-names>А. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Potapova</surname><given-names>A. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522, Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-2692-7942</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Семашко</surname><given-names>А. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Semashko</surname><given-names>A. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522, Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-0267-217X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Попкова</surname><given-names>Т. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Popkova</surname><given-names>T. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522, Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-6404-0042</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Диатроптов</surname><given-names>М. Е.</given-names></name><name name-style="western" xml:lang="en"><surname>Diatroptov</surname><given-names>M. E.</given-names></name></name-alternatives><bio xml:lang="ru"><p>115522, Москва, Каширское шоссе, 34А</p></bio><bio xml:lang="en"><p>34A, Kashirskoe Shosse, Moscow 115522</p></bio><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>V.A. Nasonova Research Institute of Rheumatology</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2025</year></pub-date><pub-date pub-type="epub"><day>22</day><month>12</month><year>2025</year></pub-date><volume>19</volume><issue>6</issue><fpage>35</fpage><lpage>41</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Кириллова И.Г., Потапова А.С., Семашко А.С., Попкова Т.В., Диатроптов М.Е., 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder xml:lang="ru">Кириллова И.Г., Потапова А.С., Семашко А.С., Попкова Т.В., Диатроптов М.Е.</copyright-holder><copyright-holder xml:lang="en">Kirillova I.G., Potapova A.S., Semashko A.S., Popkova T.V., Diatroptov M.E.</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://mrj.ima-press.net/mrj/article/view/1876">https://mrj.ima-press.net/mrj/article/view/1876</self-uri><abstract><p>Цель исследования – изучить взаимосвязь провоспалительных цитокинов, включая интерлейкин (ИЛ) 6, фактор некроза опухоли α (ФНОα), антагонист рецептора ИЛ1 (ИЛ1-Ра), c субклинической дисфункцией левого желудочка (ЛЖ) у больных ревматоидным артритом (РА).</p><sec><title>Материал и методы</title><p>Материал и методы. В исследование включен 61 больной РА, соответствовавший критериям ACR/EULAR 2010 г. В этой группе было 80% женщин, средний возраст – 47,8±10,1 года, медиана длительности заболевания до назначения генно-инженерных биологических препаратов – 120 [54; 165] мес. У всех больных определяли сывороточный уровень мозгового натрийуретического пептида (NT-proBNP), ИЛ6, ФНОα, ИЛ1-Ра, проводили эхокардиографию с оценкой глобальной продольной деформации (ГПД) ЛЖ с помощью методики спекл-трекинг.</p></sec><sec><title>Результаты и обсуждение</title><p>Результаты и обсуждение. У больных РА уровни ИЛ6 и ФНО были статистически значимо выше, чем в контроле. У больных РА с субклинической дисфункцией миокарда уровень ИЛ6 был значимо выше, чем у пациентов с сохраненной миокардиальной функцией (медиана –14,7 [0,76; 38,5] и 7,8 [0,11; 17,5] пг/мл соответственно; р&lt;0,05). Уровни ФНОα и ИЛ1-Ра в этих группах значимо не различались. Больные РА были разделены на четыре группы. В 1-ю группу включены пациенты с повышением уровня всех трех цитокинов (n=9), во 2-ю – двух (n=19) и в 3-ю – одного (n=23), в 4-й группе (n=10) содержание цитокинов было нормальным. Показатели СОЭ, DAS28 (Disease Activity Score 28) и СРБ в 1–3-й группах были выше, чем в 4-й. Все группы значимо различались по уровню фракции выброса (ФВ) и скорости движения латеральной части фиброзного кольца (Е’) ЛЖ. Показатель ГПД ЛЖ был значимо ниже в 1-й группе, чем в 4-й. Уровень ИЛ6 коррелировал с ГПД ЛЖ (r=-0,4); ИЛ1-Ра – с ФВ (r=-0,5), Е’ЛЖ (r=-0,4) и отношением максимальной скорости раннего диастолического трансмитрального потока (Е)/Е’ (r=0,3); ФНО – с Е’ЛЖ (r=0,3), р&lt;0,05 во всех случаях.</p></sec><sec><title>Заключение</title><p>Заключение. У больных РА с дисфункцией миокарда статистически значимо повышен уровень ИЛ6. Одновременное увеличение концентрации ИЛ6, ИЛ1-Ра и ФНО приводит к более выраженному ухудшению систолической и диастолической функции миокарда. Воспаление при РА способствует ухудшению миокардиальной функции сердца.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Objective</title><p>Objective: to investigate the association of pro-inflammatory cytokines, including interleukin (IL)-6, tumor necrosis factor α (TNFα), IL-1 receptor antagonist (IL-1Ra), with subclinical left ventricular (LV) dysfunction in patients with rheumatoid arthritis (RA).</p></sec><sec><title>Material and methods</title><p>Material and methods. The study included 61 patients with RA who met the 2010 ACR/EULAR (American College of Rheumatology / European Alliance of Associations for Rheumatology) criteria. In this group, 80% were women, mean age was 47.8±10.1 years, and the median disease duration before initiation of biologics was 120 [54; 165] months. All patients underwent determination of serum N-terminal pro-brain natriuretic peptide (NT-proBNP), IL-6, TNFα, IL-1Ra levels, and echocardiography with assessment of global longitudinal myocardial deformation (GLSLV) of the LV using speckle-tracking.</p></sec><sec><title>Results and discussion</title><p>Results and discussion. In patients with RA, IL-6 and TNFα levels were significantly higher than in controls. In RA patients with subclinical myocardial dysfunction, IL-6 levels were significantly higher than in patients with preserved myocardial function (median 14.7 [0.76; 38.5] and 7.8 [0.11; 17.5] pg/ml, respectively; p&lt;0.05). TNFα and IL-1Ra levels did not differ significantly between these groups. RA patients were divided into four groups. Group 1 included patients with elevation of all three cytokines (n=9), group 2 – of two cytokines (n=19), group 3 – of one cytokine (n=23), and group 4 (n=10) had normal cytokine levels. ESR, DAS28 (Disease Activity Score 28), and CRP levels in groups 1–3 were higher than in group 4. All groups differed significantly in ejection fraction (EF) and LV lateral mitral annular velocity (E’). GLSLV was significantly lower in group 1 than in group 4. IL-6 level correlated with GLSLV (r=-0.4); IL-1Ra level– with EF (r=-0.5), LV E’ (r=-0.4), and the ratio of early transmitral flow velocity (E)/E’ (r=0.3); TNFα level – with LV E’ (r=-0.3), p&lt;0.05 for all comparisons.</p></sec><sec><title>Conclusion</title><p>Conclusion. In RA patients with myocardial dysfunction, IL-6 levels are significantly elevated. Simultaneous elevation of IL-6, IL-1Ra, and TNFα leads to more pronounced impairment of systolic and diastolic myocardial function. Inflammation in RA contributes to the deterioration of cardiac myocardial function.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>ревматоидный артрит</kwd><kwd>цитокины</kwd><kwd>эхокардиография</kwd><kwd>спекл-трекинг</kwd><kwd>дисфункция миокарда</kwd></kwd-group><kwd-group xml:lang="en"><kwd>rheumatoid arthritis</kwd><kwd>cytokines</kwd><kwd>echocardiography</kwd><kwd>speckle-tracking</kwd><kwd>myocardial dysfunction</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Статья подготовлена в рамках государственного задания № 124061300101-9 «Персонифицированный подход к ранней диагностике хронической сердечной недостаточности при ревматических заболеваниях»</funding-statement><funding-statement xml:lang="en">The article was prepared within the framework of the state assignment № 124061300101-9 “Personalized approach to the early diagnosis of chronic heart failure in rheumatic diseases.”</funding-statement></funding-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Насонов ЕЛ, Каратеев ДЕ, Чичасова НВ. Новые рекомендации по лечению ревматоидного артрита (EULAR, 2013): место метотрексата. Научно-практическая ревматология. 2014;52(1):8-26.</mixed-citation><mixed-citation xml:lang="en">Nasonov EL, Karateev DE, Chichasova NV. New recommendations for the management of rheumatoid arthritis (EULAR, 2013): the role of methotrexate. Nauchno-prakticheskaya revmatologiya. 2014;52(1):8-26. (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Nicola PJ, Maradit-Kremers H, Roger VL, et al. The risk of congestive heart failure in rheumatoid arthritis: a population-based study over 46 years. Arthritis Rheum. 2005 Feb;52(2): 412-20. doi: 10.1002/art.20855.</mixed-citation><mixed-citation xml:lang="en">Nicola PJ, Maradit-Kremers H, Roger VL, et al. The risk of congestive heart failure in rheumatoid arthritis: a population-based study over 46 years. Arthritis Rheum. 2005 Feb;52(2): 412-20. doi: 10.1002/art.20855.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Myasoedova E, Crowson CS, Nicola PJ, et al. The influence of rheumatoid arthritis disease characteristics on heart failure. J Rheumatol. 2011 Aug;38(8):1601-6. doi: 10.3899/jrheum.100979.</mixed-citation><mixed-citation xml:lang="en">Myasoedova E, Crowson CS, Nicola PJ, et al. The influence of rheumatoid arthritis disease characteristics on heart failure. J Rheumatol. 2011 Aug;38(8):1601-6. doi: 10.3899/jrheum.100979.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Хроническая сердечная недостаточность. Клинические рекомендации 2024. Российский кардиологический журнал. 2024;29(11):6162.</mixed-citation><mixed-citation xml:lang="en">Chronic heart failure. Clinical guidelines 2024. Rossiiskii kardiologicheskii zhurnal. 2024;29(11):6162. (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Toldo S, Gallone G, Abbate A. Inhibitors of the Interleukin-1 Receptor Accessory Protein Signaling: Another Asset in the Cardio-Immunology Toolbox. Circ Heart Fail. 2024 Dec; 17(12):e012244. doi: 10.1161/CIRCHEARTFAILURE.124.012244.</mixed-citation><mixed-citation xml:lang="en">Toldo S, Gallone G, Abbate A. Inhibitors of the Interleukin-1 Receptor Accessory Protein Signaling: Another Asset in the Cardio-Immunology Toolbox. Circ Heart Fail. 2024 Dec; 17(12):e012244. doi: 10.1161/CIRCHEARTFAILURE.124.012244.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Васюк ЮА, Дударенко ОП, Ющук ЕН и др. «Цитокиновая» модель патогенеза хронической сердечной недостаточности и возможности нового терапевтического подхода в лечении декомпенсированных больных. Рациональная фармакотерапия в кардиологии. 2006;2(4):63-70.</mixed-citation><mixed-citation xml:lang="en">Vasuk UA, Dudarenko OP, Uschuk EN, et al. “Cytokine” model of pathogenesis of chronic heart failure and the opportunities of new therapeutic strategy in decompensated patients. Ratsional'naya farmakoterapiya v kardiologii. 2006;2(4):63-70. (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Park E, Griffin J, Bathon JM. Myocardial Dysfunction and Heart Failure in Rheumatoid Arthritis. Arthritis Rheumatol. 2022 Feb; 74(2):184-199. doi: 10.1002/art.41979.</mixed-citation><mixed-citation xml:lang="en">Park E, Griffin J, Bathon JM. Myocardial Dysfunction and Heart Failure in Rheumatoid Arthritis. Arthritis Rheumatol. 2022 Feb; 74(2):184-199. doi: 10.1002/art.41979.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification. Eur J Echocardiogr. 2006 Mar;7(2): 79-108. doi: 10.1016/j.euje.2005.12.014.</mixed-citation><mixed-citation xml:lang="en">Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification. Eur J Echocardiogr. 2006 Mar;7(2): 79-108. doi: 10.1016/j.euje.2005.12.014.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Nagueh SF, Smiseth OA, Appleton CP, et al. Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging. 2016 Dec;17(12):1321-1360. doi: 10.1093/ehjci/jew082.</mixed-citation><mixed-citation xml:lang="en">Nagueh SF, Smiseth OA, Appleton CP, et al. Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging. 2016 Dec;17(12):1321-1360. doi: 10.1093/ehjci/jew082.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Voigt JU, Pedrizzetti G, Lysyansky P, et al. Definitions for a common standard for 2D speckle tracking echocardiography: consensus document of the EACVI/ASE/Industry Task Force to standardize deformation imaging. Eur Heart J Cardiovasc Imaging. 2015 Jan; 16(1):1-11. doi: 10.1093/ehjci/jeu184.</mixed-citation><mixed-citation xml:lang="en">Voigt JU, Pedrizzetti G, Lysyansky P, et al. Definitions for a common standard for 2D speckle tracking echocardiography: consensus document of the EACVI/ASE/Industry Task Force to standardize deformation imaging. Eur Heart J Cardiovasc Imaging. 2015 Jan; 16(1):1-11. doi: 10.1093/ehjci/jeu184.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Лапкина НА, Баранов АА, Колинько АА и др. Провоспалительные цитокины при ревматоидном артрите: связь с активностью и субтипами заболевания. Русский медицинский журнал. 2024;(6):47-51.</mixed-citation><mixed-citation xml:lang="en">Lapkina NA, Baranov A, Kolinko AA, et al. Pro-inflammatory cytokines in rheumatoid arthritis: relationship with activity and subtypes of the disease. Russkii meditsinskii zhurnal. 2024;(6):47-51. (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Liang KP, Myasoedova E, Crowson CS, et al. Increased prevalence of diastolic dysfunction in rheumatoid arthritis. Ann Rheum Dis. 2010 Sep;69(9):1665-70. doi: 10.1136/ard.2009.124362.</mixed-citation><mixed-citation xml:lang="en">Liang KP, Myasoedova E, Crowson CS, et al. Increased prevalence of diastolic dysfunction in rheumatoid arthritis. Ann Rheum Dis. 2010 Sep;69(9):1665-70. doi: 10.1136/ard.2009.124362.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Su JH, Luo MY, Liang N, et al. Interleukin-6: A Novel Target for Cardio-Cerebrovascular Diseases. Front Pharmacol. 2021 Aug 24:12:745061. doi: 10.3389/fphar.2021.745061.</mixed-citation><mixed-citation xml:lang="en">Su JH, Luo MY, Liang N, et al. Interleukin-6: A Novel Target for Cardio-Cerebrovascular Diseases. Front Pharmacol. 2021 Aug 24:12:745061. doi: 10.3389/fphar.2021.745061.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Schofer N, Ludwig S, Rübsamen N, et al. Prognostic impact of Interleukin-1 receptor antagonist in patients with documented coronary artery disease. Int J Cardiol. 2018 Apr 15: 257:24-29. doi: 10.1016/j.ijcard.2018.01.055.</mixed-citation><mixed-citation xml:lang="en">Schofer N, Ludwig S, Rübsamen N, et al. Prognostic impact of Interleukin-1 receptor antagonist in patients with documented coronary artery disease. Int J Cardiol. 2018 Apr 15: 257:24-29. doi: 10.1016/j.ijcard.2018.01.055.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Herder C, de Las Heras Gala T, Carstensen-Kirberg M, et al. Circulating levels of interleukin 1-receptor antagonist and risk of cardiovascular disease: meta-analysis of six population-based cohorts. Arterioscler Thromb Vasc Biol. 2017 Jun;37(6):1222-1227. doi: 10.1161/ATVBAHA.117.309307.</mixed-citation><mixed-citation xml:lang="en">Herder C, de Las Heras Gala T, Carstensen-Kirberg M, et al. Circulating levels of interleukin 1-receptor antagonist and risk of cardiovascular disease: meta-analysis of six population-based cohorts. Arterioscler Thromb Vasc Biol. 2017 Jun;37(6):1222-1227. doi: 10.1161/ATVBAHA.117.309307.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Алиева АМ, Кисляков ВА, Воронкова КВ и др. Интерлейкин-1 — биологический маркер при сердечной недостаточности. Архивъ внутренней медицины. 2022;12(6): 422-429.</mixed-citation><mixed-citation xml:lang="en">Alieva AM, Kislyakov VA, Voronkova KV, et al. Interleukin-1 is a biological marker for heart failure. Arkhiv" vnutrennei meditsiny. 2022;12(6):422-429. (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Alieva AM, Kislyakov VA, Voronkova KV, et al. Interleukin-1 is a biological marker for heart failure. Arkhiv" vnutrennei meditsiny. 2022;12(6):422-429. (In Russ.).</mixed-citation><mixed-citation xml:lang="en">Ridker PM, Moorthy MV, Cook NR, et al. Inflammation, Cholesterol, Lipoprotein(a), and 30-Year Cardiovascular Outcomes in Women. N Engl J Med. 2024 Dec 5;391(22): 2087-2097. doi: 10.1056/NEJMoa2405182.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Ridker PM, Moorthy MV, Cook NR, et al. Inflammation, Cholesterol, Lipoprotein(a), and 30-Year Cardiovascular Outcomes in Women. N Engl J Med. 2024 Dec 5;391(22): 2087-2097. doi: 10.1056/NEJMoa2405182.</mixed-citation><mixed-citation xml:lang="en">Bahrami HSZ, Jшrgensen PG, Hove JD, et al. Association between interleukin-6, suPAR, and hsCRP with subclinical left ventricular dysfunction in type 1 diabetes: The Thousand &amp; 1 study. Diabetes Res Clin Pract. 2025 Apr:222:112071. doi: 10.1016/j.diabres. 2025.112071.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Bahrami HSZ, Jшrgensen PG, Hove JD, et al. Association between interleukin-6, suPAR, and hsCRP with subclinical left ventricular dysfunction in type 1 diabetes: The Thousand &amp; 1 study. Diabetes Res Clin Pract. 2025 Apr:222:112071. doi: 10.1016/j.diabres. 2025.112071.</mixed-citation><mixed-citation xml:lang="en">Kirillova IG, Novikova DS, Popkova TV, et al. The effect of antirheumatic therapy conducted in accordance with the principle of the "treat-to-target" strategy on diastolic dysfunction of the left and right ventricles in patients with early rheumatoid arthritis during 18 months of follow-up. Ratsional'naya Farmakoterapiya v Kardiologii. 2015;11(4):398-403. (In Russ.).</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Кириллова ИГ, Новикова ДС, Попкова ТВ и др. Влияние противоревматической терапии, проводимой в соответствии с принципом стратегии «treat-to-target», на диастолическую дисфункцию левого и правого желудочков у больных ранним ревматоидным артритом в течение 18 месяцев наблюдения. Рациональная Фармакотерапия в Кардиологии. 2015;11(4): 398-403.</mixed-citation><mixed-citation xml:lang="en">Venetsanopoulou AI, Pelechas E, Voulgari PV, et al. The lipid paradox in rheumatoid arthritis: the dark horse of the augmented cardiovascular risk. Rheumatol Int. 2020 Aug; 40(8):1181-1191. doi: 10.1007/s00296-020-04616-2.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Venetsanopoulou AI, Pelechas E, Voulgari PV, et al. The lipid paradox in rheumatoid arthritis: the dark horse of the augmented cardiovascular risk. Rheumatol Int. 2020 Aug; 40(8):1181-1191. doi: 10.1007/s00296-020-04616-2.</mixed-citation><mixed-citation xml:lang="en">Venetsanopoulou AI, Pelechas E, Voulgari PV, et al. The lipid paradox in rheumatoid arthritis: the dark horse of the augmented cardiovascular risk. Rheumatol Int. 2020 Aug; 40(8):1181-1191. doi: 10.1007/s00296-020-04616-2.</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>
