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<article 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" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="research-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Perm Medical Journal</journal-id><journal-title-group><journal-title xml:lang="en">Perm Medical Journal</journal-title><trans-title-group xml:lang="ru"><trans-title>Пермский медицинский журнал (сетевое издание "Perm medical journal")</trans-title></trans-title-group></journal-title-group><issn publication-format="print">0136-1449</issn><issn publication-format="electronic">2687-1408</issn><publisher><publisher-name xml:lang="en">Eco-Vector</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">703659</article-id><article-id pub-id-type="doi">10.17816/pmj43187-102</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Original studies</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Оригинальные исследования</subject></subj-group><subj-group subj-group-type="article-type"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Predictors of atrial fibrillation in patients with ST-segment elevation myocardial infarction</article-title><trans-title-group xml:lang="ru"><trans-title>Предикторы развития фибрилляции предсердий у больных инфарктом миокарда с подъемом сегмента ST</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0009-0007-5352-0666</contrib-id><name-alternatives><name xml:lang="en"><surname>Safarov</surname><given-names>E. N.</given-names></name><name xml:lang="ru"><surname>Сафаров</surname><given-names>Э. Н.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="ru"><p>аспирант кафедры внутренних болезней и кардиологии</p></bio><email>nakoziolova@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-7003-5186</contrib-id><name-alternatives><name xml:lang="en"><surname>Koziolova</surname><given-names>N. A.</given-names></name><name xml:lang="ru"><surname>Козиолова</surname><given-names>Н. А.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="ru"><p>доктор медицинских наук, профессор, заведующая кафедрой внутренних болезней и кардиологии</p></bio><email>nakoziolova@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-3694-3647</contrib-id><name-alternatives><name xml:lang="en"><surname>Polyanskaya</surname><given-names>E. A.</given-names></name><name xml:lang="ru"><surname>Полянская</surname><given-names>Е. А.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="ru"><p>доктор медицинских наук, профессор кафедры внутренних болезней и кардиологии</p></bio><email>nakoziolova@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid">https://orcid.org/0009-0000-4834-2905</contrib-id><name-alternatives><name xml:lang="en"><surname>Koryagin</surname><given-names>V. S.</given-names></name><name xml:lang="ru"><surname>Корягин</surname><given-names>В. С.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><bio xml:lang="ru"><p>ординатор кафедры внутренних болезней и кардиологии</p></bio><email>nakoziolova@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Ye.A. Vagner Perm State Medical University</institution></aff><aff><institution xml:lang="ru">Пермский государственный медицинский университет имени академика Е.А. Вагнера</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2026-03-03" publication-format="electronic"><day>03</day><month>03</month><year>2026</year></pub-date><volume>43</volume><issue>1</issue><issue-title xml:lang="en"/><issue-title xml:lang="ru"/><fpage>87</fpage><lpage>102</lpage><history><date date-type="received" iso-8601-date="2026-03-02"><day>02</day><month>03</month><year>2026</year></date><date date-type="accepted" iso-8601-date="2026-03-02"><day>02</day><month>03</month><year>2026</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2026, Eco-Vector</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2026, Эко-Вектор</copyright-statement><copyright-year>2026</copyright-year><copyright-holder xml:lang="en">Eco-Vector</copyright-holder><copyright-holder xml:lang="ru">Эко-Вектор</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://eco-vector.com/for_authors.php#07</ali:license_ref></license></permissions><self-uri xlink:href="https://permmedjournal.ru/PMJ/article/view/703659">https://permmedjournal.ru/PMJ/article/view/703659</self-uri><abstract xml:lang="en"><p><bold>Objective.</bold><bold> </bold>To determine the predictors of atrial fibrillation (AF) development in patients with ST-segment elevation myocardial infarction (STEMI).</p> <p><bold>Materials</bold><bold> and methods. </bold>The study presents the results of the first (in-hospital) stage of a prospective, two-stage, open-label, observational clinical trial with a retrospective assessment of the patient data prior to their enrollment in the study. Over a 2-year period, 167 patients with STEMI were sequentially included into the study on admission to a multidisciplinary hospital according to the inclusion and exclusion criteria. To determine the predictors of AF development in STEMI patients, they were divided into 2 groups: Group 1 comprised 140 patients (83.8 %) with STEMI and no AF during hospitalization or in their medical history; Group 2 included 27 patients (16.2 %) with STEMI who experienced an AF paroxysm during hospitalization.</p> <p><bold>Results.</bold><bold> </bold>The prevalence of AF among 167 hospitalized patients with STEMI was 16.2 % (<italic>n</italic>=27). In 9.6 % of cases, AF paroxysm was verified for the first time, while in 6.8 % it was a manifestation of a pre-existing paroxysmal form. Systolic blood pressure BP &lt; 90 mmHg, heart rate &lt; 50 bpm and &gt;110 bpm, and Killip class &gt;1 increased the relative risk (RR) of AF paroxysm in MI patients by 2.3-fold, 6.1-fold, and 3.0-fold, respectively. Comorbid conditions such as obesity, chronic heart failure, and a history of pulmonary pathology increased the RR of AF by 2.6-fold, 2.3-fold, and 2.2-fold, respectively. Pre-admission use of renin-angiotensin-aldosterone system (RAAS) blockers and beta-blockers reduced the RR of AF development by 71 %, whereas the need for insulin therapy increased by 3.1-fold. In addition to the well-known predictors of AF development in MI associated with cardiac and renal remodeling, new ones were identified: left atrial contractile dysfunction index &lt; 40 %; left ventricular ejection fraction (LVEF)-to-indexed left atrial volume ratio &lt; 1.1; cystatin-based glomerular filtration rate &lt; 45 ml/min/1.73 m<sup>2</sup>; urinary albumin-to-creatinine ratio &gt; 300 mg/g; and creatinine-to-LVEF ratio. These increased the RR by 7.1-fold, 6.7-fold, 2.7-fold, 3.1-fold, and 2.7-fold, respectively. Among the new biomarkers associated with AF development in MI, the following were identified: blood apolipoprotein B100 (ApoB100) concentration &gt; 100 mg/dL; monocytes-to-high-density lipoprotein cholesterol ratio &gt; 26.5; tissue inhibitor of matrix metalloproteinase type 1 (TIMP-1) &gt; 124.2 ng/ml; platelet-to-lymphocyte ratio &gt; 212.1; inflammatory burden index &gt;36.85; the combination of the GG genotype of the ApoB gene polymorphism Arg3500Gln (rs5742904) with the ID genotype of the fibrinogen alpha (FGA) gene polymorphism rs35496957. These increased the RR by 3.5-fold, 2.8-fold, 5.6-fold, 2.5-fold, 3.3-fold, and 3.6-fold, respectively.</p> <p><bold>Conclusions.</bold><bold> </bold>The study confirmed the clinical and historical predictors of AF paroxysm development in patients with STEMI and identified novel predictors associated with coupled structural and functional remodeling of the left and right ventricles, in combination with renal dysfunction, lipid metabolism disorders involving the apolipoprotein system, tissue fibrosis due to increased TIMP-1 levels, activation of nonspecific inflammation, anemia and pathological polymorphism of the ApoB100 and FGA genes.</p></abstract><trans-abstract xml:lang="ru"><p><bold>Цель. </bold>Определить предикторы развития фибрилляции предсердий (ФП) у больных инфарктом миокарда (ИМ) с подъемом сегмента ST.</p> <p><bold>Материалы и методы.</bold> Представлены результаты первого этапа (госпитального) проспективного двухэтапного открытого наблюдательного клинического исследования с ретроспективной оценкой данных больных до включения их в настоящее исследование. В исследование в течение 2 лет при поступлении в многопрофильный стационар последовательно включено 167 больных с ИМ с подъемом сегмента ST в соответствии с критериями включения и невключения. Для определения предикторов развития ФП больных ИМ с подъемом сегмента ST разделили на две группы: в первую группу включили 140 пациентов (83,8 %) с ИМ с подъемом сегмента ST без ФП во время госпитализации и в анамнезе, во вторую группу – 27 человек (16,2 %) с ИМ с подъемом сегмента ST и пароксизмом ФП во время госпитализации.</p> <p><bold>Результаты.</bold> Распространенность возникновения ФП среди 167 госпитализированных с ИМ с подъемом сегмента ST составила 16,2 % (<italic>n</italic> = 27), у 9,6 % пароксизм ФП верифицирован впервые, у 6,8 % – эпизод аритмии был проявлением пароксизмальной формы, существовавшей ранее. Систолическое АД &lt; 90 мм рт. ст., частота сердечных сокращений ниже 50 и более 110 в минуту, Killip &gt; I степени увеличивали относительный риск (ОР) возникновения пароксизма ФП у больных ИМ в 2,3; 6,1 и 3,0 раза соответственно. Коморбидная патология, такая как ожирение, хроническая сердечная недостаточность, патология легких, в анамнезе увеличивала ОР развития ФП в 2,6; 2,3 и 2,2 раза соответственно. Догоспитальный прием блокаторов ренинангиотензинальдостероновой системы и бета-адреноблокаторов снижал ОР развития ФП на 71 %, а потребность в инсулинотерапии – увеличивала в 3,1 раза. Кроме известных предикторов развития ФП при ИМ, связанных с ремоделированием сердца и почек, найдены новые, такие как индекс нарушения сократительной функции левого предсердия &lt; 40 %, соотношение фракции выброса левого желудочка (ФВ ЛЖ) к индексированному объему левого предсердия &lt; 1,1, скорость клубочковой фильтрации, рассчитанная по цистатину, &lt; 45 мл/мин/1,73м<sup>2</sup>, соотношение «альбумин/креатинин мочи» &gt; 300 мг/г, соотношение «креатинин/ФВ ЛЖ», которые увеличивали ОР в 7,1; 6,7; 2,7; 3,1; 2,7 раза соответственно. Среди новых биомаркеров, которые взаимосвязаны с развитием ФП при ИМ, выявлены такие, как концентрация аполипопротеина B100 (ApoB100) в крови &gt; 100 мг/дл, соотношение моноцитов к холестерину липопротеидов высокой плотности &gt; 26,5, тканевый ингибитор матриксных металлопротеиназ 1-го типа (TIMP-1) &gt; 124,2 нг/мл, соотношение тромбоцитов к лимфоцитам &gt; 212,1, воспалительный индекс бремени &gt; 36,85, комбинация генотипа GG полиморфизма Arg3500Gln вариант rs5742904 гена ApoB+генотипа ID полиморфизма rs35496957 гена фибриногена альфа (FGA), которые увеличивали ОР в 3,5; 2,8; 5,6; 2,5; 3,3; 3,6 раза соответственно.</p> <p><bold>Выводы. </bold>В исследовании подтверждены клинико-анамнестические предикторы развития пароксизма ФП у больных ИМ с подъемом сегмента ST и выявлены новые, связанные со структурно-функциональной сопряженной перестройкой левого и правого желудочков в сочетании с ренальной дисфункцией, нарушениями липидного метаболизма в системе аполипопротеинов, формированием фиброза в тканях за счет увеличения TIMP-1, активацией неспецифического воспаления, анемией и патологическим полиморфизмом генов ApoB100 и FGA.</p></trans-abstract><kwd-group xml:lang="en"><kwd>myocardial infarction</kwd><kwd>predictors of atrial fibrillation</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>инфаркт миокарда</kwd><kwd>предикторы фибрилляции предсердий</kwd></kwd-group><funding-group/></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Kodani E. 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