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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">10.20996/1819-6446-2024-3037</article-id><article-id custom-type="edn" pub-id-type="custom">OPRKXD</article-id><article-id custom-type="elpub" pub-id-type="custom">rpcardio-3037</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>ORIGINAL STUDIES</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯ</subject></subj-group></article-categories><title-group><article-title>Platelet reactivity clinical and biochemical markers when taking acetylsalicylic acid as part of dual antiplatelet therapy in the myocardial infarction subacute period</article-title><trans-title-group xml:lang="ru"><trans-title>Клинико-биохимические маркеры реактивности тромбоцитов при приеме ацетилсалициловой кислоты (в составе двойной антитромбоцитарной терапии) в подострый период инфаркта миокарда</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-2126-5246</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Пронько</surname><given-names>Т. П.</given-names></name><name name-style="western" xml:lang="en"><surname>Pronko</surname><given-names>T. P.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Пронько Татьяна Павловна</p><p>Гродно</p></bio><bio xml:lang="en"><p>Tatyana P. Pronko</p><p>Grodno </p></bio><email xlink:type="simple">tanya_pronko@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/0000-0002-1706-1243</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Снежицкий</surname><given-names>В. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Snezhitskiy</surname><given-names>V. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Снежицкий Виктор Александрович</p><p>Гродно</p></bio><bio xml:lang="en"><p>Viktor A. Snezhitskiy</p><p>Grodno </p></bio><email xlink:type="simple">vsnezh@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/0000-0002-1862-4300</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Копыцкий</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Kapytski</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Копыцкий Андрей Витальевич</p><p>Гродно</p></bio><bio xml:lang="en"><p>Andrei V. Kapytski</p><p>Grodno </p></bio><email xlink:type="simple">andrey_cop@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Гродненский государственный медицинский университет</institution><country>Беларусь</country></aff><aff xml:lang="en"><institution>Grodno State Medical University</institution><country>Belarus</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2024</year></pub-date><pub-date pub-type="epub"><day>28</day><month>11</month><year>2024</year></pub-date><volume>20</volume><issue>6</issue><fpage>618</fpage><lpage>624</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Pronko T.P., Snezhitskiy V.A., Kapytski A.V., 2025</copyright-statement><copyright-year>2025</copyright-year><copyright-holder xml:lang="ru">Пронько Т.П., Снежицкий В.А., Копыцкий А.В.</copyright-holder><copyright-holder xml:lang="en">Pronko T.P., Snezhitskiy V.A., Kapytski A.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.rpcardio.online/jour/article/view/3037">https://www.rpcardio.online/jour/article/view/3037</self-uri><abstract><sec><title>Aim</title><p>Aim. To study markers that determine residual platelet reactivity in the subacute period of myocardial infarction (MI) during the administration of acetylsalicylic acid (ASA) as part of dual antiplatelet therapy.</p></sec><sec><title>Material and methods</title><p>Material and methods. 405 patients with MI (79.5% men and 20.5% women, average age 58.0 years) were divided into groups based on aggregometry results. Group 1 — 11 patients with low residual platelet reactivity, group 2 — 236 patients with optimal platelet reactivity, group 3 — 158 patients with high residual platelet reactivity (HRPR). All studies were performed on days 12-14 after MI: aggregometry on a Multiplate aggregometer (Germany) with several aggregation inducers, a blood test and a study of platelet indices, determination of endothelin-1, von Willebrand factor, sP-selectin and soluble CD40 ligand levels.</p></sec><sec><title>Results</title><p>Results. Parameters influencing the ASPItest value according to univariate linear regression analysis: body mass index (β=0.53, 95% CI: 0.11-0.96; p=0.013); waist circumference (β=0.31, 95% CI: 0.14-0.49; p=0.0004); erythrocyte sedimentation rate (β=0.27, 95% CI: 0.12-0.42; p=0.0004); white blood cells count (β=1.47, 95% CI: 0.51-2.42; p=0.0027); platelets count (β=0.042, 95% CI: 0.019-0.064; p=0.00025); thrombocrit (β=36.8, 95% CI: 14.6-59.1; p=0.0012); mean platelet volume (β=1.94, 95% CI: 0.06-3.84; p=0.043); platelet distribution width (β=1.36, 95% CI: 0.22-2.51; p=0.02); creatinine (β=0.11, 95% CI: 0.011-0.21; p=0.03); C-reactive protein (β=0.18, 95% CI: 0.05-0.32; p=0.007); TRAP-test (β=0.18, 95% CI: 0.11-0.24; p=0.000001); fibrinogen (β=2.6, 95% CI: 1.17-4.02; p=0.0004). The binary logistic regression model to calculate the probability of developing HRPR to ASA included the following factors: platelet count, percentage of large platelet volume (PLCR), fibrinogen, endothelin-1 and von Willebrand factor. With a probability cutoff p₀=0.5412 for this model: sensitivity — 81.08%, specificity — 73.21%, classification accuracy — 76.34%, area under the ROC curve — 0.79 (CI: 0.696 - 0.883).</p></sec><sec><title>Conclusion</title><p>Conclusion. There are 2.7% of patients with an excessive response to ASA and 39.0% with an insufficient response to ASA on days 12-14 of MI. Clinical and biochemical markers of HRPR to ASA in the subacute period of MI are the number of platelets, PLCR, fibrinogen, endothelin-1 and von Willebrand factor.</p></sec></abstract><trans-abstract xml:lang="ru"><sec><title>Цель</title><p>Цель. Исследовать маркеры, определяющие резидуальную тромбоцитарную активность в подострый период инфаркта миокарда (ИМ) при приеме ацетилсалициловой кислоты (АСК) в составе двойной антитромбоцитарной терапии.</p></sec><sec><title>Материал и методы</title><p>Материал и методы. По результатам агрегометрии 405 пациентов с ИМ (79,5% мужчин и 20,5% женщин, средний возраст — 58,0 лет) были разделены на группы: 11 пациентов с низкой резидуальной тромбоцитарной активностью (группа 1), 236 пациентов с оптимальной тромбоцитарной активностью (группа 2) и 158 пациентов с высокой резидуальной тромбоцитарной активностью (ВРТА, группа 3). Все исследования выполнялись на 12-14 сутки ИМ: агрегометрия на агрегометре Multiplate (Германия) с несколькими индукторами агрегации, общий анализ крови и исследование тромбоцитарных индексов, определение содержания эндотелина-1, фактора Виллебранда, sP-селектина и растворимого лиганда CD40.</p></sec><sec><title>Результаты</title><p>Результаты. Параметры, влияющие на значение ASPItest по данным однофакторного линейного регрессионного анализа: индекс массы тела (β=0,53, 95% ДИ 0,11-0,96; р=0,013); окружность талии (β=0,31, 95% ДИ 0,14-0,49; р=0,0004); скорость оседания эритроцитов (β=0,27, 95% ДИ 0,12-0,42; р=0,0004); количество лейкоцитов (β=1,47, 95% ДИ 0,51-2,42; р=0,0027); количество тромбоцитов (β=0,042, 95% ДИ 0,019-0,064; р=0,00025); тромбокрит (β=36,8, 95% ДИ 14,6-59,1; р=0,0012); средний объем тромбоцитов (β=1,94, 95% ДИ 0,06-3,84; р=0,043); ширина распределения тромбоцитов (β=1,36, 95% ДИ 0,22-2,51; р=0,02); креатинин (β=0,11, 95% ДИ 0,011-0,21; р=0,03); С-реактивный белок (β=0,18, 95% ДИ 0,05-0,32; р=0,007); TRAP-test (β=0,18, 95% ДИ 0,11-0,24; р=0,000001); фибриноген (β=2,6, 95% ДИ 1,17-4,02; р=0,0004). В модель бинарной логистической регрессии для расчета вероятности развития ВРТА к АСК вошли следующие факторы: количество тромбоцитов, процент объема больших тромбоцитов, содержание фибриногена, эндотелина-1 и фактора Виллебранда. При пороге отсечения по вероятности p₀=0,5412 для данной модели: чувствительность — 81,08%, специфичность — 73,21%, точность классификации — 76,34%, площадь под ROC-кривой — 0,79 (ДИ 0,696-0,883).</p></sec><sec><title>Заключение</title><p>Заключение. На 12-14 сутки ИМ чрезмерный ответ на АСК выявлен у 2,7% пациентов; недостаточный ответ на АСК — у 39,0%. Клинико-биохимическими маркерами ВРТА к АСК в подострый период ИМ являются количество тромбоцитов, процент объема больших тромбоцитов, содержание фибриногена, эндотелина-1 и фактора Виллебранда.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>инфаркт миокарда</kwd><kwd>подострый период</kwd><kwd>ацетилсалициловая кислота</kwd><kwd>двойная антитромбоцитарная терапия</kwd><kwd>высокая и низкая резидуальная тромбоцитарная активность</kwd><kwd>агрегометрия</kwd><kwd>тромбоциты</kwd><kwd>тромбоцитарные индексы</kwd></kwd-group><kwd-group xml:lang="en"><kwd>myocardial infarction</kwd><kwd>subacute period</kwd><kwd>acetylsalicylic acid</kwd><kwd>dual antiplatelet therapy</kwd><kwd>high and low residual platelet reactivity</kwd><kwd>aggregometry</kwd><kwd>platelets</kwd><kwd>platelet indices</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Работа выполнена при поддержке Гродненского государственного медицинского университета и ГНТП "Новые методы оказания медицинской помощи 2016-2020 годы", подпрограмма "Болезни системы кровообращения", договор 02.11/2017.</funding-statement><funding-statement xml:lang="en">The study was supported by the Grodno State Medical University, SSTP "New methods of providing medical care 2016-2020", subprogram "Diseases of the circulatory system", agreement 02.11/2017.</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">Салухов В. 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