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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">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">10.15829/1728-8800-2022-3230</article-id><article-id custom-type="elpub" pub-id-type="custom">cardiovascular-3230</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>ХРОНИЧЕСКАЯ СЕРДЕЧНАЯ НЕДОСТАТОЧНОСТЬ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>CHRONIC HEART FAILURE</subject></subj-group></article-categories><title-group><article-title>Уровни маркеров ангиогенеза у пациентов с различными фенотипами хронической сердечной недостаточности</article-title><trans-title-group xml:lang="en"><trans-title>Levels of angiogenesis markers in patients with different heart failure phenotypes</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-8984-9056</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Шепель</surname><given-names>Р. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Shepel</surname><given-names>R. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Научный сотрудник отдела фундаментальных и  прикладных аспектов ожирения, заместительдиректора по перспективному развитию медицинской деятельности</p><p>Москва</p></bio><bio xml:lang="en"><p>Moscow</p></bio><email xlink:type="simple">r.n.shepel@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/0000-0002-4453-8430</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Драпкина</surname><given-names>О. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Drapkina</surname><given-names>O. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Директор, доктор медицинских наук, профессор, член-корреспондент РАН</p><p>Москва</p></bio><bio xml:lang="en"><p>Moscow</p></bio><email xlink:type="simple">cardiovasc.journal@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБУ «Национальный медицинский исследовательский центр терапии и профилактической медицины» Минздрава России</institution></aff><aff xml:lang="en"><institution>National Medical Research Center for Therapy and Preventive Medicine</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2022</year></pub-date><pub-date pub-type="epub"><day>06</day><month>03</month><year>2022</year></pub-date><volume>21</volume><issue>3</issue><fpage>3230</fpage><lpage>3230</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Шепель Р.Н., Драпкина О.М., 2022</copyright-statement><copyright-year>2022</copyright-year><copyright-holder xml:lang="ru">Шепель Р.Н., Драпкина О.М.</copyright-holder><copyright-holder xml:lang="en">Shepel R.N., Drapkina O.M.</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/3230">https://cardiovascular.elpub.ru/jour/article/view/3230</self-uri><abstract><sec><title>Цель</title><p>Цель. Оценить взаимосвязь между уровнями маркеров ангиогенеза и различными фенотипами хронической сердечной недостаточности (ХСН) у пациентов с ХСН ишемического генеза II-IV функционального класса (ФК).</p></sec><sec><title>Материал и методы</title><p>Материал и методы. Проведено одномоментное когортное исследование на базе клинических отделений стационара ФГБУ “НМИЦ ТПМ” Минздрава России. В исследовании приняли участие 180 пациентов в возрасте 30-85 лет с ХСН ишемического генеза II-IV ФК: 90 пациентов с  метаболическим синдромом и  90  — без метаболического синдрома. Пациенты были разделены на 3 группы: ХСН с низкой фракцией выброса (ХСНнФВ) — ФВ левого желудочка (ЛЖ) &lt;40%, ХСН с промежуточной ФВ ЛЖ (ХСНпФВ) — ФВ ЛЖ — 40-49%, ХСН с  сохраненной ФВ ЛЖ (ХСНсФВ)  — ФВ ЛЖ &gt;49%. Помимо стандартного инструментально-лабораторного исследования проведен анализ маркеров ангиогенеза с  определением уровней трансформирующего фактора роста β (TGF-β), сосудистого эндотелиального фактора роста А (VEGF-A), пентраксина-3 (PTX-3). Для выполнения статистического анализа использовались программные пакеты Microsoft Office Excel, STATISTICA 10.0 (Statsoft, USA).</p></sec><sec><title>Результаты</title><p>Результаты. При проведении трансторакальной эхокардиографии определено, что 74 (41,1%) пациента имели ФВ ЛЖ &lt;50%, у 71 (39,4%) пациента данный показатель оказался &lt;40%. Для группы пациентов с  ХСНсФВ отмечена ассоциация с  повышением TGF-β ≥7,2 нг/мл (p=0,011). Пороговый уровень РТХ-3 ≥55 нг/мл с  высокой степенью достоверности (p=0,001) ассоциирован с развитием ХСНсФВ. Для фенотипа ХСНпФВ определены пороговые значения VEGF-A, TGF-β и  PTX-3, которые не достигали уровня статистической значимости, однако отмечена четкая тенденция повышения VEGF-A &gt;200 нг/мл (p=0,052). Для пациентов с  низкой ФВ определено статистически значимое пороговое значение VEGF-A &gt;195 нг/мл (p=0,001), ассоциированное с низкой ФВ ЛЖ.</p></sec><sec><title>Заключение</title><p>Заключение. Настоящая работа показала актуальность использования PTX-3, VEGF-A и TGF-β в качестве дополнительных маркеров оценки течения ХСН: поскольку среди пациентов с  ХСНсФВ отмечено повышение уровней PTX-3 и  TGF-β, а  у  пациентов с  ХСНпФВ и ХСНнФВ — повышение уровня VEGF-A, целесообразно для улучшения эффективности диагностики и лечения пациентов с различными фенотипами ХСН ишемического генеза II-IV ФК проводить определение уровня этих маркеров ангиогенеза.</p></sec><sec><title> </title><p> </p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Aim</title><p>Aim. To assess the relationship between the levels of angiogenesis markers and various heart failure (HF) phenotypes in patients with class II-IV HF of ischemic origin.</p></sec><sec><title>Material and methods</title><p>Material and methods. This cross-sectional cohort study was based on the clinical departments of the National Medical Research Center for Therapy and Preventive Medicine. The study involved 180 patients aged 30-85 years with class II-IV HF of ischemic origin as follows with (n=90) and without (n=90) metabolic syndrome (MS). All patients included in the study signed an informed consent to personal data processing, participation in a clinical trial and consent to blood biobanking. All patients were divided into three groups: HF with reduced ejection fraction (HFrEF)  — left ventricular (LV) EF &lt;40%, HF with mildly reduced EF (HFmrEF) — LVEF from 40 to 49%, HF with preserved EF (HFpEF)  — LVEF &gt;49%. In addition to the standard paraclinical investigations, angiogenesis markers were analyzed with the determination of transforming growth factor β (TGF-β), vascular endothelial growth factor A (VEGF-A), pentraxin-3 (PTX-3). Statistical analysis was performed using Microsoft Office Excel, STATISTICA 10.0 software packages (Statsoft, USA).</p></sec><sec><title>Results</title><p>Results. Transthoracic echocardiography determined that 74 (41,1%) patients had LVEF &lt;50%, while 71 (39,4%)  — &lt;40%. For the group of patients with HFpEF, there was an association with an increase in TGF-β ≥7,2 ng/ml (p=0,011). The threshold level of PTX-3 ≥55 ng/ml is associated with the development of HFpEF (p=0,001). For the HFmrEF phenotype, the threshold values of VEGF-A, TGF-β and PTX-3 were determined, which did not reach the significance level. However, an upward trend in VEGF-A &gt;200 ng/ml was noted (p=0,052). In HFrEF patients, a threshold value of VEGF-A &gt;195 ng/ml (p=0,001) associated with reduced LVEF was determined.</p></sec><sec><title>Conclusion</title><p>Conclusion. Thus, the present work showed the relevance of using PTX-3, VEGF-A and TGF-β as additional markers for assessing the HF course. So, patients with HFpEF had increased levels of PTX-3 and TGF-β, while patients with HFmrEF and HFrEF  — increased VEGF-A values. Determination of the level of these angiogenesis markers should be used to improve the efficiency of diagnosis and treatment of patients with various class II-IV HF phenotypes.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>маркеры ангиогенеза</kwd><kwd>фенотипы</kwd><kwd>хроническая сердечная недостаточность</kwd></kwd-group><kwd-group xml:lang="en"><kwd>angiogenesis markers</kwd><kwd>phenotypes</kwd><kwd>heart failure</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">Фомин И.В. Хроническая сердечная недостаточность в Российской Федерации: что сегодня мы знаем и что должны делать. Российский кардиологический журнал. 2016;(8):7-13. doi:10.15829/1560-4071-2016-8-7-13.</mixed-citation><mixed-citation xml:lang="en">Fomin IV. Chronic heart failure in Russian Federation: what do we know and what to do. Russian Journal of Cardiology. 2016;(8):7- 13. 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