Epidemiоlоgy and infectious diseases. Сurrent itemsEpidemiоlоgy and infectious diseases. Сurrent itemsЭпидемиология и инфекционные болезни. Актуальные вопросы2226-69762414-9640Bionika Media71630510.18565/epidem.2026.16.2.93-100Reviews and LecturesОбзоры и лекцииReview ArticleA modern pathogenetic concept for developing diagnostic criteria for cardiac injury in patients with past COVID-19 infectionСовременная патогенетическая концепция формирования диагностических критериев поражения сердца у пациентов с перенесенной инфекцией COVID-19https://orcid.org/0000-0001-5092-4744AgeikinAlexey V.АгейкинАлексей Викторович
Russian Federation

Cand. Med. Sci., Associate Professor, Department of Infectious Diseases, Medical Institute

к.м.н., доцент кафедры инфекционных болезней, Медицинский институт

ageykinav@yandex.ruhttps://orcid.org/0000-0001-9257-0171GorelovAlexander V.ГореловАлександр Васильевич
Russian Federation

Academician of the Russian Academy of Sciences, MD, Professor, Deputy Director for Research

академик РАН, д.м.н., профессор, заместитель директора по научной работе

agorelov_05@mail.ruhttps://orcid.org/0000-0001-5232-7337UsenkoDenis V.УсенкоДенис Валерьевич
Russian Federation

MD, Associate Professor, Department of Infectious Diseases, Medical Institute; Leading Researcher, Clinical Department of Infectious Pathology

д.м.н., доцент кафедры инфекционных болезней, Медицинский институт; ведущий научный сотрудник клинического отдела инфекционной патологии

dusenko@rambler.ruhttps://orcid.org/0000-0002-2933-5758RybalkinSergey B.РыбалкинСергей Борисович
Russian Federation

Honored Doctor of the Russian Federation, Cand. Med. Sci., Associate Professor, Department of Infectious Diseases, Medical Institute

заслуженный врач РФ, к.м.н., доцент кафедры инфекционных болезней, Медицинский институт

svmp@penzadom.ruhttps://orcid.org/0000-0001-7989-7647KurmaevaDzhamilya Yu.КурмаеваДжамиля Юсуповна
Russian Federation

Cand. Med. Sci., Associate Professor, Department of Infectious Diseases, Medical Institute

к.м.н., доцент кафедры инфекционных болезней, Медицинский институт

d.kurmaeva@yandex.ruhttps://orcid.org/0009-0004-2518-4034BogoninaVeronika E.БогонинаВероника Евгеньевна
Russian Federation

5th-year student, Faculty of Medicine, Pediatrics specialty, Medical Institute

студентка 5-го курса лечебного факультета по специальности «Педиатрия», Медицинский институт

bogoninaveronika@yandex.ruhttps://orcid.org/0009-0003-8919-7136DavydovaRamziya R.ДавыдоваРамзия Ряшитовна
Russian Federation

5th-year student, Faculty of Medicine, Pediatrics specialty, Medical Institute

студентка 5-го курса лечебного факультета по специальности «Педиатрия», Медицинский институт

davydova03rr@list.ruPenza State UniversityПензенский государственный университетCentral Research Institute of Epidemiology, Russian Federal Service for Supervision of Consumer Rights Protection and Human Well-BeingЦентральный НИИ эпидемиологии Роспотребнадзора10072026162931001007202610072026Copyright ©; 2026, Bionika MediaCopyright ©; 2026, ООО «Бионика Медиа»2026Bionika MediaООО «Бионика Медиа»https://journals.eco-vector.com/2226-6976/about/editorialPolicies#purchaseIssuehttps://journals.eco-vector.com/2226-6976/article/view/716305

The COVID-19 pandemic was accompanied not only by the development of acute respiratory pathology but also by an increase in the incidence of delayed cardiovascular complications, indicating the presence of complex pathogenetic interactions in the virus-host system. The multisystem nature of the disease, driven by several key mechanisms, has now been established. The first is related to the virus’s tropism for tissues expressing the angiotensin-converting enzyme 2 receptor, leading to an imbalance in the renin-angiotensin system (RAAS) with predominant proinflammatory, vasoconstrictor, and prothrombotic effects. The second is the ability of SARS-CoV-2, which has a tropism for cardiac tissue, to initiate a signaling cascade of cardiomyocyte necroptosis. The third mechanism is mediated by virus-induced hypomethylation of the promoter regions of genes encoding proinflammatory cytokines, which contributes to the development of chronic systemic inflammation and damage to the vascular endothelium.

Conclusion. To identify the leading pathogenetic mechanism, promptly predict the risk of cardiovascular complications, and determine patient management strategies, it is necessary to develop and implement a strategy for the qualitative and quantitative assessment of specific biological markers into clinical practice. Their implementation will reduce disability and mortality rates among individuals who have recovered from COVID-19.

Пандемия COVID-19 сопровождалась не только развитием острой респираторной патологии, но и ростом частоты отсроченных сердечно-сосудистых осложнений, что указывает на наличие сложных патогенетических взаимодействий в системе «вирус–хозяин». В настоящее время установлен мультисистемный характер поражения, обусловленный несколькими ключевыми механизмами. Первый связан с тропизмом вируса к тканям, экспрессирующим рецептор ангиотензинпревращающего фермента 2, что приводит к дисбалансу ренин-ангиотензин-альдостероновой системы с преобладанием провоспалительных, вазоконстрикторных и протромботических эффектов. Второй заключается в способности SARS-CoV-2, обладающего тропностью к сердечной ткани, инициировать сигнальный каскад некроптоза кардиомиоцитов. Третий механизм реализуется посредством вирус-индуцированного гипометилирования промоторных регионов генов, кодирующих провоспалительные цитокины, что способствует формированию хронического системного воспаления и повреждению сосудистого эндотелия.

Заключение. Для идентификации ведущего патогенетического механизма, своевременного прогнозирования риска сердечно-сосудистых осложнений и определения тактики ведения пациентов необходима разработка и внедрение в клиническую практику стратегии качественной и количественной оценки специфических биологических маркеров. Их реализация позволит снизить показатели инвалидизации и смертности среди лиц, перенесших COVID-19.

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