mvjrМедицинский вестник Юга РоссииMedical Herald of the South of Russia2219-80752618-7876The Rostov State Medical University10.21886/2219-8075-2025-16-2-75-82mvjr-2030Research Article3.1.18. ВНУТРЕННИЕ БОЛЕЗНИ3.1.18. INTERNAL DISEASESЭпикардиальная жировая ткань как предиктор неблагоприятного прогнозаEpicardial adipose tissue as a predictor of adverse prognosishttps://orcid.org/0009-0007-9944-7062МещеряковаА. С.MeshcheryakovaA. S.

Мещерякова Анастасия Сергеевна — студентка 3 курса лечебного факультета 

Ростов-на-Дону 

Anastasia S. Meshcheryakova — 3rd year student of the Faculty of Medicine 

Rostov-on-Don 

mesheryakova03@gmail.comhttps://orcid.org/0000-0001-7681-2900АлексееваН. С.AlekseevaN. S.

Алексеева Наталья Сергеевна — к.м.н., доцент кафедры нормальной физиологии 

Ростов-на-Дону 

Natalya S. Alekseeva — Cand. Sci. (Med.), Lecturer at the Department of Normal Physiology 

Rostov-on-Don 

NataAlexeeva@gmail.comhttps://orcid.org/0000-0002-2419-4319ХаишеваЛ. А.KhaishevaL. A.

Хаишева Лариса Анатольевна — д.м.н., заведующий кафедрой терапии 

Ростов-на-Дону 

Larisa A. Khaisheva — Dr. Sci. (Med.), Head of the Department of Therapy 

Rostov-on-Don 

katelnitskaya@mail.ruРостовский государственный медицинский университетРоссияRostov State Medical University Russian Federation2025020720251627582Copyright © Мещерякова А.С., Алексеева Н.С., Хаишева Л.А., 20252025Мещерякова А.С., Алексеева Н.С., Хаишева Л.А.Meshcheryakova A.S., Alekseeva N.S., Khaisheva L.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.medicalherald.ru/jour/article/view/2030

Сердечно-сосудистые заболевания (ССЗ) занимают лидирующую позицию среди причин смертности по всему миру. Ожирение, относящееся к метаболическим факторам риска ССЗ, является распространённой в мире и в России проблемой. Однако общепринятые критерии ожирения не могут в полной мере отразить риск возникновения ССЗ. Согласно современным представлениям, висцеральное ожирение является более чувствительным маркером ССЗ. Для определения висцерального ожирения предлагается использование толщины эпикардиальной жировой ткани (тЭЖТ). Растущий интерес к потенциальному влиянию эпикардиальной жировой ткани (ЭЖТ) на сердечно-сосудистый риск привёел к углубленному изучению её функций. Генетические, эпигенетические и экологические факторы могут способствовать сдвигу в сторону дисфункциональной ЭЖТ, характеризуясь провоспалительным и профибротическим фенотипом. Из-за близкой анатомической близости к коронарным артериям более толстая и дисфункциональная ЭЖТ активно способствует развитию и прогрессированию коронарного атеросклероза. Помимо классической паракринной передачи, ЭЖТ может напрямую выделять медиаторы в vasa vasorum стенки коронарной артерии, механизм, называемый «вазокринным». Аналогичным образом, провоспалительный и профиброзный секретом, характеризующий дисфункциональную ЭЖТ, может нарушать структуру и функцию сердца, таким образом участвуя в патогенезе большого количества сердечно-сосудистых заболеваний. Цель данного обзора — анализ данных о связи между эпикардиальной жировой тканью и сердечно-сосудистыми заболеваниями, возможность использования ЭЖТ как предиктора неблагоприятных сердечно-сосудистых событий.

Cardiovascular diseases (CVD) rank as the leading cause of mortality worldwide. Obesity, which is related to metabolic risk factors for CVD, is a common problem globally and in Russia. However, the generally accepted criteria for obesity cannot fully reflect the risk of developing CVD. According to modern concepts, visceral obesity is a more sensitive marker of CVD. The use of epicardial adipose tissue thickness (EAT thickness) is proposed for the determination of visceral obesity. In this regard, the presented review examines studies aimed at determining the threshold values of EAT thickness for more accurate risk prediction of CVD development. Growing interest in the potential influence of epicardial adipose tissue (EAT) on cardiovascular risk has led to an in-depth study of its functions. Genetic, epigenetic, and environmental factors may contribute to a shift toward dysfunctional EAT, characterized by a proinflammatory and profibrotic phenotype. Due to its close anatomical proximity to the coronary arteries, thicker and dysfunctional EAT actively contributes to the development and progression of coronary atherosclerosis. In addition to classical paracrine transmission, EAT can directly release mediators into the vasa vasorum of the coronary artery wall, a mechanism termed “vasocrine.” Similarly, the proinflammatory and profibrotic secretome that characterizes dysfunctional EAT can impair cardiac structure and function, thus contributing to the pathogenesis of a large number of cardiovascular diseases.

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The authors declare that there are no conflicts of interest present.