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Role of epicardial adipose tissue in the pathogenesis of chronic inflammation in heart failure with preserved ejection fraction

https://doi.org/10.15829/1728-8800-2024-3928

EDN: DGYKKN

Abstract

According to the recent World Health Organization statistics, cardiovascular disease (CVD) is one of the leading causes of high mortality worldwide. While obesity is a major and persistent risk factor for CVD, the cause of this condition, the pathological molecular connection between peripheral fat depots and the heart, remains poorly understood. The aim of this review is to introduce the reader to the metabolic activity of epicardial adipose tissue (EAT), the consequences of excessive epicardial fat accumulation and the development of heart failure (HF).

EAT is visceral adipose tissue that is in direct contact with the myocardium and coronary vessels and can influence cardiac function through both mechanical effects and more subtle paracrine molecular mechanisms. HF with preserved ejection fraction (HFpEF) is closely associated with obesity and patterns in fat distribution. Excessive amounts of EAT are associated with abnormal hemodynamics in HFpEF, with the potential for direct mechanical effects on the heart causing a constriction-like effect and local myocardial remodeling effects resulting from the secretion of inflammatory mediators. However, patients with excess EAT tend to have more subcutaneous adipose tissue, making it difficult to determine a cause-and-effect relationship between epicardial fat and HFpEF. This review provides evidence that excess EAT is an important part of HFpEF pathogenesis.

About the Authors

O. N. Dzhioeva
National Medical Research Center for Therapy and Preventive Medicine
Russian Federation

Moscow



Yu. S. Timofeev
National Medical Research Center for Therapy and Preventive Medicine
Russian Federation

Moscow



V. A. Metelskaya
National Medical Research Center for Therapy and Preventive Medicine; Russian Medical Academy of Continuous Professional Education
Russian Federation

Moscow



A. A. Bogdanova
National Medical Research Center for Therapy and Preventive Medicine; I.M. Sechenov First Moscow State Medical University
Russian Federation

Moscow



T. Yu. Vedenikin
V.V. Veresaev City Clinical Hospital
Russian Federation

Moscow



O. M. Drapkina
National Medical Research Center for Therapy and Preventive Medicine
Russian Federation

Moscow



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Supplementary files

What is already known about the subject?

  • Obesity is a key risk factor for cardiovascular disease, but the pathogenesis of the relationship between adipose tissue (AT) and the heart remains poorly understood.
  • AT produces and secretes biologically active compounds into the bloodstream, which also affect the cardiovascular system.
  • Epicardial AT (EAT) is visceral AT that is in direct contact with the myocardium and has complex biological effects on the heart.

What might this study add?

  • EAT is a metabolically active tissue, the bio­chemical products of which enter the myocardium and cause its structural and functional change, which contributes to heart failure (HF) develop­ment.
  • EAT thickness ≥5 mm according to transthoracic echocardiography in a patient with HF with pre­served ejection fraction is a marker of an unfavo­rable disease course.
  • Excessive accumulation of EAT contributes to an imbalance in the secretion of adipokines and hypersecretion of activin A, pro-inflammatory cytoins and activation of the NLRP3 inflamasome, contributing to chronic inflammation, insulin resistance, fibrosis and other pathogenetic factors of HF.

Review

For citations:


Dzhioeva O.N., Timofeev Yu.S., Metelskaya V.A., Bogdanova A.A., Vedenikin T.Yu., Drapkina O.M. Role of epicardial adipose tissue in the pathogenesis of chronic inflammation in heart failure with preserved ejection fraction. Cardiovascular Therapy and Prevention. 2024;23(3):3928. (In Russ.) https://doi.org/10.15829/1728-8800-2024-3928. EDN: DGYKKN

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ISSN 1728-8800 (Print)
ISSN 2619-0125 (Online)