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Epicardial adipose tissue in contemporary cardiology
Open accessAbstract
Interest in epicardial adipose tissue (EAT) is growing rapidly, and research in this area appeals to a broad, multidisciplinary audience. EAT is unique in its anatomy and unobstructed proximity to the heart and has a transcriptome and secretome very different from that of other fat depots. EAT has physiological and pathological properties that vary depending on its location. It can be highly protective for the adjacent myocardium through dynamic brown fat-like thermogenic function and harmful via paracrine or vasocrine secretion of pro-inflammatory and profibrotic cytokines. EAT is a modifiable risk factor that can be assessed with traditional and novel imaging techniques. Coronary and left atrial EAT are involved in the pathogenesis of coronary artery disease and atrial fibrillation, respectively, and it also contributes to the development and progression of heart failure. In addition, EAT might have a role in coronavirus disease 2019 (COVID-19)-related cardiac syndrome. EAT is a reliable potential therapeutic target for drugs with cardiovascular benefits such as glucagon-like peptide 1 receptor agonists and sodium-glucose co-transporter 2 inhibitors. This Review provides a comprehensive and up-to-date overview of the role of EAT in cardiovascular disease and highlights the translational nature of EAT research and its applications in contemporary cardiology.
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“Perivascular and epicardial adipose tissue impose direct adverse effects on the vascular endothelium and myocardium. 30”
From Semaglutide and Cardiovascular Outcomes in Obesity without Diabetes (2023) · cites this paper as [30]
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“Visceral adiposity in particular has been causally implicated in adverse cardiovascular outcomes via the release of proinflammatory cytokines.6”
From Semaglutide and cardiovascular outcomes by baseline and changes in adiposity measurements: a prespecified analysis of the SELECT trial (2025) · cites this paper as [6]
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“Paracardiac adipose tissue has been hypothesized to act in a paracrine manner, with release of proinflammatory and profibrotic adipocytokines and excess free fatty acids with resultant intramyocardial lipid accumulation and myocardial inflammation and fibrosis.19”
From Tirzepatide Reduces LV Mass and Paracardiac Adipose Tissue in Obesity-Related Heart Failure (2025) · cites this paper as [19]
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Metadata
- Authors
- Iacobellis, G.
- Affiliations
- University of Miami (US)
- Corresponding author
- Iacobellis, Gianluca
- ORCID
- Iacobellis, Gianluca
- Venue
- Nature Reviews Cardiology
- Published
- 2022-03-16
- Volume
- 19
- Issue
- 9
- Pages
- 593-606
- ISSN
- 1759-5002 (ISSN-L)
- 1759-5010
- PMC
- PMC8926097
- OpenAlex
- W4220961850
- Cited by
- 797
- References
- 161
- Citations by year
- 2026: 195 · 2025: 236 · 2024: 214 · 2023: 118 · 2022: 32
- FWCI
- 31.35
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Nature Reviews Cardiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Cardiac Imaging and Diagnostics
- Keywords
- epicardial adipose tissue, coronary artery disease, atrial fibrillation, heart failure, brown fat thermogenesis, inflammatory cytokines, profibrotic cytokines, GLP-1 receptor agonists, SGLT2 inhibitors, cardiovascular risk factors
- MeSH terms
- COVID-19, Adipose Tissue, Atrial Fibrillation, Cardiology, Humans, Pericardium
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