Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (786 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A fat deposit localized between the myocardium and the visceral layer of the serous pericardium. Epicardial adipose tissue is a risk factor for various cardiovascular diseases.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Adipose Tissue, Epicardial; Epicardial Adipose Tissues; Tissue, Epicardial Adipose; Epicardial Fat; Epicardial Fats; Fat, Epicardial; Epicardial Fat Tissue; Epicardial Fat Tissues.
Where it fits in the MeSH classification
- Broader topics
- Adipose Tissue
Related concepts
Research landscape
PubMed indexes 526 records tagged with the MeSH heading “Epicardial Adipose Tissue” (counts retrieved 2026-10-31). 526 of them (100.0%) were published from 2020 onward, and the busiest period so far is 2020 onward with 526 records.
Reviews account for 78 records (14.8%) and meta-analyses for 13. Randomized controlled trials number 14 (2.7%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 0 |
| 2010-2019 | 0 |
| 2020 onward | 526 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 78 | 14.8% |
| Meta-analyses | 13 | 2.5% |
| Randomized controlled trials | 14 | 2.7% |
Method: PubMed query "Epicardial Adipose Tissue"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Radiomics analysis of lesion-specific pericoronary adipose tissue to predict major adverse cardiovascular events in coronary artery disease | 2024 | Research article Design not recorded in structured metadata | 14 | cc by PMID 38886653 · DOI · PMC11184685 |
| Single-nucleus transcriptomics of epicardial adipose tissue from female pigs reveals effects of exercise training on resident innate and adaptive immune cells | 2024 | Research article Design not recorded in structured metadata | 13 | cc by PMID 38671495 · DOI · PMC11046969 |
| Epicardial and pericardial adipose tissue: anatomy, physiology, imaging, segmentation, and treatment effects | 2026 | Review article Design not recorded in structured metadata | 9 | cc by PMID 40971601 · DOI · PMC13623221 |
Radiomics analysis of lesion-specific pericoronary adipose tissue to predict major adverse cardiovascular events in coronary artery disease [1]
Abstract reading summary — source excerpts
- Opening excerpt
- ObjectiveTo investigate the prognostic performance of radiomics analysis of lesion-specific pericoronary adipose tissue (PCAT) for major adverse cardiovascular events (MACE) with the guidance of CT derived fractional flow reserve (CT-FFR) in coronary artery disease (CAD).
- Closing excerpt
- Combination of lesion-specific Rad-score and CT-FFR shows incremental value over traditional risk factors.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (193 words)
ObjectiveTo investigate the prognostic performance of radiomics analysis of lesion-specific pericoronary adipose tissue (PCAT) for major adverse cardiovascular events (MACE) with the guidance of CT derived fractional flow reserve (CT-FFR) in coronary artery disease (CAD).Materials and methodsThe study retrospectively analyzed 608 CAD patients who underwent coronary CT angiography. Lesion-specific PCAT was determined by the lowest CT-FFR value and 1691 radiomic features were extracted. MACE included cardiovascular death, nonfatal myocardial infarction, unplanned revascularization and hospitalization for unstable angina. Four models were generated, incorporating traditional risk factors (clinical model), radiomics score (Rad-score, radiomics model), traditional risk factors and Rad-score (clinical radiomics model) and all together (combined model). The model performances were evaluated and compared with Harrell concordance index (C-index), area under curve (AUC) of the receiver operator characteristic.ResultsLesion-specific Rad-score was associated with MACE (adjusted HR = 1.330, p = 0.009). The combined model yielded the highest C-index of 0.718, which was higher than clinical model (C-index = 0.639), radiomics model (C-index = 0.653) and clinical radiomics model (C-index = 0.698) (all p ConclusionRadiomics analysis of lesion-specific PCAT is useful in predicting MACE. Combination of lesion-specific Rad-score and CT-FFR shows incremental value over traditional risk factors.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38886653 · DOI · PMC11184685
Single-nucleus transcriptomics of epicardial adipose tissue from female pigs reveals effects of exercise training on resident innate and adaptive immune cells [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundCoronary artery disease (CAD) is a leading cause of death in women.
- Closing excerpt
- These findings lay the foundation for future work focused on the impact of exercise on cell types in EAT.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (427 words)
BackgroundCoronary artery disease (CAD) is a leading cause of death in women. Epicardial adipose tissue (EAT) secretes cytokines to modulate coronary artery function, and the release of fatty acids from EAT serves as a readily available energy source for cardiomyocytes. However, despite having beneficial functions, excessive amounts of EAT can cause the secretion of proinflammatory molecules that increase the instability of atherosclerotic plaques and contribute to CAD progression. Although exercise mitigates CAD, the mechanisms by which exercise impacts EAT are unknown. The Yucatan pig is an excellent translational model for the effects of exercise on cardiac function. Therefore, we sought to determine if chronic aerobic exercise promotes an anti-inflammatory microenvironment in EAT from female Yucatan pigs.MethodsSexually mature, female Yucatan pigs (n = 7 total) were assigned to sedentary (Sed, n = 3) or exercise (Ex, n = 4) treatments, and coronary arteries were occluded (O) with an ameroid to mimic CAD or remained non-occluded (N). EAT was collected for bulk (n = 7 total) and single nucleus transcriptomic sequencing (n = 2 total, 1 per exercise treatment).ResultsBased on the bulk transcriptomic analysis, exercise upregulated S100 family, G-protein coupled receptor, and CREB signaling in neurons canonical pathways in EAT. The top networks in EAT affected by exercise as measured by bulk RNA sequencing were SRC kinase family, fibroblast growth factor receptor, Jak-Stat, and vascular endothelial growth factor. Single nucleus transcriptomic analysis revealed that exercise increased the interaction between immune, endothelial, and mesenchymal cells in the insulin-like growth factor pathway and between endothelial and other cell types in the platelet endothelial cell adhesion molecule 1 pathway. Sub-clustering revealed nine cell types in EAT, with fibroblast and macrophage populations predominant in O-Ex EAT and T cell populations predominant in N-Ex EAT. Unlike the findings for exercise alone as a treatment, there were not increased interactions between endothelial and mesenchymal cells in O-Ex EAT. Coronary artery occlusion impacted the most genes in T cells and endothelial cells. Genes related to fatty acid metabolism were the most highly upregulated in non-immune cells from O-Ex EAT. Sub-clustering of endothelial cells revealed that N-Ex EAT separated from other treatments.ConclusionsAccording to bulk transcriptomics, exercise upregulated pathways and networks related to growth factors and immune cell communication. Based on single nucleus transcriptomics, aerobic exercise increased cell-to-cell interaction amongst immune, mesenchymal, and endothelial cells in female EAT. Yet, exercise was minimally effective at reversing alterations in gene expression in endothelial and mesenchymal cells in EAT surrounding occluded arteries. These findings lay the foundation for future work focused on the impact of exercise on cell types in EAT.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38671495 · DOI · PMC11046969
Epicardial and pericardial adipose tissue: anatomy, physiology, imaging, segmentation, and treatment effects [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Epicardial adipose tissue (EAT) and pericardial adipose tissue (PAT) are increasingly recognized as distinct fat depots with implications for cardiovascular disease.
- Closing excerpt
- Understanding and accurately quantifying EAT and PAT is essential for cardiovascular risk stratification and may open new pathways for therapeutic interventions.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (166 words)
Epicardial adipose tissue (EAT) and pericardial adipose tissue (PAT) are increasingly recognized as distinct fat depots with implications for cardiovascular disease. This review discusses their anatomical and physiological characteristics, as well as their pathophysiological roles. EAT, in direct contact with the myocardium, exerts local inflammatory and metabolic effects on the heart, while PAT influences cardiovascular health rather systemically. We sought to discuss the currently used imaging modalities to assess these fat compartments-CT, MRI, and echocardiography-emphasizing their advantages, limitations, and the urgent need for standardization for both scanning and image reconstruction. Advances in image segmentation, particularly deep learning-based approaches, have improved the accuracy and reproducibility of EAT and PAT quantification. This review also explores the role of EAT and PAT as risk factors for cardiovascular outcomes, summarizing conflicting evidence across studies. Finally, we summarize the effects of medical therapy and lifestyle interventions on reducing EAT volume. Understanding and accurately quantifying EAT and PAT is essential for cardiovascular risk stratification and may open new pathways for therapeutic interventions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40971601 · DOI · PMC13623221
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Epicardial fat and ventricular arrhythmias [4]
- Research article Epicardial Adipose Tissue as a Cardiometabolic Target in Atrial Fibrillation: Implications for Ablation Strategies and Emerging Metabolic Therapies [5]
- Research article Epicardial adipose tissue as a determinant of heart failure prognosis: insights across ejection fraction phenotypes [6]
- Research article SGLT2 inhibitors are associated with reductions in epicardial adipose tissue volume and thickness: a meta-analysis [7]
- Research article Aging epicardial adipose tissue: a metabolic-endocrine network driving vascular calcification [8]
- Research article Epicardial and Visceral Adipose Tissue and Global Longitudinal Strain: A Review of Cardiac Imaging Insights in Subclinical Myocardial Dysfunction [9]
References
- Chen M, Hao G, Xu J, Liu Y, Yu Y, Hu S, et al.. Radiomics analysis of lesion-specific pericoronary adipose tissue to predict major adverse cardiovascular events in coronary artery disease. . 2024. PMID 38886653 · DOI · PMC11184685
- Ahmad I, Gupta S, Faulkner P, Mullens D, Thomas M, Sytha SP, et al.. Single-nucleus transcriptomics of epicardial adipose tissue from female pigs reveals effects of exercise training on resident innate and adaptive immune cells. . 2024. PMID 38671495 · DOI · PMC11046969
- Demmert TT, Klambauer K, Moser LJ, Mergen V, Eberhard M, Alkadhi H. Epicardial and pericardial adipose tissue: anatomy, physiology, imaging, segmentation, and treatment effects. . 2026. PMID 40971601 · DOI · PMC13623221
- Załęska-Kocięcka M, Wojdyńska Z, Kalisz M, Litwiniuk A, Mączewski M, Leszek P, et al.. Epicardial fat and ventricular arrhythmias. Heart Rhythm. 2024. PMID 37972673 · DOI
- Cacciapuoti F. Epicardial Adipose Tissue as a Cardiometabolic Target in Atrial Fibrillation: Implications for Ablation Strategies and Emerging Metabolic Therapies. Med Sci (Basel). 2026. PMID 41892842 · DOI · PMC13027828
- Nowakowski M, Mazuruk M, Nogajski Ł, Mączewski M, Czerwińska H, Kurpias M, et al.. Epicardial adipose tissue as a determinant of heart failure prognosis: insights across ejection fraction phenotypes. Cardiovasc Diabetol. 2026. PMID 41803855 · DOI · PMC13020216
- Khanna S, Kalman E, Thungathurthi K, Thakur U, Vasanthakumar S, Virk S, et al.. SGLT2 inhibitors are associated with reductions in epicardial adipose tissue volume and thickness: a meta-analysis. Int J Obes (Lond). 2026. PMID 42191874 · DOI · PMC13391349
- Zhou L, Li J, Dong Z, Du X, Sun Y, Tong S. Aging epicardial adipose tissue: a metabolic-endocrine network driving vascular calcification. Front Endocrinol (Lausanne). 2026. PMID 42077457 · DOI · PMC13132759
- Vicardi M, Farzaneh-Far A, Fava C, Dalle Carbonare L, Romano S. Epicardial and Visceral Adipose Tissue and Global Longitudinal Strain: A Review of Cardiac Imaging Insights in Subclinical Myocardial Dysfunction. Nutrients. 2026. PMID 41901184 · DOI · PMC13029081
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.