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: 4 complete abstracts (813 words), 10 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 conical fibro-serous sac surrounding the heart and the roots of the great vessels (aorta; venae cavae; pulmonary artery). Pericardium consists of two sacs: the outer fibrous pericardium and the inner serous pericardium. The latter consists of an outer parietal layer facing the fibrous pericardium, and an inner visceral layer (epicardium) resting next to the heart, and a pericardial cavity between these two layers.
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: Visceral Pericardium; Pericardium, Visceral; Epicardium; Fibrous Pericardium; Pericardium, Fibrous; Pericardiums, Fibrous; Parietal Pericardium; Pericardium, Parietal.
Where it fits in the MeSH classification
- Broader topics
- Heart; Serous Membrane
- Narrower topics
- Pericardial Fluid
- See also
- Pericardiectomy
Related concepts
- Heart
- Aorta
- Venae Cavae
- Pulmonary Artery
Research landscape
PubMed indexes 18,279 records tagged with the MeSH heading “Pericardium” (counts retrieved 2026-10-31). 2,632 of them (14.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 7,388 records.
Reviews account for 1,305 records (7.1%) and meta-analyses for 64. Randomized controlled trials number 148 (0.8%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 7,388 |
| 2000-2009 | 3,202 |
| 2010-2019 | 5,057 |
| 2020 onward | 2,632 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,305 | 7.1% |
| Meta-analyses | 64 | 0.4% |
| Randomized controlled trials | 148 | 0.8% |
Method: PubMed query "Pericardium"[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 |
|---|---|---|---|---|
| Epicardioid single-cell genomics uncovers principles of human epicardium biology in heart development and disease | 2023 | Research article Design not recorded in structured metadata | 85 | cc by PMID 37012447 · DOI · PMC10713454 |
| Effect of SGLT2-Inhibitors on Epicardial Adipose Tissue: A Meta-Analysis | 2021 | Meta-analysis Design not recorded in structured metadata | 83 | cc by PMID 34440918 · DOI · PMC8391573 |
| Regenerative potential of epicardium-derived extracellular vesicles mediated by conserved miRNA transfer | 2022 | Research article Design not recorded in structured metadata | 70 | cc by PMID 33599250 · DOI · PMC8803084 |
| A Computational Journey Toward an Optimal Design for Metamaterial Epicardial Passive Sleeves | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 41131867 · DOI · PMC12836452 |
Epicardioid single-cell genomics uncovers principles of human epicardium biology in heart development and disease [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The epicardium, the mesothelial envelope of the vertebrate heart, is the source of multiple cardiac cell lineages during embryonic development and provides signals that are essential to myocardial growth and repair.
- Closing excerpt
- As such, epicardioids offer a unique testing ground of epicardial activity in heart development, disease and regeneration.
- 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 (157 words)
The epicardium, the mesothelial envelope of the vertebrate heart, is the source of multiple cardiac cell lineages during embryonic development and provides signals that are essential to myocardial growth and repair. Here we generate self-organizing human pluripotent stem cell-derived epicardioids that display retinoic acid-dependent morphological, molecular and functional patterning of the epicardium and myocardium typical of the left ventricular wall. By combining lineage tracing, single-cell transcriptomics and chromatin accessibility profiling, we describe the specification and differentiation process of different cell lineages in epicardioids and draw comparisons to human fetal development at the transcriptional and morphological levels. We then use epicardioids to investigate the functional cross-talk between cardiac cell types, gaining new insights into the role of IGF2/IGF1R and NRP2 signaling in human cardiogenesis. Finally, we show that epicardioids mimic the multicellular pathogenesis of congenital or stress-induced hypertrophy and fibrotic remodeling. As such, epicardioids offer a unique testing ground of epicardial activity in heart development, disease and regeneration.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37012447 · DOI · PMC10713454
Effect of SGLT2-Inhibitors on Epicardial Adipose Tissue: A Meta-Analysis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- (1) Sodium-glucose cotransporter-2 inhibitors (SGLT2-i) reduce adipose tissue and cardiovascular events in patients with type 2 diabetes (T2D).
- Closing excerpt
- (4) Conclusions: This meta-analysis suggests that the amount of EAT is significantly reduced in T2D patients with SGLT2-i treatment.
- 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 (161 words)
(1) Sodium-glucose cotransporter-2 inhibitors (SGLT2-i) reduce adipose tissue and cardiovascular events in patients with type 2 diabetes (T2D). Accumulation of epicardial adipose tissue (EAT) is associated with increased cardio-metabolic risks and obstructive coronary disease events in patients with T2D. (2) We performed a systematic review and meta-analysis of SGLT2-i therapy on T2D patients, reporting data on changes in EAT after searching the PubMed/MEDLINE, Embase, Science Direct, Scopus, Google Scholar, and Cochrane databases. A random effects or fixed effects model meta-analysis was then applied. (3) Results: A total of three studies (n = 64 patients with SGLT2-i, n = 62 with standard therapy) were included in the final analysis. SGLT2 inhibitors reduced EAT (SMD: -0.82 (-1.49; -0.15); p < 0.0001). An exploratory analysis showed that HbA1c was significantly reduced with SGLT2-i use, while body mass index was not significantly reduced with this drug. (4) Conclusions: This meta-analysis suggests that the amount of EAT is significantly reduced in T2D patients with SGLT2-i treatment.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34440918 · DOI · PMC8391573
Regenerative potential of epicardium-derived extracellular vesicles mediated by conserved miRNA transfer [3]
Abstract reading summary — source excerpts
- Opening excerpt
- AimsAfter a myocardial infarction, the adult human heart lacks sufficient regenerative capacity to restore lost tissue, leading to heart failure progression.
- Closing excerpt
- Analysis of exosome cargo in mouse and human identified conserved pro-regenerative miRs, which in combination recapitulated the therapeutic effects of promoting cardiomyocyte proliferation.
- 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 (298 words)
AimsAfter a myocardial infarction, the adult human heart lacks sufficient regenerative capacity to restore lost tissue, leading to heart failure progression. Finding novel ways to reprogram adult cardiomyocytes into a regenerative state is a major therapeutic goal. The epicardium, the outermost layer of the heart, contributes cardiovascular cell types to the forming heart and is a source of trophic signals to promote heart muscle growth during embryonic development. The epicardium is also essential for heart regeneration in zebrafish and neonatal mice and can be reactivated after injury in adult hearts to improve outcome. A recently identified mechanism of cell-cell communication and signalling is that mediated by extracellular vesicles (EVs). Here, we aimed to investigate epicardial signalling via EV release in response to cardiac injury and as a means to optimize cardiac repair and regeneration.Methods and resultsWe isolated epicardial EVs from mouse and human sources and targeted the cardiomyocyte population. Epicardial EVs enhanced proliferation in H9C2 cells and in primary neonatal murine cardiomyocytes in vitro and promoted cell cycle re-entry when injected into the injured area of infarcted neonatal hearts. These EVs also enhanced regeneration in cryoinjured engineered human myocardium (EHM) as a novel model of human myocardial injury. Deep RNA-sequencing of epicardial EV cargo revealed conserved microRNAs (miRs) between human and mouse epicardial-derived exosomes, and the effects on cell cycle re-entry were recapitulated by administration of cargo miR-30a, miR-100, miR-27a, and miR-30e to human stem cell-derived cardiomyocytes and cryoinjured EHM constructs.ConclusionHere, we describe the first characterization of epicardial EV secretion, which can signal to promote proliferation of cardiomyocytes in infarcted mouse hearts and in a human model of myocardial injury, resulting in enhanced contractile function. Analysis of exosome cargo in mouse and human identified conserved pro-regenerative miRs, which in combination recapitulated the therapeutic effects of promoting cardiomyocyte proliferation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33599250 · DOI · PMC8803084
A Computational Journey Toward an Optimal Design for Metamaterial Epicardial Passive Sleeves [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Heart failure (HF) following myocardial infarction (MI) is a major clinical challenge with severe complications.
- Closing excerpt
- Ultimately, this work contributes to an improved understanding of passive sleeve-heart interactions and improves the targeted biomechanical support therapies following MI.
- 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 (197 words)
Heart failure (HF) following myocardial infarction (MI) is a major clinical challenge with severe complications. Epicardial sleeves and patches are increasingly investigated to improve heart function post-MI, yet their passive mechanical effects remain underexplored. This has resulted in limited insight into how sleeves mechanically interact with the infarct and remote myocardium. This study used 3-D in-silico cardiac models to examine how sleeve shape, material properties, and architecture affect global and regional mechanics. A high-fidelity biventricular model is used to investigate how a continuum cardiac sleeve alters function. Designs that improve regional mechanics successfully limited pathological bulging, modulated fiber strains, and influenced torsional behavior without over-constraining remote tissue, whereas overly restrictive and stiff sleeves penalized healthy myocardium and reduced the intended relief of infarct bulging. These findings highlight the importance of considering regional biomechanical markers when developing sleeve designs. Building on these continuum sleeve insights, a spheroidal left ventricle model demonstrated the proof-of-concept advantage of an "auxetic" metamaterial sleeve, engineered with a negative Poisson ratio. This programmed architecture provided region-specific benefits beyond those of conventional continuum sleeves. Ultimately, this work contributes to an improved understanding of passive sleeve-heart interactions and improves the targeted biomechanical support therapies following MI.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41131867 · DOI · PMC12836452
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 Adipose Tissue May Mediate Deleterious Effects of Obesity and Inflammation on the Myocardium [5]
- Research article American Society of Echocardiography clinical recommendations for multimodality cardiovascular imaging of patients with pericardial disease: endorsed by the Society for Cardiovascular Magnetic Resonance and Society of Cardiovascular Computed Tomography [6]
- Research article Epicardial and perivascular adipose tissues and their influence on cardiovascular disease: basic mechanisms and clinical associations [7]
- Research article The epicardium and epicardially derived cells (EPDCs) as cardiac stem cells [8]
- Research article Pericardial disease [9]
- Research article The epicardium as a hub for heart regeneration [10]
References
- Meier AB, Zawada D, De Angelis MT, Martens LD, Santamaria G, Zengerle S, et al.. Epicardioid single-cell genomics uncovers principles of human epicardium biology in heart development and disease. . 2023. PMID 37012447 · DOI · PMC10713454
- Masson W, Lavalle-Cobo A, Nogueira JP. Effect of SGLT2-Inhibitors on Epicardial Adipose Tissue: A Meta-Analysis. . 2021. PMID 34440918 · DOI · PMC8391573
- Del Campo CV, Liaw NY, Gunadasa-Rohling M, Matthaei M, Braga L, Kennedy T, et al.. Regenerative potential of epicardium-derived extracellular vesicles mediated by conserved miRNA transfer. . 2022. PMID 33599250 · DOI · PMC8803084
- Naeini V, Mendiola EA, Rafsanjani A, Coulter FB, Xiang Q, Zhang J, et al.. A Computational Journey Toward an Optimal Design for Metamaterial Epicardial Passive Sleeves. . 2026. PMID 41131867 · DOI · PMC12836452
- Packer M. Epicardial Adipose Tissue May Mediate Deleterious Effects of Obesity and Inflammation on the Myocardium. J Am Coll Cardiol. 2018. PMID 29773163 · DOI
- Klein AL, Abbara S, Agler DA, Appleton CP, Asher CR, Hoit B, et al.. American Society of Echocardiography clinical recommendations for multimodality cardiovascular imaging of patients with pericardial disease: endorsed by the Society for Cardiovascular Magnetic Resonance and Society of Cardiovascular Computed Tomography. J Am Soc Echocardiogr. 2013. PMID 23998693 · DOI
- Fitzgibbons TP, Czech MP. Epicardial and perivascular adipose tissues and their influence on cardiovascular disease: basic mechanisms and clinical associations. J Am Heart Assoc. 2014. PMID 24595191 · DOI · PMC4187500
- Wessels A, Pérez-Pomares JM. The epicardium and epicardially derived cells (EPDCs) as cardiac stem cells. Anat Rec A Discov Mol Cell Evol Biol. 2004. PMID 14699633 · DOI
- Little WC, Freeman GL. Pericardial disease. Circulation. 2006. PMID 16567581 · DOI
- Cao J, Poss KD. The epicardium as a hub for heart regeneration. Nat Rev Cardiol. 2018. PMID 29950578 · DOI · PMC6143401
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.