Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMCOpen access

Epicardial adipose tissue in coronary microvascular disease

Gašpárková V., Tran BT., Ošťádal P., Lambert L., Hájek P., Kala P.

Narrative Review on Cardiovascular Disease, published in Am Heart J Plus (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Am Heart J Plus (2026)
Reported sample size
—
Source database
Europe PMC
PMID
41694543
PMCID
PMC12906140
DOI
10.1016/j.ahjo.2026.100734

Abstract (original English)

Epicardial adipose tissue (EAT) is a metabolically active visceral fat depot located between the myocardium and visceral pericardium, characterized by direct microvascular, paracrine, and vasocrine continuity with the heart. Under physiological conditions, EAT exhibits beige- and brown-fat-like features that support myocardial energy homeostasis, thermoregulation, and local cardioprotection. In obesity, diabetes, and aging, EAT undergoes pathological remodeling toward a pro-inflammatory and profibrotic phenotype. Accumulating evidence implicates excess and dysfunctional EAT in the pathophysiology of multiple cardiovascular diseases, including coronary artery disease, coronary microvascular dysfunction (CMD), vasospastic angina, atrial fibrillation, and heart failure. Through inflammatory signaling, immune activation, extracellular matrix remodeling, autonomic dysregulation, and mechanical pericardial restraint, EAT contributes to myocardial fibrosis, impaired diastolic function, CMD, and reduced exercise capacity. This review focuses on the biological characteristics of EAT, current imaging approaches for its detection and quantification using echocardiography, cardiac computed tomography, and cardiac magnetic resonance imaging, and the relationship between EAT, CMD, and other cardiovascular pathologies. We also summarize therapeutic strategies targeting EAT, including pharmaco

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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