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.
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
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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