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Peer-reviewedCC BY 4.0Clinical Cardiology

Epicardial Adipose Tissue as a Dynamic Modulator of Coronary Artery Disease Phenotypes: Pathophysiology and Therapeutic Implications

  • Seyed Amirhossein Dormiani Tabatabaei1
  • Mehrnazsadat Dormiani Tabatabaei2
  1. 1Isfahan Cardiovascular Research Center, Cardiovascular Research Institute Isfahan University of Medical Sciences Isfahan Iran
  2. 2School of Medicine Isfahan University of Medical Sciences Isfahan Iran
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Abstract

Background: Epicardial adipose tissue (EAT) represents a localized visceral adipose depot uniquely situated between the myocardium and the visceral layer of the pericardium. Given its proximity to the coronary vasculature and distinct transcriptomic and secretory profile, EAT has been associated with the extent and severity of coronary artery disease (CAD).

Hypothesis: Systemic therapeutic interventions may affect distinct CAD phenotypes through modulation of EAT characteristics.

Methods: This review integrates evidence on EAT pathophysiology and therapeutic modulation in relation to distinct CAD phenotypes. A structured search of PubMed, EMBASE, and the Cochrane Library was conducted using combinations of terms related to EAT, distinct CAD phenotypes, and lifestyle, surgical, and pharmacological interventions. Studies were selected based on their relevance to the review objectives.

Results: EAT has been implicated in a broad spectrum of CAD phenotypes, ranging from microvascular dysfunction to the development of high‐risk atherosclerotic plaque. Advanced imaging modalities enable depot‐specific characterization of EAT as an objectively measurable biomarker. Lifestyle interventions, bariatric surgery, and several pharmacological classes, including glucagon‐like peptide‐1 receptor agonists, sodium–glucose cotransporter‐2 inhibitors, lipid‐lowering agents, and anti‐inflammatory therapies, have been reported to modify EAT.

Conclusions: EAT represents a potential therapeutic target across CAD phenotypes. However, whether therapeutic modification of EAT independently improves cardiovascular outcomes remains uncertain.

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Cite

BibTeXRIS
BibTeX
@article{tabatabaei2026epicardial,
  title = {{Epicardial Adipose Tissue as a Dynamic Modulator of Coronary Artery Disease Phenotypes: Pathophysiology and Therapeutic Implications}},
  author = {Seyed Amirhossein Dormiani Tabatabaei and Mehrnazsadat Dormiani Tabatabaei},
  journal = {Clinical Cardiology},
  year = {2026},
  month = oct,
  doi = {10.1002/clc.70509},
  url = {https://doi.org/10.1002/clc.70509},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Epicardial Adipose Tissue as a Dynamic Modulator of Coronary Artery Disease Phenotypes: Pathophysiology and Therapeutic Implications
AU  - Seyed Amirhossein Dormiani Tabatabaei
AU  - Mehrnazsadat Dormiani Tabatabaei
PY  - 2026
DA  - 2026/10/27
JO  - Clinical Cardiology
DO  - 10.1002/clc.70509
UR  - https://doi.org/10.1002/clc.70509
AB  - Background: Epicardial adipose tissue (EAT) represents a localized visceral adipose depot uniquely situated between the myocardium and the visceral layer of the pericardium. Given its proximity to the coronary vasculature and distinct transcriptomic and secretory profile, EAT has been associated with the extent and severity of coronary artery disease (CAD).  Hypothesis: Systemic therapeutic interventions may affect distinct CAD phenotypes through modulation of EAT characteristics.  Methods: This review integrates evidence on EAT pathophysiology and therapeutic modulation in relation to distinct CAD phenotypes. A structured search of PubMed, EMBASE, and the Cochrane Library was conducted using combinations of terms related to EAT, distinct CAD phenotypes, and lifestyle, surgical, and pharmacological interventions. Studies were selected based on their relevance to the review objectives.  Results: EAT has been implicated in a broad spectrum of CAD phenotypes, ranging from microvascular dysfunction to the development of high‐risk atherosclerotic plaque. Advanced imaging modalities enable depot‐specific characterization of EAT as an objectively measurable biomarker. Lifestyle interventions, bariatric surgery, and several pharmacological classes, including glucagon‐like peptide‐1 receptor agonists, sodium–glucose cotransporter‐2 inhibitors, lipid‐lowering agents, and anti‐inflammatory therapies, have been reported to modify EAT.  Conclusions: EAT represents a potential therapeutic target across CAD phenotypes. However, whether therapeutic modification of EAT independently improves cardiovascular outcomes remains uncertain.
SN  - 0160-9289
SN  - 1932-8737
ER  -