ReviewClinical cardiology2026
Epicardial Adipose Tissue as a Dynamic Modulator of Coronary Artery Disease Phenotypes: Pathophysiology and Therapeutic Implications.
Review in Clinical cardiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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2 authors.
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Abstract
backgroundEpicardial 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.
methodsThis 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.
resultsEAT 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.
conclusionsEAT represents a potential therapeutic target across CAD phenotypes. However, whether therapeutic modification of EAT independently improves cardiovascular outcomes remains uncertain.
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