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Updated: Sep 10, 2025

Epicardial Outgrowth Culture Assay and Ex Vivo Assessment of Epicardial-derived Cell Migration
Published on: March 18, 2016
Earlier Prediction of Cardiovascular Risk with Epicardial Fat Assessment.
Giuseppe Calcaterra1, Ron T Varghese2, Maurizio Baroni3
1Former Professor of Pediatric Cardiology, Postgraduate Medical School of Cardiology, University of Palermo, Italy.
Epicardial adipose tissue, a unique fat depot, offers cardioprotection but can become detrimental in disease. Its measurement is a reliable cardiovascular risk marker and a target for new therapies.
Area of Science:
- Cardiology
- Metabolic Research
- Adipose Tissue Biology
Background:
- Epicardial adipose tissue (EAT) is a distinct visceral fat depot with unique anatomical and metabolic characteristics.
- EAT shares microcirculation with the heart, suggesting potential interactions and influencing cardiac health.
- While normally protective, EAT can become detrimental in pathological conditions, impacting the myocardium and coronary arteries.
Purpose of the Study:
- To review the emerging evidence on epicardial adipose tissue's role in cardiac risk.
- To highlight EAT as an active player in cardiac pathology development.
- To discuss EAT as a potentially modifiable therapeutic target for cardiovascular diseases.
Main Methods:
- Review of scientific literature on epicardial adipose tissue.
- Analysis of EAT's anatomical, metabolic, and transcriptomic features.
- Correlation of EAT measurement with various cardiovascular and metabolic conditions.
Main Results:
- EAT exhibits properties similar to brown fat, offering metabolic and cardioprotective functions.
- Downregulation of EAT transcriptome occurs in advanced coronary artery disease.
- EAT thickness/volume measurement correlates with visceral adiposity, CAD, metabolic syndrome, and cardiac dysfunction.
Conclusions:
- Epicardial adipose tissue serves as a reliable marker for cardiovascular risk.
- EAT is an active participant in cardiac pathology and a potential therapeutic target.
- Interventions like improved vascularization, weight loss, and drugs can restore EAT's protective functions.
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