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Purpose of Review <p>This review explores the unique anatomy and pathophysiology of pericardial fat (including both epicardial adipose tissue [EAT] and paracardial fat), its clinical significance, and its potential role as a therapeutic target. It addresses key questions regarding the contribution of EAT to cardiometabolic conditions such as coronary artery disease, heart failure, atrial fibrillation, and ventricular arrhythmias, and explores interventions that reduce EAT to possibly improve cardiovascular outcomes.</p> Recent Findings <p>Recent studies have established EAT as a metabolically active, pro-inflammatory fat depot directly affecting the myocardium and coronary arteries. Imaging and metabolomic studies have advanced the assessment of EAT burden. Clinical evidence supports lifestyle modification, pharmacologic therapies including GLP-1 RA and SGLT2i, and bariatric surgery to effectively reduce EAT volume. Emerging data link EAT reduction with improved cardiac function and arrhythmia risk, although causality remains unclear.</p> Summary <p>EAT is a modifiable cardiometabolic risk factor associated with adverse outcomes in coronary artery disease, heart failure, atrial fibrillation, and ventricular arrhythmias. Targeting EAT through cardiometabolic risk reduction strategies may improve prognosis. Future research should focus on determining whether reducing EAT directly improves clinical outcomes.</p>

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The Role of Pericardial Fat in Cardiometabolic Disease: Emerging Evidence and Therapeutic Potential

  • 期刊论文

  • 发表日期：

    2025年10月10日

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  • Zaid Shahrori,
  • Michel Chedid El Helou,
  • Sherin Sallam,
  • Gianluca Iacobellis,
  • Ian J. Neeland

摘要

Purpose of Review

This review explores the unique anatomy and pathophysiology of pericardial fat (including both epicardial adipose tissue [EAT] and paracardial fat), its clinical significance, and its potential role as a therapeutic target. It addresses key questions regarding the contribution of EAT to cardiometabolic conditions such as coronary artery disease, heart failure, atrial fibrillation, and ventricular arrhythmias, and explores interventions that reduce EAT to possibly improve cardiovascular outcomes.

Recent Findings

Recent studies have established EAT as a metabolically active, pro-inflammatory fat depot directly affecting the myocardium and coronary arteries. Imaging and metabolomic studies have advanced the assessment of EAT burden. Clinical evidence supports lifestyle modification, pharmacologic therapies including GLP-1 RA and SGLT2i, and bariatric surgery to effectively reduce EAT volume. Emerging data link EAT reduction with improved cardiac function and arrhythmia risk, although causality remains unclear.

Summary

EAT is a modifiable cardiometabolic risk factor associated with adverse outcomes in coronary artery disease, heart failure, atrial fibrillation, and ventricular arrhythmias. Targeting EAT through cardiometabolic risk reduction strategies may improve prognosis. Future research should focus on determining whether reducing EAT directly improves clinical outcomes.