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

Q: What is the clinical evidence from this study?

Study design: Review. Population: Cardiometabolic disease (coronary artery disease, heart failure with preserved ejection fraction, atrial fibrillation, and ventricular arrhythmias). Intervention: Lifestyle modification, pharmacologic therapies (GLP-1 receptor agonists, SGLT2 inhibitors, statins, PCSK9 inhibitors), and bariatric surgery targeting epicardial adipose tissue.

Q: What does this research mean for the field?

Epicardial adipose tissue is a modifiable risk factor linked to major adverse cardiovascular events, HFpEF hospitalization, and arrhythmias that can be reduced through lifestyle interventions, GLP-1 receptor agonists, SGLT2 inhibitors, and bariatric surgery. Novelty: ClaimNovelty.SYNTHESIS. Consensus alignment: ConsensusAlignment.NEUTRAL.

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

doi:10.1007/s11886-025-02305-9

October 10, 2025Current Cardiology ReportsOpen Access

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

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Why the study?

The clinical significance and therapeutic potential of pericardial fat, including epicardial adipose tissue, in cardiometabolic diseases remain to be fully elucidated.

Do lifestyle, pharmacologic (GLP-1 receptor agonists, SGLT2 inhibitors), and surgical interventions reduce epicardial adipose tissue burden and improve cardiovascular outcomes in patients with cardiometabolic disease?

Key Points

To review the anatomy, pathophysiology, clinical significance, and therapeutic potential of pericardial and epicardial adipose tissue across various cardiometabolic disorders.
Narrative review synthesizing clinical, imaging, and metabolomic evidence evaluating pericardial fat and epicardial adipose tissue (EAT).
Assessed cardiac imaging modalities (echocardiography, CT, MRI) and the impact of lifestyle modification, GLP-1 RA, SGLT2i, and bariatric surgery on EAT volume.
Greater EAT volume independently correlates with coronary artery disease and increased risk of major adverse cardiac events (HR 1.35–2.05), myocardial infarction (OR 2.63), and atrial fibrillation (adjusted OR 4.04).
Higher EAT is significantly increased in heart failure with preserved ejection fraction versus controls (standardized mean difference 0.61, 95% CI 0.27–0.94) and links to increased heart failure hospitalization and mortality (HR 1.28, 95% CI 1.12–1.45, p = 0.0002).
Increased EAT thickness predicts post-ablation recurrence of atrial fibrillation (RR 1.73, 95% CI 1.04–2.87, P = 0.040) and ventricular tachycardia (HR 1.20 per mm increase, 95% CI 1.06–1.39, P = 0.004).

Structured PICO

Do lifestyle, pharmacologic (GLP-1 receptor agonists, SGLT2 inhibitors), and surgical interventions reduce epicardial adipose tissue burden and improve cardiovascular outcomes in patients with cardiometabolic disease?

P

Population

Patients with cardiometabolic conditions including coronary artery disease, heart failure with preserved ejection fraction, atrial fibrillation, and ventricular arrhythmias evaluated in the context of pericardial and epicardial adipose tissue burden.

I

Intervention

Cardiometabolic risk and weight reduction strategies targeting epicardial adipose tissue (EAT), including lifestyle modification (caloric restriction, aerobic and resistance exercise), pharmacologic therapies (GLP-1 receptor agonists, SGLT2 inhibitors such as dapagliflozin 10 mg daily, statins, PCSK9 inhibitors), and metabolic/bariatric surgery (Roux-en-Y gastric bypass, sleeve gastrectomy).

Limitations

There is no standardized clinical protocol for routine pericardial fat measurement
Causality remains unclear as to whether EAT is a direct cause of cardiometabolic conditions or an indicator of underlying risk
No medication has been specifically studied to target EAT nor is officially approved for EAT reduction
Randomized trials are still needed to determine whether reducing EAT directly improves clinical outcomes
Lack of standardized clinical protocol for routine pericardial fat measurement
Unclear causality regarding whether epicardial adipose tissue directly causes adverse cardiovascular outcomes or reflects broader cardiometabolic risk
No pharmacologic therapy is specifically approved for epicardial adipose tissue reduction
Lack of dedicated randomized controlled trials testing whether targeted reduction of epicardial adipose tissue directly improves clinical outcomes

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Implication

Epicardial adipose tissue is a metabolically active, modifiable cardiometabolic risk factor strongly linked to CAD, HFpEF, and arrhythmias that responds favorably to weight loss, exercise, GLP-1 RAs, SGLT2 inhibitors, and bariatric surgery.

Abstract

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. 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.

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Cite This Study

Shahrori et al. (2025) conducted a review in Cardiometabolic disease (coronary artery disease, heart failure with preserved ejection fraction, atrial fibrillation, and ventricular arrhythmias). Lifestyle modification, pharmacologic therapies (GLP-1 receptor agonists, SGLT2 inhibitors, statins, PCSK9 inhibitors), and bariatric surgery targeting epicardial adipose tissue was evaluated.

synapsesocial.com/papers/6ab9b2962a90f6e7a3034564 https://doi.org/10.1007/s11886-025-02305-9

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

Figures

Key Points

Structured PICO

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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

Figures

Key Points

Structured PICO

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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