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Epicardial Adipose Tissue in Diabetic Heart Disease: Impact on Cardiac Function and Modulation Strategies, a
Ana Đuzel Čokljat1, Petra Grubić Rotkvić2, Zdravko Babić3
1Department of Internal Medicine, General Hospital Dubrovnik, 20000 Dubrovnik, Croatia.
Medicina (Kaunas, Lithuania)
|July 28, 2026
Summary
Excess epicardial adipose tissue (EAT) in type 2 diabetes mellitus (T2DM) promotes inflammation and myocardial dysfunction. Interventions targeting EAT are crucial for managing this diabeto-cardiometabolic continuum.
Area of Science:
- Cardiology
- Endocrinology
- Metabolic Syndrome
Background:
- Epicardial adipose tissue (EAT) is metabolically active visceral fat surrounding the heart.
- Excessive EAT is prevalent in type 2 diabetes mellitus (T2DM) and linked to early diabetic myocardial disease.
- EAT exhibits a proinflammatory profile impacting myocardial function.
Purpose of the Study:
- To review the role of excessive EAT in T2DM-related myocardial dysfunction.
- To analyze the crosstalk between EAT and myocardium.
- To discuss interventions within the diabeto-cardiometabolic continuum.
Main Methods:
- Literature review of studies on EAT, T2DM, and myocardial function.
- Analysis of molecular and hemodynamic mechanisms.
- Exploration of therapeutic interventions.
Main Results:
- Excess EAT releases proinflammatory and profibrotic cytokines affecting the myocardium.
- Enlarged EAT causes hemodynamic changes, leading to pericardial constraint.
- T2DM, obesity, and inflammation interact with EAT to cause myocardial stiffness and dysfunction.
Conclusions:
- Excessive EAT is a key player in T2DM-associated myocardial dysfunction.
- EAT's immunometabolic activity offers an exoluminal perspective on coronary artery disease.
- Targeting EAT through lifestyle or pharmacological means is critical for managing diabeto-cardiometabolic disease.
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