ASSOCIATION OF GHRELIN RECEPTOR AND INFLAMMATION IN PERI-ATRIAL ADIPOSE TISSUE FROM OBESE PATIENTS WITH POSTOPERATIVE...

Area of Science:

• Cardiology
• Immunology
• Metabolic Syndrome

Background:

• Atrial fibrillation (AF) is a common arrhythmia, increasingly linked to inflammation.
• Obesity drives adipose tissue (AT) inflammation.
• Ghrelin (GHRL) may modulate AT inflammation via its receptor (GHS-R) on adipose tissue macrophages (ATMs).

Purpose of the Study:

• To investigate the role of ATMs and GHS-R in right atrial appendage (RAA) adipose tissue samples.
• To explore the association between epicardial adipose tissue characteristics and postoperative atrial fibrillation (POAF).

Main Methods:

• RAA biopsies were obtained from 10 obese patients undergoing coronary artery bypass graft (CABG) surgery who developed POAF.
• Immunohistochemistry was used to quantify CD68 (macrophage marker) and GHS-R expression in epicardial adipose tissue (EAT).

Main Results:

• Epicardial adipose tissue (EAT) with inflammation showed larger mean adipocyte diameter (MAD) compared to non-inflamed EAT.
• CD68 expression, indicating macrophage infiltration, was higher in inflamed EAT.
• GHS-R expression was also elevated in inflamed EAT samples.

Conclusions:

• Increased epicardial fat area, macrophage infiltration (CD68+ ATMs), and GHS-R expression in ATMs are associated with POAF in obese patients.
• These findings suggest a potential inflammatory pathway linking obesity, epicardial fat, and AF development.