Abstract
Background: Although electrical and structural remodeling has been recognized to be important in the pathophysiology of atrial fibrillation, the mechanisms underlying remodeling process are unknown. There has been increasing interest in the involvement of inflammatory molecules and adipokines released from the epicardial fat tissue in the pathophysiology of atrial fibrillation. Objectives: In our study, we aimed to investigate the relationship of atrial fibrillation with increased epicardial adipose tissue, inflammatory molecules released from this tissue and omentin. Methods: Thirty-six patients [...]
Highlights
Electrical and structural remodeling has been recognized to be important in the pathophysiology of atrial fibrillation, the mechanisms underlying remodeling process are unknown
It has been suggested that that epicardial fat tissue, adipokines and inflammatory molecules released from this tissue may play a role in the pathophysiology of Atrial fibrillation (AF).[4,5,6]
The relation of inflammatory molecules released from epicardial adipose tissue and adipokines with AF will provide a better understanding of the pathophysiology of the disease.[18,19]
Summary
Electrical and structural remodeling has been recognized to be important in the pathophysiology of atrial fibrillation, the mechanisms underlying remodeling process are unknown. There has been increasing interest in the involvement of inflammatory molecules and adipokines released from the epicardial fat tissue in the pathophysiology of atrial fibrillation. Objectives: In our study, we aimed to investigate the relationship of atrial fibrillation with increased epicardial adipose tissue, inflammatory molecules released from this tissue and omentin. Epicardial adipose tissue thickness of patients was measured by echocardiography. Results: Epicardial adipose tissue thickness was significantly greater in the patient group (6mm [4-5.5]) than controls (4mm [3-5.5]) (p
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