Epicardial adipose tissue acts as an independent risk factor for atrial fibrillation, with its volume or thickness predicting the presence, severity, and recurrence of the arrhythmia.
What is the role of epicardial adipose tissue in the pathogenesis and management of atrial fibrillation?
Epicardial adipose tissue is an independent risk factor for atrial fibrillation and represents a promising therapeutic target for improving AF outcomes.
Obesity plays an important role in the pathogenesis of atrial fibrillation (AF). Recently, rather than general fat distribution, epicardial adipose tissue (EAT) gains a growing concern. EAT is the local adipose deposition between myocardium and pericardium. Accumulated evidence revealed several distinguishing characteristics of EAT. It lies contiguously with the myocardium and could infiltration into myocardium, actively secrets cytokines and adipokines mediating inflammation or remodeling, and contains abundant ganglionated plexi. Clinical research also found EAT may be an independent risk factor of AF. Volume or thickness of EAT measured on CT or MRI could be applied as a predictor of presence, severity, and recurrence of AF. Some drugs, like antidiabetic drugs and lipid-lowing drugs, show ability to reduce EAT. Additional surgical ablation of EAT was also proved that it could improve outcome of pulmonary vein isolation for AF. In present review, we summarize recent epidemic, biological, and clinical findings about EAT and its possible role in AF.
Zhou et al. (Mon,) conducted a review in Atrial fibrillation. Epicardial adipose tissue (EAT) was evaluated. Epicardial adipose tissue acts as an independent risk factor for atrial fibrillation, with its volume or thickness predicting the presence, severity, and recurrence of the arrhythmia.