We read the recent report “Relation of proinflammatory activity of epicardial adipose tissue to the occurrence of atrial fibrillation” by Mazurek et al. 1 Their purpose was to investigate epicardial adipose tissue (EAT) inflammatory activity using 18-fluorodeoxyglucose-positron emission tomography in patients with atrial fibrillation (AF) and in controls. The authors very clearly discussed inflammatory activity of EAT reflected by standardized uptake value is greater in patients with AF than that in controls. Inflammatory activity of EAT adjacent to left atrium, atrioventricular groove, and left main artery is greater than in subcutaneous or visceral thoracic tissue. In addition to their discussion, we aimed to emphasize the possible other relative mechanism between epicardial fat and AF, the contribution of cardioautonomic nervous system function.
We read the recent report “Relation of proinflammatory activity of epicardial adipose tissue to the occurrence of atrial fibrillation” by Mazurek et al.
1
Their purpose was to investigate epicardial adipose tissue (EAT) inflammatory activity using 18-fluorodeoxyglucose-positron emission tomography in patients with atrial fibrillation (AF) and in controls. The authors very clearly discussed inflammatory activity of EAT reflected by standardized uptake value is greater in patients with AF than that in controls. Inflammatory activity of EAT adjacent to left atrium, atrioventricular groove, and left main artery is greater than in subcutaneous or visceral thoracic tissue. In addition to their discussion, we aimed to emphasize the possible other relative mechanism between epicardial fat and AF, the contribution of cardioautonomic nervous system function.
