We read the recent report “Relation of proinflammatory activity of epicardial adipose tissue to the occurrence of atrial fibrillation” by Mazurek et al. 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.

Several published studies show the associations between alterations in autonomic nervous system and development of AF. Cherniavskiĭ et al. focused on the role and mechanism of autonomous nervous system (ANS) disbalance in AF. They showed that disbalance in the ANS is a leading cause of AF. There is definitive evidence of the relations between vegetative innervations, initiation, and maintenance of AF, the main contributors being hyperactivity of ANS and uncontrolled release of neurotransmitters that shorten atrial refractoriness. The neurotransmitters have been responsible for triggering mechanism of AF. Shen et al. investigated importance of baseline autonomic nerve activity in development of pacing-induced AF and showed good linear sympathovagal correlation. The result of these previous studies, impairment in autonomic nervous system function, is believed to play a role in the development of AF.

Previous studies obviously revealed that the close relation between EAT and cardioautonomic function. Zhou et al. showed that the cardiac ganglionated plexus in the EAT integrates the autonomic innervation between the extrinsic and intrinsic cardiac autonomic nervous system and affects atrial electrophysiology and pathophysiology. Carnevalli et al. concluded that EAT deficiency in mice leads to an imbalance of the autonomic neural modulation of cardiac function in the sympathetic direction and to a potentially proarrhythmic remodeling of electrical and structural properties of the heart. Balcioğlu et al. showed that sympathovagal imbalance, detected by heart rate variability and heart rate turbulence parameters, is related to EAT thickness. As sympathovagal imbalance is a predictor of arrhythmic events, EAT may play an important arrhythmogenic role.

As a consequence, we believe that the relation between impairment on cardiac autonomic nervous system function may have a role in the result of the report by Mazurek et al. We hope that the aforementioned items would add to the value of the well-written report of Mazurek et al. regarding the relation between EAT and AF.