Epicardial Adipose Tissue and Neural Mechanisms of Atrial Fibrillation

In this issue of the Circulation: Arrhythmia and Electrophysiology, Nagashima et al 1 reported that there is higher epicardial adipose tissue (EAT) volume and greater serum inflammatory biomarker levels in patients with persistent atrial fibrillation (PerAF) than in patients with paroxysmal atrial fibrillation (PAF).Furthermore, they noted that high dominant frequency (DF) sites are located adjacent to EAT sites.The authors proposed two possible explanations for these findings.One is that EAT secrets proinflammatory cytokines that alter local atrial and pulmonary vein (PV) electrophysiology and facilitates the development of atrial fibrillation (AF).Two is that EAT contains abundant ganglionated plexi (GP).Activation of the autonomic nerves in the GP facilitates the maintenance of AF.The results of the present study extended their previous observation on EAT 2 by providing new data on the correlation between high DF sites and EAT sites.These novel observations provide new insights into the anatomical and physiological differences between PAF and PerAF.After the initial diagnosis of PAF, there is a slow (5-10% per year) but steady progression to chronic (permanent or persistent) AF. 3 Baseline echocardiographic variables, age, cardiomyopathy and heart rate are independently associated with progression to chronic AF.On the other hand, PerAF is also frequently the initial diagnosis without preceding PAF episodes.How often PerAF and permanent forms of AF are preceded by recurrent PAF remains unclear.Improving the understanding of PAF to PerAF progression may help secondary prevention efforts to reduce the complications associated with AF.Wijffels et al 4 performed intermittent rapid atrial pacing in goats to study the progression of PAF to PerAF.They found that when AF is maintained artificially, the duration of the paroxysms progressively increases, until after 1 to 3 weeks AF becomes sustained.The transition from PAF to PerAF is associated with a marked shortening of atrial effective refractory period and wavelength, which the authors propose as major factors responsible for