Association between GP and ATP-induced AF
Pharmacologically, adenosine shortens atrial action potential duration and refractory period mainly through the activation of specific G protein-coupled adenosine A1 receptors and the downstream outward potassium channel, which is also regulated by acetylcholine via M2 muscarinic receptors.5
Anatomical studies have shown that about a half of atrial ganglia are present on the surface of the RA adjacent to the intertribal groove (posterior RA GP), around the SVC (superior RA GP), and about one-third of atrial ganglia are present between the inferior vena cava, CS ostium and around CS (posteromedial LA GP).12, 13
Previous clinical studies have suggested that adenosine/ATP could provoke the RA or CS triggers more frequently as compared to ISP.,8, 11
Zhang et al. reported that about 70% of ATP-provoked triggers were located in SVC. They postulated the hyperactivity of the SVC–aorta–GP induced by ATP could lead to rapid firing from the SVC.9
Thus, considering the pharmacological mechanisms of ATP, the anatomical characteristics of GP, the distribution of the ATP-induced foci observed in previous studies, and the efficacy of the GP-based approach in our patients, ATP-induced AF following PV/Box and SVC isolation must be associated with the hyperactivity of GP.