Sinoatrial node electrical activity modulates pulmonary vein arrhythmogenesis

Background: Sinoatrial node (SAN) dysfunction increases the occurrences of atrial fibrillation (AF). The pulmonary veins (PVs) play a critical role in the pathophysiology of AF. The purpose of this study was to evaluate whether SAN electrical activity can modulate PV arrhythmogenesis. Methods: Conventional microelectrodes and multi-electrode array system were used to simultaneously record the electrical activity and conduction properties of rabbit SAN and PV tissue preparations with and without SAN-PV interruptions before and after perfusion with Anemonia sulcata toxin (ATX)-II (100 nM) or isoproterenol (1 mu M). Results: ATX-II significantly increased PV beating rates, which overdrove SAN electrical activity with the occurrences of PV burst firings in 5 (56%) of 9 tissue preparations, and induced SAN-PV conduction block in 6 (67%) of 9 preparations. After SAN-PV disconnection, ATX-II induced burst firing and early afterdepolarizations in 8 (89%) of 9 PVs. Moreover, themulti-electrode array found that ATX-II reversed the electrical conduction between the SAN and PV with an increase in electrical activity from 1.8 +/- 0.6 to 2.9 +/- 0.6 Hz (P < 0.05) in SAN-PV preparations (n = 7). In contrast, isoproterenol did not reverse electrical conduction between the SAN and PV with an increase in electrical activity from 1.8 +/- 0.2 to 3.0 +/- 0.3 Hz (P < 0.005) in SAN-PV preparations (n = 7). Conclusions: SAN electrical activity modulates PV arrhythmogenesis. SAN-PV conduction blocks can increase PV arrhythmogenesis. (C) 2014 Elsevier Ireland Ltd. All rights reserved.