title: Sinoatrial node electrical activity modulates pulmonary vein arrhythmogenesis.
abstract: 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 μM).
  
  
  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, the multi-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.
authors.affiliation: Department of Biomedical Engineering, National Defense Medical Center, Taipei, Taiwan; Department of Marine Biotechnology and Resources, National Sun Yat-sen University, Kaohsiung, Taiwan.
authors.forename: Yao-Chang
authors.initials: YC
authors.lastname: Chen
authors.affiliation: Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; Division of Cardiology, Sijhih Cathay General Hospital, New Taipei City, Taiwan.
authors.forename: Yen-Yu
authors.initials: YY
authors.lastname: Lu
authors.affiliation: Division of Cardiology, Chi-Mei Medical Center, Tainan, Taiwan.
authors.forename: Chen-Chuan
authors.initials: CC
authors.lastname: Cheng
authors.affiliation: Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; Division of Cardiovascular Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
authors.forename: Yung-Kuo
authors.initials: YK
authors.lastname: Lin
authors.affiliation: National Yang-Ming University, School of Medicine, Taipei, Taiwan; Division of Cardiology and Cardiovascular Research Center, Veterans General Hospital-Taipei, Taipei, Taiwan.
authors.forename: Shih-Ann
authors.initials: SA
authors.lastname: Chen
authors.affiliation: Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; Division of Cardiovascular Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan. Electronic address: yjchen@tmu.edu.tw.
authors.forename: Yi-Jen
authors.initials: YJ
authors.lastname: Chen
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000175:diagnosis / Q000503:physiopathology*; D008297:Male; D009431:Neural Conduction / Q000502:physiology*; D009924:Organ Culture Techniques; D011667:Pulmonary Veins / Q000503:physiopathology*; D011817:Rabbits; D012849:Sinoatrial Node / Q000502:physiology*
keywords: Atrial fibrillation; Pulmonary vein; Sinoatrial dysfunction