TY - JOUR
T1 - Unique Autonomic Profile of the Pulmonary Veins and Posterior Left Atrium
AU - Arora, Rishi
AU - Ng, Jason
AU - Ulphani, Joseph
AU - Mylonas, Ilias
AU - Subacius, Haris
AU - Shade, Greg
AU - Gordon, David
AU - Morris, Alexander
AU - He, Xiang
AU - Lu, Yi
AU - Belin, Rashad
AU - Goldberger, Jeffrey J.
AU - Kadish, Alan H.
PY - 2007/3/27
Y1 - 2007/3/27
N2 - Objectives: The purpose of this study was to investigate the electrophysiologic profile of the pulmonary veins (PVs) and left atrium (LA) in response to autonomic manipulation. Background: The parasympathetic innervation of the PVs and posterior left atrium (PLA) is thought to contribute to focal atrial fibrillation (AF). We hypothesized that autonomic effects would be more prominent in these regions. Methods: In 14 dogs, epicardial mapping was performed in the PVs, PLA, and left atrial appendage (LAA) under the following conditions: baseline, 20-Hz cervical vagal stimulation (VS), propranolol (P), P + VS, and P + atropine. Effective refractory periods (ERPs) were measured, and conduction vectors were computed at multiple sites. Western blotting and immunostaining were performed for IKAch (Kir3.1/3.4). Results: The VS and P + VS caused more ERP shortening in the PV and PLA than in the LAA. The P + atropine caused greatest ERP prolongation in the LAA. Cumulative ERP change (ERP difference between P + VS and P + atropine) was greatest in the LAA and corresponded with expression of Kir3.1/3.4 (LAA > PLA ≥ PV). The ERP change in response to vagal manipulation was most heterogeneous in the PLA; this corresponded with a pronounced heterogeneity of Kir3.1 distribution in the PLA. With VS and/or P, there was evidence of regional conduction delay in the PVs with a significant change in activation direction. Similar activation changes were not seen in the PLA and LAA. Conclusions: The PVs and PLA demonstrate unique activation and repolarization characteristics in response to autonomic manipulation. The heterogeneity of vagal responses correlates with the pattern of IKAch distribution in the LA. The peculiar autonomic characteristics of the PVs and PLA might create substrate for re-entry and AF.
AB - Objectives: The purpose of this study was to investigate the electrophysiologic profile of the pulmonary veins (PVs) and left atrium (LA) in response to autonomic manipulation. Background: The parasympathetic innervation of the PVs and posterior left atrium (PLA) is thought to contribute to focal atrial fibrillation (AF). We hypothesized that autonomic effects would be more prominent in these regions. Methods: In 14 dogs, epicardial mapping was performed in the PVs, PLA, and left atrial appendage (LAA) under the following conditions: baseline, 20-Hz cervical vagal stimulation (VS), propranolol (P), P + VS, and P + atropine. Effective refractory periods (ERPs) were measured, and conduction vectors were computed at multiple sites. Western blotting and immunostaining were performed for IKAch (Kir3.1/3.4). Results: The VS and P + VS caused more ERP shortening in the PV and PLA than in the LAA. The P + atropine caused greatest ERP prolongation in the LAA. Cumulative ERP change (ERP difference between P + VS and P + atropine) was greatest in the LAA and corresponded with expression of Kir3.1/3.4 (LAA > PLA ≥ PV). The ERP change in response to vagal manipulation was most heterogeneous in the PLA; this corresponded with a pronounced heterogeneity of Kir3.1 distribution in the PLA. With VS and/or P, there was evidence of regional conduction delay in the PVs with a significant change in activation direction. Similar activation changes were not seen in the PLA and LAA. Conclusions: The PVs and PLA demonstrate unique activation and repolarization characteristics in response to autonomic manipulation. The heterogeneity of vagal responses correlates with the pattern of IKAch distribution in the LA. The peculiar autonomic characteristics of the PVs and PLA might create substrate for re-entry and AF.
UR - https://www.scopus.com/pages/publications/33947505844
UR - https://www.scopus.com/inward/citedby.url?scp=33947505844&partnerID=8YFLogxK
U2 - 10.1016/j.jacc.2006.10.075
DO - 10.1016/j.jacc.2006.10.075
M3 - Article
C2 - 17394967
AN - SCOPUS:33947505844
SN - 0735-1097
VL - 49
SP - 1340
EP - 1348
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 12
ER -