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Updated: Jun 4, 2026

High-Resolution Endocardial and Epicardial Optical Mapping in a Sheep Model of Stretch-Induced Atrial Fibrillation
Published on: July 29, 2011
Neural mechanism of atrial fibrillation: insight from global high density frequency mapping
Li-Wei Lo1, Chuen-Wang Chiou, Yenn-Jiang Lin
1Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Background:
It has been demonstrated that intrinsic cardiac autonomic activation of ganglionated plexi (GPs) exhibits a frequency gradient from the center to the periphery with limited mapping.
Objective:
We aimed to use a global mapping tool (Ensite Array) to identify the frequency distribution and clarify the interaction between the extrinsic/intrinsic autonomic systems.
Methods:
A mid sternal thoractomy was performed in anesthetized dogs. High frequency stimulation (20 Hz, 0.1 ms duration) was applied to locate the GPs and achieve vagosympathetic stimulation (VNS). There were 4 major GPs, which were located near the 4 pulmonary vein (PV) ostia, and a third fat pad (SVC-Ao) GP that was located near the superior vena cava (SVC)-right atrial (RA) junction.
Results:
Without VNS (n = 12), the left atrial (LA) mean (8.20 ± 0.11 vs 7.95 ± 0.30 Hz, P = 0.04) and max (9.86 ± 0.28 vs 9.43 ± 0.29 Hz, P = 0.03) DFs were higher during the PV ostial GP stimulation than the SVC-Ao GP stimulation. The LA max DFs were located not only at the primary GPs but also the nearby secondary PV ostial GPs. The RA mean DF (8.36 ± 0.05 vs 7.99 ± 0.19 Hz, P = 0.04) was higher during SVC-Ao GP stimulation than PV ostial GP stimulation. The max DF was located inside the SVC during SVC-Ao GP stimulation and at the RA septum during PV ostial GP stimulation. With VNS (n = 12), the LA mean and max DFs between the PV ostial and SVC-Ao GP stimulation were similar. The DF distribution shifted to non-GP LA sites during both the PV ostial and SVC-Ao GP stimulation.
Conclusion:
The findings indicate that the AF was caused by an interaction between the PV ostial GPs during intrinsic autonomic stimulation, whereas the non-GP LA sites were responsible for the AF induced by an extrinsic neural input.
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