Transverse versus longitudinal electrical propagation within the atrioventricular node during dual pathway conduction: Basis of dual pathway electrophysiology and His electrogram alternans (Zhang's phenomenon)
详细信息    查看全文
文摘

Background

We have discovered and validated that AV node dual pathway conduction results in a new phenomenon termed His electrogram alternans (HEA), which indicates dual inputs rather than a final common pathway from the AV node into the His bundle. However, the electrophysiological basis for AV node dual pathway conduction and HEA has not been clarified. This study was designed to elucidate the electrophysiological basis for dual pathway conduction and HEA.

Methods

By using HEA as an index of dual pathway electrophysiology, action potentials from multiple locations in the superior and inferior AV nodal domains were obtained to monitor electrical propagation during dual pathway conduction in 8 isolated rabbit hearts.

Results

Fibers inside the AV node were generally aligned along the AV conduction axis. During fast pathway (FP) conduction, electrical excitation in the AV node was propagated in a superior to inferior direction across the major fiber orientation. In contrast, slow pathway (SP) conduction occurred when the superior-inferior propagation failed within the superior nodal domain, permitting electrical propagation to proceed in the inferior nodal domain along the fiber orientation in a posterior to anterior direction. In effect, FP activated first the superior distal node, while SP activated first the inferior distal node. This functional dissociation of superior-fast and inferior-slow domains in distal node produced dual inputs into the His bundle.

Conclusions

Transverse versus longitudinal electrical propagation within the AV node produces functional dissociation in the distal node, resulting in superior-fast and inferior-slow inputs into the His bundle and HEA during dual pathway conduction.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700