Open Access

On the nature of delays allowing anatomical re-entry involving the Purkinje network: a simulation study

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Date: 27 January 2021
Journal: EP Europace Journal , Volume 23 , Issue Supplement_1 , Pages i71 - i79
Authors: E. Vigmond , J. Bouyssier , J. Bayer , M. Haïssaguerre , H. Ashikaga

ESC Journals

AbstractAims

Clinical observations suggest that the Purkinje network can be part of anatomical re-entry circuits in monomorphic or polymorphic ventricular arrhythmias. However, significant conduction delay is needed to support anatomical re-entry given the high conduction velocity within the Purkinje network.

Methods and results

We investigated, in computer models, whether damage rendering the Purkinje network as either an active lesion with slow conduction or a passive lesion with no excitable ionic channel, could explain clinical observations. Active lesions had compromised sodium current and a severe reduction in gap junction coupling, while passive lesions remained coupled by gap junctions, but modelled the membrane as a fixed resistance. Both types of tissue could provide significant delays of over 100 ms. Electrograms consistent with those obtained clinically were reproduced. However, passive tissue could not support re-entry as electrotonic coupling across the delay effectively increased the proximal refractory period to an extremely long interval. Active tissue, conversely, could robustly maintain re-entry.

Conclusion

Formation of anatomical re-entry using the Purkinje network is possible through highly reduced gap junctional coupling leading to slowed conduction.

About the contributors

Edward J Vigmond

Bordeaux (IHU Liryc)

Role: Author

Julien Bouyssier

Role: Author

Jason Bayer

Role: Author