Edward J Vigmond1,2, Julien Bouyssier1,2, Jason Bayer1,2, Michel Haïssaguerre1,3,4, Hiroshi Ashikaga1,5. 1. IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, F-33600 Pessac-Bordeaux, France. 2. Univ. Bordeaux, IMB, UMR 5251, F-33400 Talence, France. 3. Univ. Bordeaux, Centre de recherche Cardio-Thoracique de Bordeaux, U1045, F-33000 Bordeaux, France. 4. Bordeaux University Hospital (CHU), Electrophysiology and Ablation Unit, F-33600 Pessac, France. 5. Cardiac Arrhythmia Service, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Abstract
AIMS: 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. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: 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. Published on behalf of the European Society of Cardiology. All rights reserved.
Authors: Michel Haissaguerre; Ghassen Cheniti; Meleze Hocini; Frederic Sacher; F Daniel Ramirez; Hubert Cochet; Laura Bear; Romain Tixier; Josselin Duchateau; Rick Walton; Elodie Surget; Tsukasa Kamakura; Hugo Marchand; Nicolas Derval; Pierre Bordachar; Sylvain Ploux; Takamitsu Takagi; Thomas Pambrun; Pierre Jais; Louis Labrousse; Mark Strik; Hiroshi Ashikaga; Hugh Calkins; Ed Vigmond; Koonlawee Nademanee; Olivier Bernus; Remi Dubois Journal: Eur Heart J Date: 2022-03-21 Impact factor: 29.983