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Purkinje network and myocardial substrate at the onset of human ventricular fibrillation: implications for catheter ablation

AIMS: Mapping data of human ventricular fibrillation (VF) are limited. We performed detailed mapping of the activities underlying the onset of VF and targeted ablation in patients with structural cardiac abnormalities. METHODS AND RESULTS: We evaluated 54 patients (50 ± 16 years) with VF in the sett...

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Autores principales: Haissaguerre, Michel, Cheniti, Ghassen, Hocini, Meleze, Sacher, Frederic, Ramirez, F. Daniel, Cochet, Hubert, Bear, Laura, Tixier, Romain, Duchateau, Josselin, Walton, Rick, Surget, Elodie, Kamakura, Tsukasa, Marchand, Hugo, Derval, Nicolas, Bordachar, Pierre, Ploux, Sylvain, Takagi, Takamitsu, Pambrun, Thomas, Jais, Pierre, Labrousse, Louis, Strik, Mark, Ashikaga, Hiroshi, Calkins, Hugh, Vigmond, Ed, Nademanee, Koonlawee, Bernus, Olivier, Dubois, Remi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8934691/
https://www.ncbi.nlm.nih.gov/pubmed/35134898
http://dx.doi.org/10.1093/eurheartj/ehab893
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author Haissaguerre, Michel
Cheniti, Ghassen
Hocini, Meleze
Sacher, Frederic
Ramirez, F. Daniel
Cochet, Hubert
Bear, Laura
Tixier, Romain
Duchateau, Josselin
Walton, Rick
Surget, Elodie
Kamakura, Tsukasa
Marchand, Hugo
Derval, Nicolas
Bordachar, Pierre
Ploux, Sylvain
Takagi, Takamitsu
Pambrun, Thomas
Jais, Pierre
Labrousse, Louis
Strik, Mark
Ashikaga, Hiroshi
Calkins, Hugh
Vigmond, Ed
Nademanee, Koonlawee
Bernus, Olivier
Dubois, Remi
author_facet Haissaguerre, Michel
Cheniti, Ghassen
Hocini, Meleze
Sacher, Frederic
Ramirez, F. Daniel
Cochet, Hubert
Bear, Laura
Tixier, Romain
Duchateau, Josselin
Walton, Rick
Surget, Elodie
Kamakura, Tsukasa
Marchand, Hugo
Derval, Nicolas
Bordachar, Pierre
Ploux, Sylvain
Takagi, Takamitsu
Pambrun, Thomas
Jais, Pierre
Labrousse, Louis
Strik, Mark
Ashikaga, Hiroshi
Calkins, Hugh
Vigmond, Ed
Nademanee, Koonlawee
Bernus, Olivier
Dubois, Remi
author_sort Haissaguerre, Michel
collection PubMed
description AIMS: Mapping data of human ventricular fibrillation (VF) are limited. We performed detailed mapping of the activities underlying the onset of VF and targeted ablation in patients with structural cardiac abnormalities. METHODS AND RESULTS: We evaluated 54 patients (50 ± 16 years) with VF in the setting of ischaemic (n = 15), hypertrophic (n = 8) or dilated cardiomyopathy (n = 12), or Brugada syndrome (n = 19). Ventricular fibrillation was mapped using body-surface mapping to identify driver (reentrant and focal) areas and invasive Purkinje mapping. Purkinje drivers were defined as Purkinje activities faster than the local ventricular rate. Structural substrate was delineated by electrogram criteria and by imaging. Catheter ablation was performed in 41 patients with recurrent VF. Sixty-one episodes of spontaneous (n = 10) or induced (n = 51) VF were mapped. Ventricular fibrillation was organized for the initial 5.0 ± 3.4 s, exhibiting large wavefronts with similar cycle lengths (CLs) across both ventricles (197 ± 23 vs. 196 ± 22 ms, P = 0.9). Most drivers (81%) originated from areas associated with the structural substrate. The Purkinje system was implicated as a trigger or driver in 43% of patients with cardiomyopathy. The transition to disorganized VF was associated with the acceleration of initial reentrant activities (CL shortening from 187 ± 17 to 175 ± 20 ms, P < 0.001), then spatial dissemination of drivers. Purkinje and substrate ablation resulted in the reduction of VF recurrences from a pre-procedural median of seven episodes [interquartile range (IQR) 4–16] to 0 episode (IQR 0–2) (P < 0.001) at 56 ± 30 months. CONCLUSIONS: The onset of human VF is sustained by activities originating from Purkinje and structural substrate, before spreading throughout the ventricles to establish disorganized VF. Targeted ablation results in effective reduction of VF burden. KEY QUESTION: The initial phase of human ventricular fibrillation (VF) is critical as it involves the primary activities leading to sustained VF and arrhythmic sudden death. The origin of such activities is unknown. KEY FINDING: Body-surface mapping shows that most drivers (≈80%) during the initial VF phase originate from electrophysiologically defined structural substrates. Repetitive Purkinje activities can be elicited by programmed stimulation and are implicated as drivers in 37% of cardiomyopathy patients. TAKE-HOME MESSAGE: The onset of human VF is mostly associated with activities from the Purkinje network and structural substrate, before spreading throughout the ventricles to establish sustained VF. Targeted ablation reduces or eliminates VF recurrence.
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spelling pubmed-89346912022-03-21 Purkinje network and myocardial substrate at the onset of human ventricular fibrillation: implications for catheter ablation Haissaguerre, Michel Cheniti, Ghassen Hocini, Meleze Sacher, Frederic Ramirez, F. Daniel Cochet, Hubert Bear, Laura Tixier, Romain Duchateau, Josselin Walton, Rick Surget, Elodie Kamakura, Tsukasa Marchand, Hugo Derval, Nicolas Bordachar, Pierre Ploux, Sylvain Takagi, Takamitsu Pambrun, Thomas Jais, Pierre Labrousse, Louis Strik, Mark Ashikaga, Hiroshi Calkins, Hugh Vigmond, Ed Nademanee, Koonlawee Bernus, Olivier Dubois, Remi Eur Heart J Clinical Research AIMS: Mapping data of human ventricular fibrillation (VF) are limited. We performed detailed mapping of the activities underlying the onset of VF and targeted ablation in patients with structural cardiac abnormalities. METHODS AND RESULTS: We evaluated 54 patients (50 ± 16 years) with VF in the setting of ischaemic (n = 15), hypertrophic (n = 8) or dilated cardiomyopathy (n = 12), or Brugada syndrome (n = 19). Ventricular fibrillation was mapped using body-surface mapping to identify driver (reentrant and focal) areas and invasive Purkinje mapping. Purkinje drivers were defined as Purkinje activities faster than the local ventricular rate. Structural substrate was delineated by electrogram criteria and by imaging. Catheter ablation was performed in 41 patients with recurrent VF. Sixty-one episodes of spontaneous (n = 10) or induced (n = 51) VF were mapped. Ventricular fibrillation was organized for the initial 5.0 ± 3.4 s, exhibiting large wavefronts with similar cycle lengths (CLs) across both ventricles (197 ± 23 vs. 196 ± 22 ms, P = 0.9). Most drivers (81%) originated from areas associated with the structural substrate. The Purkinje system was implicated as a trigger or driver in 43% of patients with cardiomyopathy. The transition to disorganized VF was associated with the acceleration of initial reentrant activities (CL shortening from 187 ± 17 to 175 ± 20 ms, P < 0.001), then spatial dissemination of drivers. Purkinje and substrate ablation resulted in the reduction of VF recurrences from a pre-procedural median of seven episodes [interquartile range (IQR) 4–16] to 0 episode (IQR 0–2) (P < 0.001) at 56 ± 30 months. CONCLUSIONS: The onset of human VF is sustained by activities originating from Purkinje and structural substrate, before spreading throughout the ventricles to establish disorganized VF. Targeted ablation results in effective reduction of VF burden. KEY QUESTION: The initial phase of human ventricular fibrillation (VF) is critical as it involves the primary activities leading to sustained VF and arrhythmic sudden death. The origin of such activities is unknown. KEY FINDING: Body-surface mapping shows that most drivers (≈80%) during the initial VF phase originate from electrophysiologically defined structural substrates. Repetitive Purkinje activities can be elicited by programmed stimulation and are implicated as drivers in 37% of cardiomyopathy patients. TAKE-HOME MESSAGE: The onset of human VF is mostly associated with activities from the Purkinje network and structural substrate, before spreading throughout the ventricles to establish sustained VF. Targeted ablation reduces or eliminates VF recurrence. Oxford University Press 2022-02-04 /pmc/articles/PMC8934691/ /pubmed/35134898 http://dx.doi.org/10.1093/eurheartj/ehab893 Text en © The Author(s) 2022. Published by Oxford University Press on behalf of European Society of Cardiology. https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle Clinical Research
Haissaguerre, Michel
Cheniti, Ghassen
Hocini, Meleze
Sacher, Frederic
Ramirez, F. Daniel
Cochet, Hubert
Bear, Laura
Tixier, Romain
Duchateau, Josselin
Walton, Rick
Surget, Elodie
Kamakura, Tsukasa
Marchand, Hugo
Derval, Nicolas
Bordachar, Pierre
Ploux, Sylvain
Takagi, Takamitsu
Pambrun, Thomas
Jais, Pierre
Labrousse, Louis
Strik, Mark
Ashikaga, Hiroshi
Calkins, Hugh
Vigmond, Ed
Nademanee, Koonlawee
Bernus, Olivier
Dubois, Remi
Purkinje network and myocardial substrate at the onset of human ventricular fibrillation: implications for catheter ablation
title Purkinje network and myocardial substrate at the onset of human ventricular fibrillation: implications for catheter ablation
title_full Purkinje network and myocardial substrate at the onset of human ventricular fibrillation: implications for catheter ablation
title_fullStr Purkinje network and myocardial substrate at the onset of human ventricular fibrillation: implications for catheter ablation
title_full_unstemmed Purkinje network and myocardial substrate at the onset of human ventricular fibrillation: implications for catheter ablation
title_short Purkinje network and myocardial substrate at the onset of human ventricular fibrillation: implications for catheter ablation
title_sort purkinje network and myocardial substrate at the onset of human ventricular fibrillation: implications for catheter ablation
topic Clinical Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8934691/
https://www.ncbi.nlm.nih.gov/pubmed/35134898
http://dx.doi.org/10.1093/eurheartj/ehab893
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