Role of Purkinje-muscle junction in early ventricular fibrillation in a porcine model: Beyond the trigger concept.


Journal

Pacing and clinical electrophysiology : PACE
ISSN: 1540-8159
Titre abrégé: Pacing Clin Electrophysiol
Pays: United States
ID NLM: 7803944

Informations de publication

Date de publication:
06 2022
Historique:
revised: 01 01 2022
received: 02 11 2021
accepted: 14 01 2022
pubmed: 25 1 2022
medline: 22 6 2022
entrez: 24 1 2022
Statut: ppublish

Résumé

The role of the Purkinje network in triggering ventricular fibrillation (VF) has been studied; however, its involvement after onset and in early maintenance of VF is controversial. We studied the role of the Purkinje-muscle junctions (PMJ) on epicardial-endocardial activation gradients during early VF. In a healthy, porcine, beating-heart Langendorff model [control, n = 5; ablation, n = 5], simultaneous epicardial-endocardial dominant frequent mapping was used (224 unipolar electrograms) to calculate activation rate gradients during the onset and early phase of VF. Selective Purkinje ablation was performed using Lugol's solution, followed by VF re-induction and mapping and finally, histological evaluation. Epicardial activation rates were faster than endocardial rates for both onset and early VF. After PMJ ablation, activation rates decreased epicardially and endocardially for both onset and early VF [Epi: 9.7 ± 0.2 to 8.3 ± 0.2 Hz (p <.0001) and 10.9 ± 0.4 to 8.8 ± 0.3 Hz (p < .0001), respectively; Endo: 8.2 ± 0.3 Hz to 7.4 ± 0.2 Hz (p < .0001) and 7.0 ± 0.4 Hz to 6.6 ± 0.3 Hz (p = .0002), respectively]. In controls, epicardial-endocardial activation rate gradients during onset and early VF were 1.7 ± 0.3 Hz and 4.5 ± 0.4 Hz (p < .001), respectively. After endocardial ablation of PMJs, these gradients were reduced to 0.9 ± 0.3 Hz (onset VF, p < .001) and to 2.2 ± 0.3 Hz (early VF, p <.001). Endocardial-epicardial Purkinje fiber arborization and selective Purkinje fiber extinction after only endocardial ablation (not with epicardial ablation) was confirmed on histological analysis. Beyond the trigger paradigm, PMJs determine activation rate gradients during onset and during early maintenance of VF.

Sections du résumé

BACKGROUND
The role of the Purkinje network in triggering ventricular fibrillation (VF) has been studied; however, its involvement after onset and in early maintenance of VF is controversial.
AIM
We studied the role of the Purkinje-muscle junctions (PMJ) on epicardial-endocardial activation gradients during early VF.
METHODS
In a healthy, porcine, beating-heart Langendorff model [control, n = 5; ablation, n = 5], simultaneous epicardial-endocardial dominant frequent mapping was used (224 unipolar electrograms) to calculate activation rate gradients during the onset and early phase of VF. Selective Purkinje ablation was performed using Lugol's solution, followed by VF re-induction and mapping and finally, histological evaluation.
RESULTS
Epicardial activation rates were faster than endocardial rates for both onset and early VF. After PMJ ablation, activation rates decreased epicardially and endocardially for both onset and early VF [Epi: 9.7 ± 0.2 to 8.3 ± 0.2 Hz (p <.0001) and 10.9 ± 0.4 to 8.8 ± 0.3 Hz (p < .0001), respectively; Endo: 8.2 ± 0.3 Hz to 7.4 ± 0.2 Hz (p < .0001) and 7.0 ± 0.4 Hz to 6.6 ± 0.3 Hz (p = .0002), respectively]. In controls, epicardial-endocardial activation rate gradients during onset and early VF were 1.7 ± 0.3 Hz and 4.5 ± 0.4 Hz (p < .001), respectively. After endocardial ablation of PMJs, these gradients were reduced to 0.9 ± 0.3 Hz (onset VF, p < .001) and to 2.2 ± 0.3 Hz (early VF, p <.001). Endocardial-epicardial Purkinje fiber arborization and selective Purkinje fiber extinction after only endocardial ablation (not with epicardial ablation) was confirmed on histological analysis.
CONCLUSIONS
Beyond the trigger paradigm, PMJs determine activation rate gradients during onset and during early maintenance of VF.

Identifiants

pubmed: 35067947
doi: 10.1111/pace.14453
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

742-751

Informations de copyright

© 2022 Wiley Periodicals LLC.

Références

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Auteurs

Robert D Anderson (RD)

The Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, Toronto, Canada.

Stéphane Massé (S)

The Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, Toronto, Canada.

John Asta (J)

The Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, Toronto, Canada.

Patrick F H Lai (PFH)

The Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, Toronto, Canada.

Praloy Chakraborty (P)

The Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, Toronto, Canada.

Mohammed Ali Azam (MA)

The Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, Toronto, Canada.

Eugene Downar (E)

The Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, Toronto, Canada.

Kumaraswamy Nanthakumar (K)

The Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, Toronto, Canada.

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