Why Ablation of Sites With Purkinje Activation Is Antiarrhythmic: The Interplay Between Fast Activation and Arrhythmogenesis

Coronel, Ruben; Potse, Mark; Haı̈ssaguerre, Michel; Derval, Nicolas; Rivaud, Mathilde R.; Meijborg, Veronique M.F.; Cluitmans, Matthijs; Hocini, Mélèze; Boukens, Bastiaan J.

doi:10.3389/fphys.2021.648396

Cited by 9 publications

(7 citation statements)

References 40 publications

(43 reference statements)

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“…The propensity of distal fascicles to produce reentry has been shown in prior computer studies, especially in association with cardiac structural pathologies. 21 , 31 , 32 A reduction in VF vulnerability has also been reported in experimental studies using modelling or ablation of the Purkinje network 9 , 30 , 33 , 34 ; and a termination of long-lasting VF has recently been published using radiofrequency ablation. 35 …”

Section: Discussionmentioning

confidence: 76%

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

Haı̈ssaguerre

Cheniti

Hocini

et al. 2022

European Heart Journal

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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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Section: Discussionmentioning

confidence: 76%

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

Haı̈ssaguerre

Cheniti

Hocini

et al. 2022

European Heart Journal

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“…Hypothetically, ablation of the Purkinje tissue could also prevent VF occurrence by reducing the propagation velocity within the Purkinje system and modifying the delicate balance between the elements involved. 12 …”

Section: Discussionmentioning

confidence: 99%

Long-term freedom from ventricular fibrillation despite persistent Purkinje ectopy after catheter ablation

Surget

Duchâteau

Lavergne

et al. 2022

HeartRhythm Case Reports

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“…Evidence suggests that if the PMJ activates myocardium close to repolarization gradients or heterogeneities, this increases the likelihood of conduction block and predisposes ventricular re-entry. 26 Furthermore, asymmetrical anterograde or retrograde conduction and source-sink mismatch at the PMJ sites may explain a subset of Purkinje-triggered human VF cases in the absence of any structural abnormality. 27 Supporting this mechanism is the finding that Purkinje-directed ablation is antiarrhythmic in patients with idiopathic VF, possibly due to reducing apparent propagation velocity.…”

Section: Discussionmentioning

confidence: 99%

“…27 Supporting this mechanism is the finding that Purkinje-directed ablation is antiarrhythmic in patients with idiopathic VF, possibly due to reducing apparent propagation velocity. 26,28 Recently, the role of human Purkinje has been studied in idiopathic VF. 29,30 Both focal and reentrant drivers were shown to maintain VF from the RV or LV (or both) corresponding to regions of structurally abnormalities in 62% of patients suggesting that scarred substrate acted as anchors for reentrant waves.…”

Section: Discussionmentioning

confidence: 99%

“…Within species, there is considerable variability of the Purkinje network, especially the terminal branches and the depth of fiber penetration into the ventricular myocardium. Evidence suggests that if the PMJ activates myocardium close to repolarization gradients or heterogeneities, this increases the likelihood of conduction block and predisposes ventricular re‐entry 26 . Furthermore, asymmetrical anterograde or retrograde conduction and source‐sink mismatch at the PMJ sites may explain a subset of Purkinje‐triggered human VF cases in the absence of any structural abnormality 27 .…”

Section: Discussionmentioning

confidence: 99%

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

Anderson

Massé

Asta

et al. 2022

Pacing Clinical Electrophis

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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.

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Why Ablation of Sites With Purkinje Activation Is Antiarrhythmic: The Interplay Between Fast Activation and Arrhythmogenesis

Cited by 9 publications

References 40 publications

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

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

Long-term freedom from ventricular fibrillation despite persistent Purkinje ectopy after catheter ablation

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

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