Termination of long-duration ventricular fibrillation by catheter ablation

Hasegawa, Tomoaki; Nogami, Akihiko; Aonuma, Kazutaka; Ieda, Masaki

doi:10.1016/j.hrcr.2020.10.002

Cited by 6 publications

(3 citation statements)

References 15 publications

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“… 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: 99%

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: 99%

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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“…Of note, surrounding ablation was performed in case of early Purkinje activation during ablation. In a case report by Hasegawa et al, frequent episodes of VF were mapped under extracorporeal membrane oxygenation and a nearly regular Purkinje activation could be demonstrated during long-lasting arrhythmia episodes (17). Ablation resulted in the termination of VF within minutes after the ablation of Purkinje signals in this case.…”

Section: Mechanisms Of Initiation and Maintenance Of Ventricular Fibr...mentioning

confidence: 52%

Catheter ablation in patients with ventricular fibrillation by purkinje de-networking

Sciacca

Fink

Guckel

et al. 2022

Front. Cardiovasc. Med.

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BackgroundVentricular fibrillation (VF) is a leading cause of cardiovascular death worldwide. However, recurrence rates of arrhythmia are high leading to mortality and morbidity. Recently, Purkinje fibers have been identified as potential sources of VF initiation and maintenance.AimThe study analyzes the feasibility and effectiveness of catheter ablation in patients with recurrent VF by specific Purkinje de-networking (PDN).MethodsConsecutive patients with recurrent VF undergoing PDN were included in this observational study. The procedural endpoint was the non-inducibility of sustained ventricular arrhythmia. A three-dimensional -anatomical mapping was conducted, and the specific cardiac conduction system and Purkinje fibers were tagged. All detectable Purkinje signals were ablated in the left ventricle (LV). Additional right ventricular (RV) PDN was performed in case of VF inducibility after LV ablation. Follow-up was performed by patient visits at our outpatient clinic including device interrogation and by telephone interviews.ResultsEight patients were included in the study. Six patients were females (75%); the median age during the procedure was 43 [37;57] years and the median body mass index was 24 [23;33] kg/m2. Four patients (50%) had known structural heart disease with two cases of ischemic cardiomyopathy and two cases of dilated cardiomyopathy. In four patients (50%), no underlying structural heart disease could be identified. The median LV ejection fraction was 42 ± 16.4%. All patients had an implantable cardioverter-defibrillator (ICD) prior to ablation with documentation of recurrent VF. The median number of ICD shocks before the ablation was 5 [3;7]. LV PDN was performed in all patients. In two patients (25%), an additional RV PDN was performed. Non-inducibility of any ventricular arrhythmia was achieved in all patients after PDN. Two patients showed complete left bundle branch block post-ablation. The median follow-up duration was 264 [58;421] days. Two patients (25%) experienced ventricular arrhythmia recurrence with recurrent ICD-shock delivery. One patient died during follow-up with an unknown cause of death. Six patients (75%) experienced no arrhythmia recurrence during follow-up.ConclusionPurkinje de-networking represents a novel treatment option for patients with recurrent VF without arrhythmia substrate or specific arrhythmia triggers with promising results in terms of efficiency and feasibility. Larger and more prospective studies are needed for a systematic evaluation.

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“… 2 Its role as a trigger has been demonstrated particularly in the context of ischemic heart disease and in idiopathic VF, but also in a variety of other types of cardiac disease, including HCM. 5 , 6 , 7 Its role as a maintaining driver has been the subject of controversy, because experimentally induced VF could evolve either with or without Purkinje fiber involvement. These apparent discrepancies may be related to distinct experimental and structural conditions and the timing of VF recordings.…”

Section: Discussionmentioning

confidence: 99%

Two-to-one Purkinje-to-myocardium activation during ventricular fibrillation associated with hypertrophic cardiomyopathy

Waldmann¹,

Iserin²,

Vigmond³

et al. 2023

HeartRhythm Case Reports

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Termination of long-duration ventricular fibrillation by catheter ablation

Cited by 6 publications

References 15 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

Catheter ablation in patients with ventricular fibrillation by purkinje de-networking

Two-to-one Purkinje-to-myocardium activation during ventricular fibrillation associated with hypertrophic cardiomyopathy

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