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

Figures

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  Figure 1. A: (Left) Electrocardiogram (ECG) on admission of patient in case 1 shows a premature ventricular complex (PVC) with a short coupling interval (CI) at 280 ms. The sharp and rapid onset of the PVC and its left bundle branch block morphology are in favor of right Purkinje ectopy. (Right) Twelve-lead ECG during the follow-up shows the same PVC with a coupling interval at 300 ms. B: (Left) ECG before the ablation of patient in case 2 shows a right Purkinje ectopy with a coupling interval at 300 ms. (Right) During the follow-up, the 12-lead Holter ECG in case 2 shows right Purkinje ectopy with a short CI at 355 ms and a variation of morphology in V2, probably because of a V2 lead misplacement (inconsistent R-wave progression in V2 in sinus rhythm). C: Implantable cardioverter-defibrillator interrogation of patient in case 3 shows PVC with a short coupling interval at 300 ms.

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  Figure 2. Annual 24-hour Holters after ablation of patient in case 2. A: Premature ventricular contractions (PVCs) recorded on Holter electrocardiogram. B: Persistence of isolated PVCs after ablation. C: Mean coupling interval of the postablation PVCs.

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  Figure 3. Left: Purkinje ectopy is induced by triggered activity and spreads in the Purkinje network thanks to a mechanism of reentry essential for ventricular fibrillation (VF) initiation. Right: Ablation of the Purkinje network and the surrounding tissue prevents reentry in the Purkinje network, leading to isolated Purkinje ectopy without VF episode.