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Arrhythmia Rounds Section Editor: George J. Klein, M.D.

Disruption of the Purkinje Network Causing Polymorphic Ventricular Tachycardia TAKEKUNI HAYASHI, M.D., TAKESHI MITSUHASHI, M.D., Ph.D., HIDEO FUJITA, M.D., Ph.D., and SHIN-ICHI MOMOMURA, M.D., Ph.D. From the Division of Cardiovascular Medicine, Saitama Medical Center, Jichi Medical University, Saitama, Japan

polymorphic ventricular tachycardia, Purkinje potential, ventricular fibrillation, ventricular premature contraction Case Presentation An 18-year-old woman without structural heart disease presented with multiple episodes of syncope. A 24-hour Holter electrocardiogram revealed multiple episodes of nonsustained polymorphic ventricular tachycardia (PVT) initiated by a short-coupled ventricular premature contraction (VPC). The initiating form of the VPC consistently had a right bundle branch block (RBBB) configuration with an inferior-axis deviation; however, there was a slightly different morphology in the initiation of VPC. An implantable cardioverterdefibrillator (ICD) was implanted to prevent sudden cardiac death. One year later, she had frequent ICD shocks for PVT. After obtaining written informed consent, an electrophysiological study (EPS) was performed. Two types of PVT were recorded before the catheter was inserted (Fig. 1A). For both, the initial VPC morphology was an RBBB with inferior-axis deviation, but there was a slightly different morphology in the initiation of VPC. After an octapolar electrode catheter was placed at the left ventricular septum, multiple VPCs were recorded (Fig. 1B). Presystolic Purkinje potentials were recorded during sinus rhythm. During the VPC, Purkinje potentials were recorded at the phase of early-diastolic, middiastolic, and presystolic. The difference in the conduction time between the mid-diastolic Purkinje potential and presystolic Purkinje potential dictated the morphology of the VPC. Before VPC4, the conduction times between the early diastolic Prukinje potential and mid-diastolic Purkinje potential were gradually shortened (120–110–95 ms) with an intraPrukinje block. The next conduction time was prolonged to 125 ms, conducting VPC4 (Fig. 2A). Interestingly, variJ Cardiovasc Electrophysiol, Vol. 26, pp. 1279-1281, November 2015. Disclosures: None. Address for correspondence: Takekuni Hayashi, M.D., Division of Cardiovascular Medicine, Saitama Medical Center, Jichi Medical University, 1–847, Amanuma, Oomiya-ku, Saitama 330–8503, Japan. Fax: +81-48647-5188; E-mail: [email protected] Manuscript received 16 April 2015; Revised manuscript received 27 April 2015; Accepted for publication 5 May 2015. doi: 10.1111/jce.12735

ous intra-Purkinje conductions occurred without conducting VPC (Fig. 2B). A spontaneously nonsustained PVT is shown in Figure 3A. Based on these observations, where is the initial ablation target? Commentary Radiofrequency catheter ablation of the triggered VPC is an optional therapeutic approach in patients with multiple episodes of ventricular fibrillation (VF) or PVT that is initiated by VPC. Ha¨ıssaguerre et al. reported that catheter ablation of idiopathic VF initiates from the VPC originating in the Purkinje network, and ablation for idiopathic VF has been increasingly reported during the last decade.1 When ablation is attempted, the earliest activation site of the Purkinje potential preceding the VPC should be identified. However, catheter ablation of the triggered VPC is challenging when the earliest activation site cannot be identified or is located close to the His bundle. Therefore, a substrate modification of the Purkinje network should be considered.2 Nogami et al. showed that VF was suppressed during 14 years of follow-up after catheter ablation of the Purkinje network.3 In their case, the polymorphic QRS morphology during the initiation of the PVT has been constantly changed, which resulted from the changing propagation in the Purkinje arborization. Furthermore, the suppression of VF was achieved with catheter ablation to the Purkinje network, not ablation to the earliest Purkinje activation. Therefore, they hypothesized that reentry in the Purkinje system was essential for the initiation of VF in their case. In the present case, the morphology of the triggered VPC at the initiation of PVT, in which at least two types were recorded during the EPS, and the polymorphic QRS morphology during the initiation of PVT did not constantly change. Although the morphology of the triggered VPC was different, these were matched in terms of the RBBB and inferior-axis deviation. Initially, radiofrequency catheter ablation was applied in the left ventricular septum 13 and 14, wherein the earliest mid-diastolic Purkinje potential was recorded before VPC3, and the ablation was ceased because junctional rhythm occurred during ablation. The early-diastolic and mid-diastolic Purkinje potentials preceded the VPCs, and VPC was conducted when the conduction time between the early diastolic and mid-diastolic

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Figure 1. A: Two types of polymorphic ventricular tachycardia are recorded during the cardiac electrophysiology study. B: Intracardiac electrocardiograms showing four major types of VPCs.

Figure 2. A: Intracardiac electrocardiograms showed intra-Purkinje conduction before ventricular premature contraction (VPC) 4. B: Intracardiac electrocardiograms showing multiple intra-Purkinje conductions without conducting VPC.

Purkinje potentials was >120 ms. Interestingly, the firing of Purkinje potential was observed such as repetitive ventricular response by programmed stimulation when the coupling interval between the early-diastolic Purkinje potential and middiastolic Purkinje potential was shortened from 120 to 110 ms (Fig. 2A). Subsequently, an intra-Purkinje block occurred

when the coupling interval was shortened from 110 to 95 ms. Furthermore, at the initiation of the PVT, the intervals between the Purkinje potentials were gradually shortened, and thereby an intra-Purkinje block occurred. Hence, ablation was performed at the distal portion of the Purkinje potentials to disconnect the Purkinje network.

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Figure 3. Catheter ablation of the Purkinje network. A: Intracardiac electrocardiograms showing polymorphic ventricular tachycardia by an initiating ventricular premature contraction (VPC) 3. The earliest preceding Purkinje potential is recorded in the left ventricular (LV) septum 13–14. B: The catheter position and ablation site using the CARTO system. C: After ablation, only VPC5 remains. Before VPC5, the earliest preceding mid-diastolic Purkinje potentials are recorded near the main trunk of the left bundle. In addition, isolated delayed Purkinje potentials are recorded at the mid to distal potion of the left bundle.

After ablation, the only VPC5, of which the morphology was different from the VPC recording before ablation, remained. Before VPC5, the earliest preceding mid-diastolic Prukinje potentials were recorded near the main trunk of the left bundle, and isolated delayed Purkinje potentials were recorded at the mid to distal potion of the left bundle (Fig. 3C). One week after ablation, the patient had ICD appropriate shock. However, over the 1-year follow-up, she never had ICD shock again. Although the telemetry of ICD showed nonsustained VT >3,000 episodes per 3 months before ablation, it was dramatically reduced (

Disruption of the Purkinje Network Causing Polymorphic Ventricular Tachycardia.

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