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Idiopathic premature ventricular contraction–triggered ventricular fibrillation: Subcutaneous implantable cardioverter-defibrillator (S-ICD) template matched ablation in the absence of inducible clinical premature ventricular contraction

Open AccessPublished:January 15, 2023DOI:https://doi.org/10.1016/j.hrcr.2023.01.004

      Keywords

      Key Teaching Points
      • Premature ventricular contraction (PVC)–triggered idiopathic ventricular fibrillation requires successful elimination of the PVC.
      • In the absence of clinical PVC during the ablation procedure, implantable cardioverter-defibrillator (ICD) template matching is the next available choice.
      • Subcutaneous ICD template matching has not been previously reported and was used in this case, with a successful outcome.

      Introduction

      Idiopathic ventricular fibrillation is diagnosed in patients who have survived sudden cardiac arrest from ventricular fibrillation (VF) without identifiable structural heart disease.
      • Rattanawong P.
      • Ladia V.
      • Minaskeian N.
      • et al.
      Empirical ablation to prevent sequential Purkinje system recruitment.
      It is the main cause of unexplained sudden cardiac death, particularly in young patients under the age of 35.
      • Cheniti G.
      • Vlachos K.
      • Meo M.
      • et al.
      Mapping and ablation of idiopathic ventricular fibrillation.
      An implantable cardioverter-defibrillator (ICD) is usually recommended for the secondary prevention of sudden cardiac death. VF ablation is recommended for clinical VF recurrence and for reducing the number of ICD shocks.
      • Priori S.G.
      • Blomström-Lundqvist C.
      • Mazzanti A.
      • et al.
      ESC Scientific Document Group
      2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: The Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC). Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC).
      ,
      • Priori S.G.
      • Wilde A.A.
      • Horie M.
      • et al.
      HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes: document endorsed by HRS, EHRA, and APHRS in May 2013 and by ACCF, AHA, PACES, and AEPC in June 2013.
      In this case report, we sought a VF ablation strategy that used analysis of stored subcutaneous ICD (S-ICD) electrograms in the absence of inducible premature ventricular contractions (PVCs) for template matching during ablation.

      Case report

      The subject was a 30-year-old previously healthy female patient with no known antecedent cardiovascular disease until 2019, when she had an out-of-hospital cardiac arrest with bystander resuscitation. She was found to be in VF and was defibrillated by the paramedics twice on the way to the hospital. Later an S-ICD was placed and she was started on quinidine, which was not well tolerated. Subsequently, a different electrophysiologist switched to disopyramide, which was discontinued quickly owing to a lack of efficacy and side effects. Extensive investigations were negative, including a coronary angiogram, stress testing, magnetic resonance imaging, and genetic testing.
      She presented to our institution at the end of 2021 with 6 appropriate S-ICD shocks. Resting 12-lead electrocardiogram is normal with no significant abnormalities to suggest arrhythmogenic right ventricular dysplasia or Brugada syndrome. S-ICD transmissions showed short-coupled PVC–mediated (coupling interval 260 ms, Figure 1A ) polymorphic ventricular tachycardia falling into the category of idiopathic VF, for which ablation was planned in early 2022. Beta-blockade with nadolol was initiated.
      Figure thumbnail gr1
      Figure 1A: Premature ventricular contraction (PVC) triggered ventricular fibrillation during the clinical event recorded on subcutaneous implantable cardioverter-defibrillator. B: PVC morphology in a 12-lead electrocardiogram. C: Clinical PVC replication during ablation of targeted PVC.
      A comprehensive electrophysiology evaluation was done with 3D Mapping – NavX (Abbott, Abbott Park, IL) and an intracardiac echocardiogram (ICE; Acuson Ultrasound catheter; Biosense Webster, Irvine, CA).

      Clinical PVC

      Left bundle branch morphology, coupling interval of 260 ms with a negative concordance of the precordial leads and left superior axis, was noted during this procedure, similar to the PVC documented during hospitalization at an outside facility (Figure 1B). PVC was mapped to the moderator band area, which resolved after ablation at free wall insertion of the moderator band. Despite high doses of epinephrine infusion and atrial and ventricular burst pacing, no recurrence was noted.
      Follow-up was normal without arrhythmia, and beta-blocker was discontinued 3 months postprocedure until 5 months after ablation, when she developed 2 PVC-triggered VF episodes, which required flecainide and reablation under conscious sedation.

      Second procedure description

      An 8F sheath was placed in the right femoral vein. We advanced a 3.5 mm irrigated ablation catheter into the right ventricle (RV) over an Agilis medium curve sheath (Abbott, Abbott Park, IL) for mapping and ablation. A 6F sheath was placed in the right femoral vein, through which a deflectable quadripolar catheter was advanced into the His bundle location. A 9F sheath was placed in the right femoral vein, through which we advanced an ICE (CartoSound; Biosense Webster, Irvine, CA) catheter into the right atrium and RV. Using ICE, RV surrogate geometry, including the moderator band, was registered and used as a guide for ablation.

      Intraprocedural findings

      The patient’s S-ICD had shown 2 episodes of PVC-triggered VF with a baseline sinus cycle length of 780 ms and a coupling interval of 260 ms. Unfortunately, the ablation catheter stimulation of the RV with matching the same cycle length and extrastimulus as the clinical event did not induce any VF. Aggressive burst pacing and programmed extrastimulus testing did not trigger clinical PVC or VF. Throughout the procedure, the patient did not have the clinical PVC for mapping or comparison for pace mapping.
      Subsequently, administering isoproterenol and dopamine/dobutamine combination did not induce the arrhythmia. A different strategy was pursued to map the PVC; a 3-pronged confirmation of the clinical PVC was attempted:
      • (1)
        The clinical PVC, documented in the clinic (Figure 1B) when the patient had trigeminy, was used as a template.
      • (2)
        The PVC that was ablated in early 2022 was similar and was used for an additional template matching using 12 leads (both of the above are visual comparisons only, as they are not real-time comparisons).
      • (3)
        We used the subcutaneous ICD tracings (where the PVCs triggered VF) for an S-ICD template match (Figure 1C). This became the primary strategy during the procedure.
      The stored S-ICD electrogram of all the VF events had the same PVC morphology with almost identical coupling intervals. Within the limitations of comparison, the PVC recorded in the 12-lead electrocardiogram (ECG) closely resembled the S-ICD-recorded PVCs triggering polymorphic ventricular tachycardia. Therefore, it became relevant to target this PVC.
      All 3 confirmed that the lateral edge of the moderator band was most likely the source of the PVC that triggers VF. We hypothesized that the moderator band with terminal arborizing fibers of the right bundle branch had connections with the PVC site, which allows conduction to the rest of the Purkinje system triggering VF. Therefore, we decided to ablate the entire moderator band from the lateral edge to the septal edge, as this is a second procedure. The moderator band was imaged using ICE imaging, stored in the electroanatomical mapping system, and guided the ablation spatially (Figure 2). For the lateral edge, we used 30 W; in the middle, we used 35 W; and for the septal portions, we used 40 W with an irrigated catheter. A prolonged duration (60 seconds) of ablations was delivered to ensure significant electrogram attenuation and eliminate the possibility of connections with the rest of the Purkinje system.
      Figure thumbnail gr2
      Figure 2Intracardiac echocardiogram images of moderator band and tagged ablation lesions.
      Interestingly, the middle of the moderator band had a mass-like protrusion, and this was heavily targeted for ablation, as the fibers could be well insulated at this location. During the ablation lesion sets, there was a flurry of PVCs (Figure 3A ) and nonsustained ventricular tachycardia similar to the QRS morphology of the 12-lead ECG and matched the template on S-ICD. Multiple consolidative long-duration lesions were delivered. Owing to recording saturation, it was not possible to discern Purkinje, high-frequency near-field potential during ablation, but Purkinje potential was visible during sinus rhythm between ablation lesions (Figure 3B). We did not attempt to induce, as the patient was not inducible initially, and flecainide was discontinued.
      Figure thumbnail gr3
      Figure 3A: Nonsustained ventricular tachycardia during ablation mimicking clinical premature ventricular contractions. B: Purkinje potential during sinus rhythm between ablations.
      Follow-up 1 week later and at 4 months revealed no arrhythmia while continuing metoprolol 25 mg daily.

      Discussion

      The correct diagnosis of idiopathic VF requires extensive diagnostic testing. Routine testing excludes the most common causes of VF. Routine testing usually comprises blood chemistry (cardiac enzymes, electrolytes, and thyroid function), toxicological screening, ECG, chest radiograph, echocardiography, exercise testing, Holter or telemetry monitoring, coronary angiography with or without ventriculography, and magnetic resonance imaging.
      • Visser M.
      • van der Heijden J.F.
      • Doevendans P.A.
      • Loh P.
      • Wilde A.A.
      • Hassink R.J.
      Idiopathic ventricular fibrillation: the struggle for definition, diagnosis, and follow-up.
      Generally, genetic screening with a sudden death panel of genes is frequently done, which was negative in our patient.
      In most cases, VF is triggered by PVCs originating from the Purkinje network. Ablation of VF triggers in this setting is associated with high rates of acute success and long-term freedom from VF recurrence. In the absence of spontaneous or inducible PVCs, pace mapping may indicate the area of interest.
      • Cheniti G.
      • Vlachos K.
      • Meo M.
      • et al.
      Mapping and ablation of idiopathic ventricular fibrillation.
      In case of lack of spontaneous or provoked clinical ventricular ectopy, electrograms from the ICD are the last source of ectopy that can be used for template matching.
      Usage of stored ICD electrograms focusing on likely target areas permits ablation when triggering ectopy or VF was unable to be induced at the time of ablation.
      • Lowery C.M.
      • Tzou W.S.
      • Aleong R.G.
      • et al.
      Use of stored implanted cardiac defibrillator electrograms in catheter ablation of ventricular fibrillation.
      The transvenous ICD relies on a near-field electrogram for detection. Far-field electrogram can be recorded between the coil and the can, but the coil is intravascular, vastly different from a subcutaneous coil of the S-ICD. The subcutaneous tracing resembles the surface ECG more closely than the far-field electrogram of the transvenous ICD.
      PVC-triggered VF in patients with structurally normal hearts can originate from the Purkinje fibers of the moderator band. A recent study regarding the empiric ablation of polymorphic ventricular tachycardia/fibrillation in the absence of a mappable trigger reported that the pace map match for the stored transvenous ICD template electrograms of the clinical PVC trigger within the RV moderator band region is 14% of ablation targets (left Purkinje network, 55%).
      • Salazar P.
      • Beaser A.D.
      • Upadhyay G.A.
      • et al.
      Empiric ablation of polymorphic ventricular tachycardia/fibrillation in the absence of a mappable trigger: prospective feasibility and efficacy of pacemap matching to defibrillator electrograms.
      The RV moderator band extends from the septum to the free wall and is a muscular structure containing RV Purkinje fibers. PVCs arising from the moderator band have a distinctive ECG morphology and are not infrequently associated with PVC-induced VF in patients with structurally normal hearts. Catheter ablation of these PVCs can be challenging but is facilitated by ICE guidance and can be safely performed with excellent long-term outcomes. Ablation therapy is targeted at the body and free-wall insertion of the moderator band, and challenges include catheter contact and stability in this intracavitary structure. Intracardiac echocardiography can aid in the anatomic identification of the moderator band and catheter placement. Long-term ablation outcomes are excellent, with no sustained ventricular arrhythmias and no device therapies in follow-up. However, some patients may have recurrence after an arrhythmia-free period and require a second procedure.
      • Sadek M.M.
      • Benhayon D.
      • Sureddi R.
      • et al.
      Idiopathic ventricular arrhythmias originating from the moderator band: electrocardiographic characteristics and treatment by catheter ablation.
      Empirical fascicular ablation and mid-Purkinje transection through radiofrequency ablation in specific patients with idiopathic VF who have VF with documented short-coupled PVCs but a lack of spontaneous or inducible short-coupled PVCs were also reported.1 But, in this patient, based on available data, focusing on the moderator band alone was considered appropriate.
      In the absence of triggering spontaneous PVCs, using an S-ICD template has not been reported earlier and may have utility in these cases.

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