Catheter Ablation of Idiopathic Ventricular Fibrillation: A Role For The Moderator Band

John L. Sapp MD, Christopher Gray MD, Ratika Parkash MD, Magdy Basta MD, Josee Michaud MD, Ahmed El-Damaty MD, Ali Khadem MD, Jeremy Wood MD, Martin Gardner MD

QEII Health Sciences Centre, Dalhousie University, Halifax, Canada

Case Presentation
Case 1: A 39 y.o. man with no structural heart disease and known short-coupled PVCs initiating torsades de pointes and ventricular fibrillation was referred for ablation due to side-effects of antiarrhythmic drugs. 3D electroanatomic mapping of the very frequent PVCs during intracardiac echocardiography revealed that the earliest intracardiac activation during PVCs was associated with a discrete early potential preceding the QRS on the moderator band. At this site, a Purkinje potential was seen during sinus rhythm. Ablation at this site abolished recurrent ventricular fibrillation. Case 2: A 42 year-old man had an ICD implanted 3 years ago after a resuscitated cardiac arrest. No evidence of coronary disease, ion channelopathy, nor of structural heart disease despite extensive investigation. Presented with multiple ICD shocks and was found to have recurrent appropriate shocks for ventricular fibrillation. He received 54 internal and external shocks for recurrent ventricular fibrillation despite amiodarone, verapamil, lidocaine, procainamide, metoprolol, phenytoin, flecainide, intubation and general anaesthesia Each VF was initiated by a monomorphic PVC with left bundle branch block morphology, leftward axis, transition V5 (See figure 1). Mapping was severely limited by extremely frequent ventricular fibrillation. Two ablation procedures were performed targeting sites of early Purkinje potentials during ectopy on the moderator band. Recurrent VF resulted in approximately 100 shocks; subsequent LV ejection fraction was severely reduced. A second ablation procedure was performed with TEE guidance and ECMO support, and irrigated RF was delivered at along the entire moderator band and right bundle proximal to the moderator band. PVCs remained absent for >5 days, but then recurred and were associated with further VF. Surgical cryoablation of the distal RV septum and RV free wall as well as resection of the moderator band was performed. No further VF has been seen in follow-up. RV dysfunction has been treated medically.

ECMO removed 2 days later, EF normalized. Developed Recurrent VF 6 days later: brought to OR

Discussion
Idiopathic ventricular fibrillation initiated by shortcoupled PVCs is uncommon, but amenable to catheter ablation. Most commonly, culprit PVCs are associated with the His-Purkinje network, although PVCs arising from the RVOT have also been implicated. In the largest series, 13 of 23 patients had PVCs mapped to the distal right bundle,1 a finding seen in other case reports.2-4 Although the normal course of the right bundle is within the moderator band, the relationship of this anatomy to these arrhythmias has not been reported. We report two cases in which the distal portion of the right bundle, within the moderator band, was identified as the source of ectopy. In both cases, ectopy recurred after an apparently successful ablation, and further procedures targeted anatomically (catheter ablation in one, and surgical ablation in the other) permitted effective control of life-threatening arrhythmias. An important limitation of catheter ablation of focal ectopy which initiates VT or VF is whether the ectopy is inducible and thus mappable. Identification of anatomic correlates may permit ablation when electrophysiologic mapping cannot be performed.

Resected moderator band demonstrates ablation lesion (arrows) with coagulative necrosis surrounded by granulation tissue

Case 2: Brought to EP Laboratory: recurrent ventricular fibrillation initiated by monomorphic PVCs

Case 1: Extremely frequent ventricular ectopy, occasionally initiating nonsustained polymorphic VT. Activation mapping of the RV apex using intracardiac echo revealed early activation preceding the QRS by 20 msec, at the mid-moderator band. Ablation at this site caused a burst of ectopy which then became quiescent. No further ectopics were seen, but 5 hours later, PVCs resumed with nonsustained VT. During the second procedure, there were very rare PVCs: intracardiac echo was used to direct aggressive ablation at the moderator band. There were no recurrences of VT/VF during followup.

Infrequent PVCs which initiated VF each time; mapped to right ventricular apex; preceded by Purkinje potential (See below). Mapping severely limited by recurrent VF
Earliest Site Purk Potential

Purkinje Potential

Purk Potential -20

His

Conclusions
Prox RB Potential Prox RB Potential

Focal ectopy initiating VT/VF arising from the distal RV conduction system may originate in the moderator band. Ablation of ectopy from this structure may be aided by imaging with echocardiography.

Case 2: Almost every PVC initiated VF, severely limiting mapping. Ablation at apical RV septum and free wall, seemingly at mid-ventricular structure: moderator band. 62 shocks during procedure; ventilated throughout. Still having VF at end of procedure. Went to OR that night; Fem-Fem bypass. Echo EF 30%. Brought back to EP lab 2 days later for ICE-guided ablation targeting moderator band at septal and free-wall insertions.

References
1. 2. 3. 4. Haissaguerre M, Shoda M, Jais P et al. Circulation 2002; 106:962-967. Saliba W, Abul Karim A, Tchou P, Natale A. J Cardiovasc Electrophysiol 2002; 13:1296-1299. Betts TR, Yue A, Roberts PR, Morgan JM. J Cardiovasc Electrophysiol 2004; 15:957-959. Kohsaka S, Razavi M, Massumi A. Pacing Clin Electrophysiol 2007; 30:701-704.