Discussion:
We report here a case of long-standing frequent monomorphic PVCs of right ventricular distal conduction system embedded in the moderator band that progressed to non-sustained ventricular tachycardia. Following suppression of the arrhythmia with RF ablation, the arrhythmia recurred with PVCs at a shorter coupling interval, with frequent repetitive non-sustained polymorphic VT and triggering of sustained ventricular fibrillation. Given his prior history of several years of stable PVCs and non-sustained VT, the occurrence of short coupled PVCs triggering VF has to be considered a pro-arrhythmic effect of RF ablation. The use of a cryoballoon to ablate over the course of the moderator band resulted in complete and durable suppression of ventricular arrhythmias.
The right ventricular moderator band (MB) is increasingly being recognized as a source for PVCs and PVC-mediated ventricular fibrillation.1 The moderator band extends from the septo-marginal trabeculations on the RV side of the septum and extends to the anterior papillary muscle. It carries fascicles of the right bundle within it that serve to rapidly activate the RV free wall. There is considerable structural variation in the MB ranging from short and thick (most common) to long strands of muscle commonly extending across the distal half of the RV cavity. The MB is abundant in Purkinje tissue that is insulated from the myocardium until peripheral arborization in the RV free wall. Monomorphic PVCs, non-sustained monomorphic VT and ventricular fibrillation are all documented arrhythmias originating from the MB.1 The benign PVCs usually have a coupling interval in excess of 400 msec, as in the initial arrhythmia of the patient in this case. When PVCs trigger VF, coupling intervals are typically short, less than 300 msec.2-4
The exact mechanism for the malignant transformation of the MB PVCs is unclear. Purkinje fibers have been shown to initiate arrhythmias by triggered automaticity and re-entry. Afterdepolarizations can be initiated by travelling Ca++ waves and initiate membrane depolarization in a well polarized aggregate of Purkinje cells.5 The transient outward current (Ito) has also been implicated in Purkinje early afterdepolarizations. Strong depolarization gradients between Purkinje fibers and surrounding myocardium can result in short coupling of PVCs due to phase 2 re-entry.6 In the present case, the exact mechanism for emergence of frequent short-coupled PVCs after RF ablation of a more benign form of the arrhythmia is uncertain. The creation of a RBBB may have abolished an overdrive suppressive phenomenon. Alternatively, an inflammatory response of the Purkinje tissue as seen in the early phase of acute myocardial infarction may have been responsible.7 Such aggravation of Purkinje fiber mediated arrhythmias following ablation has not been previously documented and should be a consideration when inadequate suppression is achieved and PVCs re-emerge with coupling interval shortening.
Because of the varying anatomy of the MB, the structure may not be well visualized even with intracardiac echocardiography. Ablation with an RF catheter can be difficult due to inability to maintain consistent contact. Use of a cryocatheter or a cryoballoon can achieve better stability.8 In the present case, the use of a 23 mm Arctic Front IV Cryoballoon enabled a more diffuse ablation all along the course of the MB. Repeat voltage map showed a small area of low voltage in the apical septal area without involvement of the RV apex. RV function remained unchanged by transthoracic echocardiography.