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.