Successful Ablation of Moderator Band-Originated Ventricular Tachycardia at Its Ventricle Insertion Sites

To the Editor: Moderator band (MB) is a part of the septomarginal trabeculation, which not only supports the anterior papillary muscle (APM) of the tricuspid valve but also connects it to the free wall. Nevertheless, with the advent of intracardiac echocardiography (ICE), electrophysiologists are now aware of the arrhythmogenic role of MB besides its mechanical function. MB-originated ventricular tachycardia or ventricular fibrillation (VT/VF) is a kind of idiopathic malignant arrhythmia in the absence of structural heart disease, which is frequently triggered by a premature ventricular contraction (PVC) from the same site.[1] As the mechanism of this kind of arrhythmia is not well illustrated, previous research has reported the involvement of the Purkinje system of the right ventricle (RV), although catheter radiofrequency (RF) ablation delivered to the site displaying Purkinje potential showed limited efficacy.[2,3] Herein, we present a case of MB-originated VT/VF in a 29-year-old woman in whom ablation based on the anatomical substrate (free wall and septum insertions of MB) proved successfully.

A 29-year-old woman experienced a sudden episode of syncope and was transferred to a local hospital. Frequent unifocal PVC was observed, and the PVC showed a left bundle branch block (LBBB) pattern with precordial transition later than V4 [Figure 1a], some of which precipitated recurrent episodes of VT [Figure 1b]. Moreover, some of the PVC-induced VF that was restored to sinus rhythm through electrical cardioversion [Figure 1c] and implantable cardioverter-defibrillator (ICD, Lumax 340 VR, BIOTRONIK SE & Co. KG, Berlin, Germany) was implanted for the secondary prevention of sudden cardiac death (SCD). However, during the 4 months after ICD implantation, four shocks for repeated VF were conducted, and the patient was referred to our department. Initial workup included a baseline 12-lead electrocardiography (ECG) with frequent PVC, normal transthoracic echocardiography, and coronary angiography. The patient had no family history of SCD. Morphology of the captured PVC was identical to the one that triggered the earlier episode of VF, which was characterized by an LBBB pattern with late precordial transition (V5) and a left superior axis.

Figure 1.

The electrocardiograph and the anatomy of moderator band of the patient. (a) Characteristic PVC with a left bundle branch block pattern, late precordial transition (V5). (b) Ventricular tachycardia was induced by PVC. (c) The PVC-induced ventricular fibrillation that was restored to sinus rhythm through electrical cardioversion. (d-f) Intracardiac ultrasound showed the moderator band (red arrows), the free wall of right ventricle (white arrows), the ablation catheter (yellow arrows), and intracardiac echocardiography catheter (black arrow). PVC: Premature ventricular contraction.

Ablation catheter (Thermocool Smarttouch, Biosense Webster, Johnson and Johnson Medical, Ltd., CA, USA) was introduced to the RV through a transfemoral approach under the guidance of CARTO 3 mapping system (Biosense Webster) and ICE catheter (ICE, Soundstar, 10 French, Biosense Webster, Johnson and Johnson Medical, Ltd., CA, USA). Detailed endocardial voltage maps were created using previously established values to define normal RV bipolar and unipolar voltage. After comprehensive pace mapping and activation mapping and with the guidance of ICE [Figure 1d], the original site of the PVC was located within the MB. RF current was delivered separately to the free wall and septum insertions of MB [Figure 1e and 1f]. The RF energy was applied using a power-controlled mode with a delivered power up to 35 W and the tip temperature of 43°C for 15–60 s per site with contact force ranging from 9 to 31 g. The patient underwent an uneventful procedure with normal baseline 12-lead ECG and echocardiography and did not require antiarrhythmic drugs postablation. During the 12-month follow-up period, ICD interrogation was absent of any VT/VF event. Regardless of the fact that identical PVC pattern was recorded in Holter, no VT/VF was induced.

The exact nature of the MB-VF is not well elucidated, although some researchers have suggested a connection between MB-VF and His-Purkinje conduction system of the RV.[3,4,5] An evident sharp Purkinje system potential that preceded the ventricular activation during the culprit PVC supported the aforementioned hypothesis.[6] However, the success rate of ablation MB showing P potential was only 50%.[3,4] In this case, we focused on ablation of the free wall and septum insertions of MB, which proved successful. Despite the recurrence of PVC indistinguishable as before, the ablation was not considered a failure, as no VT/VF was triggered by those unexpected ventricular beats. However, the coupling interval of PVC had prolonged from 240 ms to 440 ms after ablation. It is therefore reasonable to speculate that the insertion sites of MB and RV play a critical role in provoking deteriorated ventricular arrhythmia. The anatomical structure of MB might determine its arrhythmogenic role. As part of the septomarginal trabeculation, the MB crosses from the septum to the RV free wall and supports the APM of the tricuspid valve. As the name suggests, MB was thought to protect against overdistention of the RV.[7] The mechanical stretch and misarranged cardiomyocyte renders the insertion sites more vulnerable to arrhythmia generation. Further, a previous study showed that the insertion sites were abundant with Purkinje fibers and cholinesterase-containing nerve fascicles, which gave rise to the possibility that a mechanical stretch of RV might influence its electrophysiological properties.[8] In addition, the APM, also a potential substrate for idiopathic ventricular arrhythmia, is anatomically connected with MB, and ablation of the ventricular insertion to papillary muscle proved a perfect target for PM-origin ventricular arrhythmia.[9]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient had given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.