53

Historically, individuals with Brugada syndrome (BrS) have been thought to have normal hearts,1 despite reports to the contrary in sporadic cases.^2,3 Therefore, ablation to suppress ventricular fibrillation (VF) in the context of BrS has aimed at targeting premature ventricular contractions (PVCs)^4,5 as well as idiopathic VF.⁵ Nagase et al.,⁶ however, described abnormal epicardial right ventricular outflow tract (RVOT) electrograms (EGMs) recorded via the conus branch of the right coronary artery in BrS patients, and subsequently, with the development of epicardial access and mapping for ventricular tachycardia (VT) ablation, Nademanee et al.⁷ clearly identified a VF substrate that could be abolished by radiofrequency (RF) ablation. In light of these results, ablation is now considered to have a class IIb indication for the treatment of recurrent VF in the context of BrS.^8,9 In this chapter, we will describe both the trigger ablation approach and the now more common substrate approach to ablation of VF in BrS patients.

The Trigger Approach

Background

Haïssaguerre et al.⁵ showed that idiopathic VF could be eliminated by ablation of the triggering PVCs in a manner analogous to ablation of focal triggers for atrial fibrillation (AF).¹⁰ Kakishita et al.¹¹ showed that in patients with BrS, PVCs were frequent before the onset of VF and of almost identical morphology to the PVCs that triggered VF. They also reported that in the case of multiple VF episodes, the initiating PVCs of each episode of VF had similar morphologies in the same patient. They rarely identified a short-long-short sequence before VF initiation, and the coupling interval of the initiating PVC was not so short as to intrude on the T wave. The site of origin was almost exclusively in the right ventricle (RV) (mainly the RVOT free wall) except in the case of 1 patient in the series of Morita et al.¹² In our experience, initiating PVCs largely arise from the RVOT but are also seen to originate from the RV free wall and the right-sided Purkinje network.

In clinical practice, it is rare to record PVC triggers on the 12-lead ECG or in the electrophysiological (EP) laboratory in patients with BrS. This approach is therefore limited to patients with frequent PVCs, particularly since the development of epicardial substrate-based ablation.

Preprocedural Planning

PVCs that trigger VF are often seen only in the period surrounding arrhythmic events, and even in this period they are usually infrequent. It is therefore crucial to have 12-lead ECG recordings of PVCs before the procedure (Figure 53.1). Long-duration ECG recordings or 12-lead Holter monitoring should be performed immediately after VF episodes to allow PVCs to be recorded. In order to match PVC morphologies, it is essential that during PVC recording, electrode positions are identical to those used in the electrophysiology (EP) laboratory. To allow this, the EP procedure must be scheduled as soon as possible after the arrhythmic event. In our experience, PVCs always arise from the RV—either from the RVOT, from lower on the ventricular free wall, or from the right Purkinje network.

All antiarrhythmic drugs should be withdrawn prior to ablation. The need for pain control and sedation should be balanced against the possibility of PVC suppression with deep sedation or general anesthesia. During the procedure, all staff should be ready for prompt defibrillation in the event of VF, and disposable defibrillator patches should be attached to the patient and connected to a defibrillator, so that the defibrillator is ready to shock on demand.

Procedure

Essentially, the procedure does not differ from standard PVC ablation.^4,13,14 We use a 3.5-mm irrigated-tip ablation catheter and a quadripolar catheter at the RV apex. The settings on the ablation catheter (amplification ×16, voltage range 1 mV; Filters: 30–250 Hz; Labsystem Pro, Bard, Lowell, MA) aim at identifying small, abnormal electrograms but require minimization of electrical noise from the EP laboratory environment. In addition to the usual bipolar channels, we use a unipolar channel between the distal ablation catheter tip and Wilson’s central terminal (WCT) (amplification ×8; voltage range 10 mV; filters: 0.05 Hz–500 Hz; Labsystem Pro, Bard). If PVCs are seen, activation mapping is performed. Where PVC morphology is compatible with a Purkinje origin, the right Purkinje network is mapped, with particular care to avoid mechanical right bundle branch block (RBBB), as RBBB would mask a Purkinje potential within the QRS electrogram (Figure 53.2). In the absence of native PVCs, pace mapping can allow approximate identification of the culprit zone but mapping and therefore ablation are not as precise.

Once the site of origin of the PVC is identified, RF ablation is delivered at 30 to 35 W. The ablation area is then enlarged to 3 to 4 cm2 around the site of earliest activation or best pace map. Before changing our standard technique to epicardial substrate ablation, we showed that large endocardial ablation at the site of origin of PVCs (in the RVOT or RV free wall) could eliminate the typical Brugada pattern of ST elevation seen on the 12-lead ECG.¹⁵

The Substrate Approach

Background

The trigger approach is limited by the very small number of PVC in BrS. A previous clinical report⁶ recorded abnormal epicardial potentials in BrS patients via the conus branch of the right coronary artery. Subsequently, an experimental report from Morita et al. described radiofrequency catheter ablation at the earliest activation site of PVCs in the epicardium, which disconnected the short and long action potential duration regions and eliminated all PVCs and VTs.¹⁶ These findings, combined with the development of epicardial VT mapping and ablation, have led to substrate ablation becoming the preferred approach to ablation for BrS. In 2011, Nademanee et al.⁷ described their experience using percutaneous epicardial access¹⁷ in this population and identified an area with fragmented potentials over the epicardial surface of the RVOT. Ablation at these sites rendered VF noninducible in 7 of 9 patients (78%) and normalized the Brugada ECG pattern in 89%. Long-term outcome (20 ± 6 months) was excellent, with no recurrent VF in any patient.⁷ We showed that these epicardial potentials were delayed during ajmaline infusion at the same time that the Brugada pattern became more pronounced.¹⁸ In our experience, Brugada pattern ST elevation can sometimes persist or increase during ablation, perhaps due to local tissue injury, but disappears afterwards. In all of the patients treated with substrate ablation in this center, we have demonstrated a negative ajmaline challenge at 3 months. In the 14 patients in whom we performed epicardial mapping, fragmented potentials covered an area of 20 ± 4 cm². More recently, Brugada et al.¹⁹ reported their experience of 14 patients with epicardial Brugada ablation. In this series, the area of abnormal electrograms covered an area on the right anterior RV free wall and RVOT of 19 cm² that increased to 27.3 cm² after flecainide infusion. In 100% of their patients, VF was noninducible at the end of the procedure and none demonstrated the Brugada pattern after flecainide infusion at 5 months.

Interestingly, one of our patients presented with monomorphic VT 18 months after epicardial ablation, whereas he had had VF before. This is likely to be due to organization of the remaining substrate by ablation, such that it allowed only VT and not VF in a manner analogous to atrial tachycardia post AF ablation.

Based on our experience on AF mapping with noninvasive ECG imaging,20,21 we performed VF recordings in 7 patients with BrS and epicardial mapping for VF ablation. Analysis of noninvasive ECG imaging showed that VF rotors were anchored within the area of fragmented potentials over the RVOT (unpublished data).

Preprocedural Planning

There are several advantages of the substrate approach. First, it does not require PVCs (which can be sometimes challenging to record), and second, the timing of the procedure is less important. However, it requires access to the pericardium and therefore awareness and prevention of potential complications.^22,23

We routinely perform CT scans before ablation to obtain cardiac anatomy, particularly coronary artery anatomy (Figure 53.3) of the right coronary artery branches for BrS ablation.

Stay updated, free articles. Join our Telegram channel

Join