Catheter Ablation
Does Electrocardiographic Normalization Predict Successful Substrate Ablation in Brugada Syndrome?
2021 Volume 85 Issue 8 Pages 1294-1295
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2021 Volume 85 Issue 8 Pages 1294-1295
Brugada syndrome (BrS) is characterized by prominent J waves and coved-type ST elevation in the right precordial leads, associated with a significant risk of ventricular fibrillation (VF) and sudden cardiac death (SCD). Since BrS was first described in 1992,1 numerous studies and BrS cases have reported on its diagnosis, risk stratification, and strategy of clinical management. Implantable cardioverter-defibrillator (ICD) is the standard therapy to prevent SCD in BrS patients.2 Pharmacologic therapies, including quinidine, bepridil, and cilostazol, have been reported to prevent VF. Although these medications are effective, there is a relatively high incidence of adverse effects. In addition, quinidine may be limited by its unavailability in countries where BrS is endemic.3
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Radiofrequency (RF) catheter ablation (CA) is a therapeutic option to suppress recurrent VF in patients with BrS. Haïssaguerre et al were the first to report the outcome of CA in 3 symptomatic patients with BrS.4 The target of ablation was the premature ventricular contractions (PVCs) triggering VF, which was ablated from the endocardial sites of the right ventricular outflow tract (RVOT). Almost a decade later, Nademanee et al reported that the ablation of arrhythmogenic substrate distributed at the epicardial RVOT is effective in preventing recurrent VF.5 The substrate is characterized by low voltage and fractionated late potentials at the RVOT epicardium. They demonstrated that ablation at these sites resulted in non-inducible VF and normalized the BrS electrocardiographic (ECG) pattern. After this landmark publication, the approach to substrate ablation of BrS rapidly evolved. Although multiple case reports and studies have supported the effectiveness of epicardial ablation, there are still several issues that need to be further investigated: the definition of local abnormal potentials for the ablation target, the procedural endpoint, the predictor of VF recurrence after the ablation procedure, and long-term follow-up data.
The study by Mamiya et al6 in this issue of the Journal is the first to systematically assess the ECG characteristics before and after ablation. The study demonstrated that ST-segment elevation and the number of abnormal spikes in the surface ECG were significantly decreased after epicardial substrate ablation. The improvements in ECG parameters were more significant in patients who had no recurrence of VF compared with those with recurrence. Interestingly, the changes in ECG gradually occurred 1 month, 6 months, and 12 months after the ablation procedure in patients without VF recurrence. These serial changes in the BrS ECG seemed to be associated with successful substrate ablation. In clinical practice, however, it is important to identify intraprocedural predictors of post-ablation prognosis because they could affect the immediate endpoint of substrate ablation. Ideally, ECG normalization, possibly indicating an adequate modification of the BrS substrate, would be observed during the ablation procedure. However, it is unfortunately not the rule. Because ECG normalization occurs during follow-up after ablation, not at the time of ablation procedure, it is not able to serve as intra-procedural evidence associated with a reduced risk of recurrent VF during follow-up.
When considering substrate ablation to treat patients with BrS, the question is: what should be the ablation endpoint? How much ablation is required? In the original publication by Nademanee et al,5 the ablation endpoint was either noninducible VT/VF or disappearance of the BrS ECG pattern. However, in the past decade, they have modified their mapping/ablation protocol, and no longer use their previous endpoint. In their recent review article, Nademanee et al described that the endpoint of BrS ablation is to eliminate all identified substrate areas with abnormal signals that are detected after sodium-channel blocker administration.7
Multiple previous publications have demonstrated the elimination of type 1 BrS ECG during follow-up after ablation.5,8–10 Persistent or recurrent ST elevation during follow-up appears to be associated with the risk of VF recurrence.11 It is important to note that the ECG manifestations of BrS can be concealed and are unmasked by sodium-channel blockers. In fact, one-quarter of patients with BrS presenting with cardiac arrest do not have the BrS ECG pattern at presentation.12
Recently, Nademanee and Haïssaguerre et al demonstrated the mapping and ablation of inferolateral J-wave with frequent VF episodes,13 where patients with a combination of BrS ECG pattern and inferolateral J-wave harbored an arrhythmogenic substrate not only in the RVOT epicardium but also at the inferior aspect of the RV. In most of the patients, ablation of all identified substrate normalized the BrS ECG pattern and resulted in disappearance of the inferolateral J-wave. In light of these findings, ablation of the RVOT epicardium yielding normalization of the BrS ECG alone may be insufficient to treat patients who have the BrS ECG with concomitant inferolateral J-wave.
In summary, the study by Mamiya et al suggests that dynamic change in the BrS ECG is an important clue for risk stratification on follow-up. However, the elimination of the BrS ECG after ablation of arrhythmia substrate distributed at the RVOT epicardium, as a predictor of favorable clinical outcome, must be interpreted with caution; that is, the absence of the BrS ECG during follow-up does not guarantee freedom from recurrence of VF. Further studies are needed to optimize the therapeutic approach for BrS patients and to more definitely determine the clinical, electrocardiographic, and electrophysiologic predictors of post-procedural prognosis.
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