Early repolarization is often also observed
Early repolarization is often also observed in Brugada syndrome patients [30–34]. In this study, 34% of Brugada syndrome patients exhibited early repolarization in inferolateral leads. Clinical characteristics, inducibility, and arrhythmic event rate were similar between patients with and without early repolarization. In a previous report from Lestas et al., risk was similar between patients with and without early repolarization in Brugada syndrome , while there were three reports which demonstrated that early repolarization was associated with higher risk [32–34]. All of these studies and the present study included different patient cohorts, which may explain the inconsistent results. In the studies by Kamakura et al. and Takagi et al., 330 and 460 patients were enrolled, respectively, but more than half of the patients studied were asymptomatic [32,33]. In both studies, arrhythmic event rate was 7–8% during 4-year follow-up. Kawata et al. enrolled 49 Brugada syndrome patients with documented VF . In their study, 71% of patients had VF during 7.8-year follow-up. It is now recognized that asymptomatic patients with Brugada type ECG are at low risk (annual arrhythmic event rate of <1%). Thus, the present study included 58 symptomatic Brugada syndrome patients and showed overall arrhythmic event rate of 21% at 5-year follow-up. The results of the studies need to be taken into account together with the enrolled patient cohorts.
Conflict of interest
Introduction Idiopathic ventricular tachyarrhythmia originating from the right ventricular outflow tract (RVOT) is one of the most frequent ventricular arrhythmias observed in clinical practice . Although RVOT arrhythmias rarely cause sudden cardiac death [2–4], frequent RVOT arrhythmias can reduce left ventricular contraction in some patients [5,6]. Therefore, radiofrequency catheter ablation (RFCA) of RVOT arrhythmia is important, especially for symptomatic patients or those with reduced left ventricular contraction. Moreover, high success rates have been achieved with RFCA, and it benfotiamine is associated with a low risk of complications [7,8]. On the other hand, various QRS morphologies have often been observed in patients with RVOT arrhythmia at the time of RFCA. It has been suggested that a shift in the site of origin of RVOT arrhythmia results in different QRS morphologies [9–11]; however, the precise mechanism underlying multiple QRS morphologies has not yet been clarified.
Results Table 1 shows patients׳ characteristics. There were 5 men and 15 women, with a mean (±standard deviation) age of 55±21 years (range, 15–77). Eleven patients had nonsustained ventricular tachycardia, and 9 patients had premature ventricular contraction (PVC). No structural heart disease was detected using transthoracic echocardiography. Forty-six QRS morphologies of RVOT arrhythmia were observed in the 20 evaluated patients. The site of origin could be identified using the non-contact mapping system in all the patients. Five patients showed monofocal QRS morphology, whereas the remaining 15 patients showed multiple QRS morphologies (from 2 to 4 morphologies each, Table 1). The mean distance between the initial site of origin and the subsequent different sites of origin of RVOT arrhythmia was 9.9±7.1mm. A shift in the site of origin of the tachycardia was observed in all the patients with multiple QRS morphologies (Table 1). In addition, different QRS morphologies were observed in 5 of these patients (Table 1), which were caused by the change in the local activation after radiofrequency energy delivery. RVOT arrhythmias in all patients were eliminated after radiofrequency energy was applied to the site of origin of the arrhythmias using non-contact mapping navigation. However, 1 patient presented RVOT arrhythmia recurrence (success rate, 95.0%) (Table 1). Fig. 1 shows the 2 different QRS morphologies, both observed before radiofrequency energy was applied in patient 9. The QRS morphology of PVC 1 was slightly different from that of PVC 2 (Fig. 1). Fig. 2 shows the activation sequence of PVC 1. The earliest ventricular activation of PVC 1 was observed at Site A; then, the activation spread centrifugally. Fig. 2a–d shows the activation sequence of PVC 1 (Fig. 2, upper panel) and the corresponding virtual unipolar electrogram morphology at Sites A and B (Fig. 2, lower panel). Since the activation was derived from Site A, virtual unipolar morphology at Site A showed a QS morphology, whereas that at Site B showed a rS pattern (Fig. 2). Fig. 3 shows the activation sequence of PVC 2 and the corresponding virtual unipolar electrogram morphology at Sites A and B (the same site presented in Fig. 2). During PVC 2, the earliest ventricular activation was observed at Site B. Therefore, virtual unipolar morphology at Site B showed a QS morphology, whereas that at Site A showed a rS pattern (Fig. 3).