Brugada electrocardiogram pattern and right bundle branch block

We read with great interest the recent case report by Eitel et al.1 entitled; ‘Postextrasystolic unmasking of Brugada electrocardiogram’. This case clearly exemplifies the challenge of detecting Brugada pattern in the presence of right bundle branch block (RBBB). We wish to commend the author’s punctilious review of serial electrocardiograms (ECG’s) to detect the Brugada Type 1 pattern that was revealed upon intermittent resolution of the RBBB. The diagnosis could have been easily overlooked. A patient presenting with syncope in combination with RBBB, right axis deviation, and borderline PQ prolongation may well have underwent a pacemaker implant alone, and have remained at risk of ventricular arrhythmias. We wish to discuss and hopefully contribute to additional aspects of this case. Firstly, it should be emphasized that cardiac conduction disease and Brugada syndrome often co-exist, as both conditions can be a manifestation of sodium channel dysfunction.2 Maury et al.2 demonstrated that RBBB was evident in 20% (29/143) of spontaneous Type 1 Brugada pattern, and 33% (61/182) of those induced by sodium channel blocker challenge. The case by Eitel et al.1 mention a manoeuvre to overcome the masking effect of RBBB. The right ventricular apex is paced at such an A-V interval to fuse ventricular activation, nullifying the effect of the RBBB delay that would have obscured the Brugada pattern. We wish to highlight that the first to perform this was in fact Pablo A. Chiale in 2012, as part of his work at the Rosenbaum School of Electrocardiology in Buenos Aires.3 This technique has been referred to as the Chiale manoeuvre.4 He has since passed and we wish to reference and acknowledge this pioneering work. In addition, Chiale’s detailed analysis of the ECG in Brugada syndrome when combined with RBBB is applicable and warrants further discussion.3 In RBBB, the ST-T wave in the early precordial leads is negative, being opposed to the main direction of the QRS electrical forces. The ST segment in the case by Eitel et al.1 was atypical as it exhibited a degree of elevation, best appreciated in lead V1. A similar finding was also evident in Chiale’s index description,3 and should alert suspicion of Brugada syndrome. However, it should be noted that Brugada pattern can be completely obscured in higher degree RBBB3 and contrary to this case report; Baranchuk et al.5 have previously described normalization of Brugada pattern post extra-systolic pauses. Such is the dynamic and complex nature of the ECG changes associated with Brugada syndrome. As a result, patients with persistent RBBB and a suspicion of Brugada syndrome should be referred to the electrophysiology lab to undergo the Chiale manoeuvre. The case report by Eitel et al.1 promotes awareness of this practice and also the additional benefit of backup ventricular pacing should a sodium channel blocker challenge be required. Conflict of interest: none declared.

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