Key result
Body surface mapping links complete RBBB in Brugada syndrome to significant RVOT conduction delay.
Why the study?
Complete right bundle-branch block in Brugada syndrome carries an increased ventricular fibrillation risk, but its pathophysiological mechanism has not been well established.
What is the pathophysiological mechanism of complete right bundle-branch block in patients with Brugada syndrome?
Observational (n=19)
What is the pathophysiological mechanism of complete right bundle-branch block in patients with Brugada syndrome?
Complete right bundle-branch block in Brugada syndrome is driven by significant conduction delay in the right ventricular outflow tract, with or without proximal RBBB.
Supports RVOT conduction delay as mechanism of complete RBBB in Brugada syndrome; hypothesis-generating for risk stratification pending larger validation.
Background The appearance of complete right bundle-branch block (CRBBB) in Brugada syndrome (BrS) is associated with an increased risk of ventricular fibrillation. The pathophysiological mechanism of CRBBB in patients with BrS has not been well established. We aimed to clarify the significance of a conduction delay zone associated with arrhythmias on CRBBB using body surface mapping in patients with BrS. Methods and Results Body surface mapping was recorded in 11 patients with BrS and 8 control patients both with CRBBB. CRBBB in control patients was transiently exhibited by unintentional catheter manipulation (proximal RBBB). Ventricular activation time maps were constructed for both of the groups. We divided the anterior chest into 4 areas (inferolateral right ventricle [RV], RV outflow tract [RVOT], intraventricular septum, and left ventricle) and compared activation patterns between the 2 groups. Excitation propagated to the RV from the left ventricle through the intraventricular septum with activation delay in the entire RV in the control group (proximal RBBB pattern). In 7 patients with BrS, excitation propagated from the inferolateral RV to the RVOT with significant regional activation delay. The remaining 4 patients with BrS showed a proximal RBBB pattern with the RVOT activation delay. The ventricular activation time in the inferolateral RV was significantly shorter in patients with BrS without a proximal RBBB pattern than in control patients. Conclusions The CRBBB morphology in patients with BrS consisted of 2 mechanisms: (1) significantly delayed conduction in the RVOT and (2) proximal RBBB with RVOT conduction delay. Significant RVOT conduction delay without proximal RBBB resulted in CRBBB morphology in patients with BrS.
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Morimoto et al. (2023) conducted an observational in Brugada syndrome with complete right bundle-branch block (n=19). Body surface mapping vs. Control patients with transient complete right bundle-branch block was evaluated on Ventricular activation patterns and time. Body surface mapping revealed that complete right bundle-branch block in Brugada syndrome is driven by significant right ventricular outflow tract conduction delay (7 of 11 patients).
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