Significant Delayed Activation on the Right Ventricular Outflow Tract Represents Complete Right Bundle‐Branch Block Pattern in Brugada Syndrome

Author:

Morimoto Yoshimasa12ORCID,Morita Hiroshi3ORCID,Ejiri Kentaro14ORCID,Mizuno Tomofumi1ORCID,Masuda Takuro1,Ueoka Akira1,Asada Saori1,Miyamoto Masakazu1,Kawada Satoshi1,Nakagawa Koji1,Nishii Nobuhiro3ORCID,Nakamura Kazufumi1ORCID,Ito Hiroshi1

Affiliation:

1. Department of Cardiovascular Medicine Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences Okayama Japan

2. Department of Cardiovascular Medicine Fukuyama City Hospital Hiroshima Japan

3. Department of Cardiovascular Therapeutics Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences Okayama Japan

4. Department of Epidemiology Johns Hopkins Bloomberg School of Public Health Baltimore MD USA

Abstract

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.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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