International Heart Journal
Clinical Studies
Right Ventricular Histological Substrate and Conduction Delay in Patients With Brugada Syndrome
Kimie OhkuboIchiro WatanabeYasuo OkumuraYasuhiro TakagiSonoko AshinoMasayoshi KofuneHidezou SugimuraToshiko NakaiYuji KasamakiAtsushi HirayamaShin-Ichiro Morimoto
Author information
JOURNALS FREE ACCESS

Volume 51 (2010) Issue 1 Pages 17-23

Details
Download PDF (2994K) Contact us
Abstract

The reported pathogenesis of Brugada syndrome is phase 2 reentry resulting from shortening of the epicardial action potential duration at the right ventricular outflow tract (RVOT). However, several studies have revealed a high incidence of ventricular late potentials and high rate of ventricular fibrillation (VF) induced by programmed ventricular stimulation (PVS). The aim of the present study was to evaluate the role of slow conduction at the RVOT for the initiation of VF by PVS and any underlying pathological conditions in Brugada syndrome. Endocardial mapping of the RVOT and endomyocardial biopsy of the right ventricle were performed in 25 patients with Brugada syndrome with inducible VF. Late potentials were positive in 11 of the 25 (44%) patients. Low-amplitude fragmented and delayed electrograms were recorded at the RVOT in 13 of 18 (72.2%) patients. Histologic examination of the biopsy samples revealed fatty tissue infiltration, interstitial fibrosis, lymphocyte infiltration, and/or myocyte disorganization in 13 patients. Slow conduction at the RVOT may contribute to the induction of VF by PVS in Brugada syndrome. Various pathomorphologic changes may contribute to slow conduction at the RVOT.

Information related to the author
© 2010 by the International Heart Journal Association
Previous article Next article

Recently visited articles
feedback
Top