Right Ventricular Histological Substrate and Conduction Delay in Patients With Brugada Syndrome

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 fi...

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Published inInternational Heart Journal Vol. 51; no. 1; pp. 17 - 23
Main Authors Ohkubo, Kimie, Watanabe, Ichiro, Okumura, Yasuo, Takagi, Yasuhiro, Ashino, Sonoko, Kofune, Masayoshi, Sugimura, Hidezou, Nakai, Toshiko, Kasamaki, Yuji, Hirayama, Atsushi, Morimoto, Shin-Ichiro
Format Journal Article
LanguageEnglish
Published Japan International Heart Journal Association 2010
Subjects
Adult
Aged
Brugada syndrome
Brugada Syndrome - diagnosis
Brugada Syndrome - pathology
Brugada Syndrome - physiopathology
Brugada Syndrome - therapy
Cardiac Catheterization
Coronary Angiography
Delayed potential
Echocardiography
Electrocardiography
Electrophysiologic study
Female
Heart - physiopathology
Heart Conduction System - pathology
Heart Conduction System - physiopathology
Heart Ventricles - pathology
Heart Ventricles - physiopathology
Humans
Male
Middle Aged
Myocardium - pathology
RV biopsy
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Summary: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.
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ISSN:1349-2365
1349-3299
DOI:10.1536/ihj.51.17