Channelpedia

PubMed 20129298


Referenced in Channelpedia wiki pages of: none

Automatically associated channels: Nav1.5



Title: Atrial electrophysiological and structural remodeling in high-risk patients with Brugada syndrome: assessment with electrophysiology and echocardiography.

Authors: Norihisa Toh, Hiroshi Morita, Satoshi Nagase, Manabu Taniguchi, Daiji Miura, Nobuhiro Nishii, Kazufumi Nakamura, Tohru Ohe, Kengo F Kusano, Hiroshi Ito

Journal, date & volume: Heart Rhythm, 2010 , 7, 218-24

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/20129298


Abstract
Atrial fibrillation (AF) often occurs in Brugada syndrome (BrS), and BrS patients with spontaneous AF often experience ventricular fibrillation (VF) attacks. Atrial vulnerability providing a substrate for AF is known to be enhanced in BrS, but there are no data on atrial structural attributes.The objective of this study was to assess atrial electrophysiological and structural characteristics in BrS and their relationships with gene mutations.We studied 57 patients with BrS. Intra-atrial conduction time (CT) was defined as the interval from the stimulus at the high right atrium to atrial deflection at the distal portion of the coronary sinus. Left atrial volume index (LAVI) was measured by the modified Simpson method at left ventricular end-systole using echocardiography. SCN5A mutations were analyzed in all patients.In patients with documented VF, spontaneous AF frequently occurred and prolonged CT and increased LAVI were observed compared with those in patients without VF (all P < .05; LAVI: 22 +/- 5 vs. 32 +/- 7 ml/m(2)). Even among patients without AF, CT and LAVI were still increased in patients with VF (all P < .05; LAVI: 22 +/- 5 vs. 29 +/- 5 ml/m(2)). The presence of SCN5A mutation was associated with prolonged CT (P < .05) and increased LAVI (P < .01), but not with arrhythmic episodes.Both atrial vulnerability and structural remodeling are enhanced in high-risk patients with BrS, even in those without AF. These morphological characteristics suggest that BrS is a form of genetic myocardial disease.