Atrial fibrillation in patients with brugada syndrome relationships of gene mutation, electrophysiology, and clinical backgrounds.

Atrial fibrillation in patients with brugada syndrome relationships of gene mutation, electrophysiology, and clinical backgrounds. Research Abstract Details 

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Atrial fibrillation in patients with brugada syndrome relationships of gene mutation, electrophysiology, and clinical backgrounds. Abstract Text:

Kengo F Kusano,Makiko Taniyama,Kazufumi Nakamura,Daiji Miura,Kimikazu Banba,Satoshi Nagase,Hiroshi Morita,Nobuhiro Nishii,Atsuyuki Watanabe,Takeshi Tada,Masato Murakami,Kohei Miyaji,Shigeki Hiramatsu,Koji Nakagawa,Masamichi Tanaka,Aya Miura,Hideo Kimura,Soichiro Fuke,Wakako Sumita,Satoru Sakuragi,Shigemi Urakawa,Jun Iwasaki,Tohru Ohe,

OBJECTIVES: The goal of our work was to examine the relationships of atrial fibrillation (AF) with genetic, clinical, and electrophysiological backgrounds in Brugada syndrome (BrS). BACKGROUND: Atrial fibrillation is often observed in patients with BrS and indicates that electrical abnormality might exist in the atrium as well as in the ventricle. SCN5A, a gene encoding the cardiac sodium channel, has been reported to be causally related to BrS. However, little is known about the relationships of atrial arrhythmias with genetic, clinical, and electrophysiological backgrounds of BrS. METHODS: Seventy-three BrS patients (49 +/- 12 years of age, men/women = 72/1) were studied. The existence of SCN5A mutation and clinical variables (syncopal episode, documented ventricular fibrillation [VF], and family history of sudden death) were compared with spontaneous AF episodes. Genetic and clinical variables were also compared with electrophysiologic (EP) parameters: atrial refractory period, interatrial conduction time (CT), repetitive atrial firing, and AF induction by atrial extra-stimulus testing. RESULTS: Spontaneous AF occurred in 10 (13.7%) of the BrS patients and SCN5A mutation was detected in 15 patients. Spontaneous AF was associated with higher incidence of syncopal episodes (60.0% vs. 22.2%, p < 0.03) and documented VF (40.0% vs. 14.3%, p < 0.05). SCN5A mutation was associated with prolonged CT (p < 0.03) and AF induction (p < 0.05) in EP study, but not related to the spontaneous AF episode and other clinical variables. In patients with documented VF, higher incidence of spontaneous AF (30.8% vs. 10.0%, p < 0.05), AF induction (53.8% vs. 20.0%, p < 0.03), and prolonged CT was observed. CONCLUSIONS: Spontaneous AF and VF are closely linked clinically and electrophysiologically in BrS patients. Patients with spontaneous AF have more severe clinical backgrounds in BrS. SCN5A mutation is associated with electrical abnormality but not disease severity.

Atrial fibrillation in patients with brugada syndrome relationships of gene mutation, electrophysiology, and clinical backgrounds. Publishing Authors By Initials

KF Kusano,M Taniyama,K Nakamura,D Miura,K Banba,S Nagase,H Morita,N Nishii,A Watanabe,T Tada,M Murakami,K Miyaji,S Hiramatsu,K Nakagawa,M Tanaka,A Miura,H Kimura,S Fuke,W Sumita,S Sakuragi,S Urakawa,J Iwasaki,T Ohe,

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Atrial fibrillation in patients with brugada syndrome relationships of gene mutation, electrophysiology, and clinical backgrounds. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Journal of the American College of Cardiology

VOLUME: 51

Page Numbers: 1169-75

Journal Abbreviation: J. Am. Coll. Cardiol.

ISSN: 1558-3597

DAY: 25

MONTH: Mar

YEAR: 2008

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LANGUAGE: eng

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

Country: United States

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MEDLINETA: J Am Coll Cardiol

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