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MINI-FOCUS ISSUE: BRUGADA SYNDROME: CLINICAL RESEARCH

Atrial Fibrillation in Patients With Brugada Syndrome

Relationships of Gene Mutation, Electrophysiology, and Clinical Backgrounds

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

Manuscript received September 19, 2007; accepted October 19, 2007.

^_* Reprint requests and correspondence: Dr. Kengo F. Kusano, Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Shikata-cho 2-5-1, Okayama 7008558, Japan. (Email: kusanokengo{at}hotmail.com).

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.

Abbreviations and Acronyms   AF = atrial fibrillation   BrS = Brugada syndrome   CS = coronary sinus   CT = conduction time   EP = electrophysiology/electrophysiological   ERP = effective refractory period   FH = family history of sudden death   ICD = implantable cardioverter-defibrillator   PCR = polymerase chain reaction   RAA = right atrial appendage   RAF = repetitive atrial firing   SCN5A = pore-forming region of the human cardiac sodium channel   VF = ventricular fibrillation

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