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Review
. 2008 Mar 25;51(12):1149-53.
doi: 10.1016/j.jacc.2007.10.062.

Atrial fibrillation and Brugada syndrome

Affiliations
Review

Atrial fibrillation and Brugada syndrome

Johnson Francis et al. J Am Coll Cardiol. .

Abstract

Brugada syndrome is characterized by right bundle branch block pattern with ST-segment elevation in leads V(1) to V(3) and a propensity for sudden cardiac death due to ventricular arrhythmias. The arrhythmogenic substrate in Brugada syndrome may not be restricted to the ventricles, and atrial arrhythmias are being increasingly reported. Incidences of spontaneous atrial arrhythmias vary from 6% to 38% and those of inducible atrial arrhythmias from 3% to 100%. Atrial fibrillation (AF) is the most common atrial arrhythmia found in Brugada syndrome. Enhanced duration of atrial action potential and increased intra-atrial conduction time may contribute to the genesis of atrial arrhythmias in Brugada syndrome. Atrial arrhythmias are an important cause of inappropriate discharge of implantable defibrillators in patients with Brugada syndrome. Hence, implantation of dual-chamber defibrillators and careful programming of single-chamber devices have been recommended. Atrial fibrillation has been associated with mutations in both the sodium and calcium channels of the heart, as well as with cases of Brugada syndrome that could not genotyped to any of the known genes associated with the disease. This observation suggests that the substrate responsible for the development of ventricular arrhythmias also may contribute to arrhythmogenesis in the atria of the heart. The presence of a prominent transient outward current in atria and the observation that episodes of AF are triggered by closely coupled atrial extrasystoles point to the possibility that a substrate similar to that responsible for ventricular arrhythmogenesis underlies the development of AF in patients with Brugada syndrome.

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References

    1. Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. J Am Coll Cardiol. 1992;20:1391–6. - PubMed
    1. Chen Q, Kirsch GE, Zhang D, et al. Genetic basis and molecular mechanisms for idiopathic ventricular fibrillation. Nature. 1998;392:293–6. - PubMed
    1. Antzelevitch C, Pollevick GD, Cordeiro JM, et al. Loss-of-function mutations in the cardiac calcium channel underlie a new clinical entity characterized by ST-segment elevation, short QT intervals, and sudden cardiac death. Circulation. 2007;115:442–9. - PMC - PubMed
    1. London B, Sanyal S, Michalec M, et al. A mutation in the Glycerol-3-Phosphate Dehydrogenase 1-Like gene (GPD1L) causes Brugada syndrome (abstr) Heart Rhythm. 2006;3:S32.
    1. Eckardt L, Kirchhof P, Loh P, Schulze-Bahr E, et al. Brugada syndrome and supraventricular tachyarrhythmias: a novel association? J Cardiovasc Electrophysiol. 2001;12:680–5. - PubMed

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