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Cardiovascular Research Advance Access originally published online on January 9, 2009
Cardiovascular Research 2009 81(4):635-636; doi:10.1093/cvr/cvp008
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org

Arrhythmogenic Brugada syndrome substrate: a proof of principle

Joachim R. Ehrlich*

Division of Cardiology, Section of Electrophysiology, J.W. Goethe-University, Theodor Stern Kai 7, 60590 Frankfurt am Main, Germany

* Corresponding author. Tel: +49 69 6301 83661, fax: +49 69 6301 4037. E-mail address: j.ehrlich@em.uni-frankfurt.de

This editorial refers to ‘A transient outward potassium current activator recapitulates the electrocardiographic manifestations of Brugada syndrome’ by Calloe et al.,4 pp. 686–694, this issue.

The first 10% of the full text of this article appears below.

The Brugada syndrome is an inherited, arrhythmogenic entity affecting predominantly young men without structural heart disease.1 It is associated with a specific ECG pattern of coved-type ST-segment elevation in right precordial leads (Figure 1). Patients are at increased risk for sudden cardiac death often triggered by vagal influence and many times occurring at rest. After its description as a distinct entity in 1992, a first genetic link was identified in 1998.2 The Brugada syndrome . . . [Full Text of this Article]


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Related Article

A transient outward potassium current activator recapitulates the electrocardiographic manifestations of Brugada syndrome
Kirstine Calloe, Jonathan M. Cordeiro, José M. Di Diego, Rie S. Hansen, Morten Grunnet, Søren Peter Olesen, and Charles Antzelevitch
Cardiovasc Res 2009 81: 686-694. [Abstract] [Full Text] [PDF]