• G Paparella, A Sarkozy, and P Brugada.
• Heart Rhythm Management Center, UZ Brussels, Brussels, Belgium. ga.pap@libero.it
• Minerva Med. 2009 Aug 1;100(4):307-19.

AbstractSince its first description in 1992 as a new clinical entity, the Brugada syndrome has stimulated great interest among physicians and basic scientists. In 2002 and 2005, two consensus conferences have respectively defined the diagnostic criteria for the syndrome. Currently the diagnosis of Brugada syndrome is based on a combination of clinical events (syncope and/or sudden cardiac death due to malignant ventricular arrhythmias) and electrocardiographic features (pathognomonic ST-segment elevation morphology). In the last years, many advances have been done in the knowledge about the genetic basis, the cellular mechanisms responsible for the typical electrocardiography features, susceptibility to ventricular arrhythmias and risk stratification. The implantable cardioverter defibrillator remains the only therapeutic option of proven efficacy for primary and secondary prophylaxis of sudden cardiac death. Identification of high risk subjects is one of the major goals in clinical decision-making. Syncope is ubiquitously recognized as a bad prognostic marker in Brugada syndrome. However, young individuals with this disease may suffer from vaso-vagal instead of arrhythmic syncope. The prognostic significance of syncope in patients with Brugada syndrome is discussed in this review.

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