Brugada syndrome: Cellular mechanisms and approaches to therapy

Charles Antzelevitch*, Sami Viskin

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

1 Scopus citations


The Brugada Syndrome, introduced as a new clinical entity 20 years ago, has attracted great interest because of its prevalence and association with high risk of sudden death, especially in males as they enter their third and fourth decade of life. Consensus reports published in 2002 and 2005 focused on diagnostic criteria, risk stratification and approaches to therapy. More recently, the risk stratification approaches have been the subject of controversy and debate. Over 21 years have transpired since the introduction of the concept of phase 2 reentry, the mechanism believed to underlie development of arrhythmogenesis in BrS. Thus, the entity initially introduced as ST segment elevation and right bundle branch block (RBBB), which came to be known as Brugada syndrome in 1996, evolved in the experimental laboratory and in the clinic along parallel but separate tracks. While the electrocardiographic and arrhythmic manifestations of BrS are well explained by abnormal repolarization in the right ventricular outflow track (RVOT), recent data have suggested conduction impairment in the RVOT as the basis for BrS, thus generating a debate as to the basis for the pathogenicity of the syndrome. This review provides an overview of the clinical, genetic, molecular and cellular aspects of the Brugada syndrome and the various approaches to therapy.

Original languageEnglish
Title of host publicationElectrical Diseases of the Heart
Subtitle of host publicationVolume 1: Basic Foundations and Primary Electrical Diseases
PublisherSpringer-Verlag London Ltd
Number of pages40
ISBN (Electronic)9781447148814
ISBN (Print)1447148800, 9781447148807
StatePublished - 1 Mar 2013


  • Electrocardiography
  • Electrophysiology
  • J Wave syndrome
  • Pharmacology
  • Quinidine
  • Sudden cardiac death


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