Brugada syndrome: recent advances and controversies

Curr Cardiol Rep. 2008 Sep;10(5):376-83. doi: 10.1007/s11886-008-0060-y.

Abstract

The Brugada syndrome, first described as a new clinical entity in 1992, is widely recognized today as a form of inherited sudden cardiac arrest. The past 16 years witnessed a progressive increase in the number of reported cases and a dramatic proliferation of articles serving to define the clinical, genetic, cellular, ionic, and molecular aspects of the disease. This article provides a brief overview of recent advances in our understanding of the clinical presentation and molecular and cellular mechanisms and an update of existing controversies.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Anti-Arrhythmia Agents / therapeutic use
  • Brugada Syndrome* / complications
  • Brugada Syndrome* / diagnosis
  • Brugada Syndrome* / genetics
  • Brugada Syndrome* / therapy
  • Death, Sudden, Cardiac / etiology
  • Defibrillators, Implantable
  • Diagnosis, Differential
  • Electrocardiography
  • Humans
  • Muscle Proteins / genetics
  • NAV1.5 Voltage-Gated Sodium Channel
  • Risk Factors
  • Sodium Channels / genetics

Substances

  • Anti-Arrhythmia Agents
  • Muscle Proteins
  • NAV1.5 Voltage-Gated Sodium Channel
  • SCN5A protein, human
  • Sodium Channels