Brugada syndrome: recent advances and controversies.
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.
Antzelevitch
Charles
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Masonic Medical Research Laboratory, 2150 Bleecker Street, Utica, NY 13501, USA. ca@mmrl.edu
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D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D053840:Brugada Syndrome / Q000150:complications / Q000175:diagnosis / Q000235:genetics / Q000628:therapy; D016757:Death, Sudden, Cardiac / Q000209:etiology; D017147:Defibrillators, Implantable; D003937:Diagnosis, Differential; D004562:Electrocardiography; D006801:Humans; D009124:Muscle Proteins / Q000235:genetics; D062554:NAV1.5 Voltage-Gated Sodium Channel; D012307:Risk Factors; D015222:Sodium Channels / Q000235:genetics
D000889:Anti-Arrhythmia Agents; D009124:Muscle Proteins; D062554:NAV1.5 Voltage-Gated Sodium Channel; C568320:SCN5A protein, human; D015222:Sodium Channels