Brugada syndrome: a decade of progress.
The Brugada syndrome has gained wide recognition throughout the world and today is believed to be responsible for 4% to 12% of all sudden deaths and approximately 20% of deaths in patients with structurally normal hearts. The incidence of the disease is on the order of 5 per 10 000 inhabitants and, apart from accidents, is the leading cause of death of men under the age of 50 in regions of the world where the inherited syndrome is endemic. This minireview briefly summarizes the progress made over the past decade in our understanding of the clinical, genetic, cellular, ionic, and molecular aspects of this disease.
Antzelevitch
C
C
Masonic Medical Research Laboratory, Utica, NY 13501, USA. ca@mmrl.edu
Brugada
P
P
Brugada
J
J
Brugada
R
R
Shimizu
W
W
Gussak
I
I
Perez Riera
A R
AR
D001145:Arrhythmias, Cardiac / Q000150:complications* / Q000175:diagnosis* / Q000235:genetics / Q000628:therapy; D002037:Bundle-Branch Block / Q000235:genetics / Q000503:physiopathology; D016757:Death, Sudden, Cardiac / Q000209:etiology*; D004562:Electrocardiography; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans; D008297:Male; D062554:NAV1.5 Voltage-Gated Sodium Channel; D015222:Sodium Channels / Q000235:genetics; D013575:Syncope / Q000209:etiology*; D017180:Tachycardia, Ventricular / Q000175:diagnosis / Q000209:etiology / Q000628:therapy; D014693:Ventricular Fibrillation / Q000175:diagnosis / Q000209:etiology / Q000628:therapy
D062554:NAV1.5 Voltage-Gated Sodium Channel; C568320:SCN5A protein, human; D015222:Sodium Channels