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J Am Coll Cardiol, 2003; 41:1665-1671, doi:10.1016/S0735-1097(03)00310-3 © 2003 by the American College of Cardiology Foundation |



* Masonic Medical Research Laboratory, Utica, New York, USA
Cardiovascular Center, OLV Hospital, Aalst, Belgium
Cardiovascular Institute, Hospital Clinic, University of Barcelona, Barcelona, Spain
Pediatrics Department, Section of Cardiology, Baylor College of Medicine, Houston, Texas, USA
|| Pacific Rim Cardiac Electrophysiology and Research, Inglewood, California, USA
Manuscript received October 30, 2002; revised manuscript received December 20, 2002, accepted January 24, 2003.
* Reprint requests and correspondence: Dr. Charles Antzelevitch, Masonic Medical Research Laboratory, 2150 Bleecker Street, Utica, New York 13501, USA.
ca{at}mmrl.edu
An intriguing new clinical entity characterized by ST-segment elevation in the right precordial electrocardiographic leads and a high incidence of sudden death in individuals with structurally normal hearts was described by Pedro and Josep Brugada in 1992. The past decade has witnessed an exponential rise in the number of reported cases and a dramatic proliferation of papers serving to define the clinical, genetic, cellular, ionic, and molecular aspects of this disease. The purpose of this brief review is to chronicle the historical highlights that have brought us to our present understanding of Brugada syndrome.
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