Circulation. 2005;111:659-670
Published online before print January 17, 2005, doi: 10.1161/01.CIR.0000152479.54298.51
Published online before print January 17, 2005, doi: 10.1161/01.CIR.0000152479.54298.51
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(Circulation. 2005;111:659-670.)
© 2005 American Heart Association, Inc.
Special Report |
Brugada Syndrome: Report of the Second Consensus Conference
Endorsed by the Heart Rhythm Society and the European Heart Rhythm Association
From the Masonic Medical Research Laboratory, Utica, NY (C.A., R.B.); Cardiovascular Center, Cardiovascular Research and Teaching Institute, Aalst, Belgium (P.B.); University of Heidelberg, University Hospital of Mannheim, Mannheim, Germany (M.B.); Cardiovascular Institute, Clinical Hospital, University of Barcelona, Barcelona, Spain (J.B.); Divisione di Cardiología, Università di Padova, Padova, Italy (D.C.); eResearch Technology, Inc, Bridgewater, NJ (I.G.); Chu de Nantes, Nantes, France (H.L.); Pacific Rim Electrophysiology Research Institute, Inglewood, Calif (K.N.); ABC’s Faculty of Medicine, ABC Foundation, Santo André, São Paulo, Brazil (A.R.P.R.); National Cardiovascular Center, Suita, Japan (W.S.); Department of Cardiology, University of Münster, and Institute for Arteriosclerosis Research, Münster, Germany (E.S.-B.); and Experimental and Molecular Cardiology Group, Academic Medical Center, Amsterdam, and the Interuniversity Cardiology Institute, Utrecht, the Netherlands (H.T., A.W.).
Correspondence to Dr Charles Antzelevitch, Gordon K. Moe Scholar, Masonic Medical Research Laboratory, 2150 Bleecker St, Utica, NY 13501. E-mail ca{at}mmrl.edu
Since its introduction as a clinical entity in 1992, the Brugada syndrome has progressed from being a rare disease to one that is second only to automobile accidents as a cause of death among young adults in some countries. Electrocardiographically characterized by a distinct ST-segment elevation in the right precordial leads, the syndrome is associated with a high risk for sudden cardiac death in young and otherwise healthy adults, and less frequently in infants and children. Patients with a spontaneously appearing Brugada ECG have a high risk for sudden arrhythmic death secondary to ventricular tachycardia/fibrillation. The ECG manifestations of Brugada syndrome are often dynamic or concealed and may be unmasked or modulated by sodium channel blockers, a febrile state, vagotonic agents, 
-adrenergic agonists, ß-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of glucose and insulin, hypo- and hyperkalemia, hypercalcemia, and alcohol and cocaine toxicity. In recent years, an exponential rise in the number of reported cases and a striking proliferation of articles defining the clinical, genetic, cellular, ionic, and molecular aspects of the disease have occurred. The report of the first consensus conference, published in 2002, focused on diagnostic criteria. The present report, which emanated from the second consensus conference held in September 2003, elaborates further on the diagnostic criteria and examines risk stratification schemes and device and pharmacological approaches to therapy on the basis of the available clinical and basic science data.
Key Words: arrhythmia • death, sudden • electrocardiography • diagnosis
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D. Darbar, T. Yang, K. Churchwell, A. A.M. Wilde, and D. M. Roden Unmasking of Brugada Syndrome by Lithium Circulation, September 13, 2005; 112(11): 1527 - 1531. [Abstract] [Full Text] [PDF]
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P. Brugada, R. Brugada, J. Brugada, S. G. Priori, C. Napolitano, P. Brugada, R. Brugada, J. Brugada, S. G. Priori, and C. Napolitano Should patients with an asymptomatic Brugada electrocardiogram undergo pharmacological and electrophysiological testing? Circulation, July 12, 2005; 112(2): 279 - 292. [Full Text] [PDF]
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