Published online before print January 10, 2005, doi: 10.1161/01.CIR.0000153267.21278.8D
(Circulation. 2005;111:257-263.)
© 2005 American Heart Association, Inc.
Arrhythmia/Electrophysiology |
Long-Term Prognosis of Individuals With Right Precordial ST-Segment–Elevation Brugada Syndrome
From the Westfälische Wilhelms University Hospital, Department of Cardiology and Angiology, Münster, Germany (L.E., E.S.B., T.W., G.B., D.B.); University Hospital, Department of Cardiology, Nantes, France (V.P., H.L.); INSERM U533, University of Nantes, Nantes, France (V.P., P.B., H.L.); Experimental and Molecular Cardiology Group, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands (J.P.P.S., A.A.M.W.); University Hospital Mannheim, University of Heidelberg, Mannheim, Germany (C.W., R.S., M.B.); and Department of Medical Informatics and Biomathematics, University of Münster, Münster, Germany.
Correspondence to PD Dr Lars Eckardt, Universitätsklinikum Münster Medizinische Klinik und Poliklinik C, Kardiologie und Angiologie, Albert Schweitzer Str 33, D-48149 Münster, Germany. E-mail l.eckardt{at}uni-muenster.de
Received June 17, 2004; revision received September 29, 2004; accepted October 11, 2004.
Background— Brugada syndrome is an arrhythmogenic disease characterized by an ECG pattern of ST-segment elevation in the right precordial leads and an increased risk of sudden cardiac death as a result of ventricular fibrillation. Controversy exists with regard to risk stratification and therapeutic management, particularly in asymptomatic individuals.
Methods and Results— A total of 212 individuals (mean age, 45±6 years) with a type 1 Brugada ECG pattern were studied. Of these, 123 (58%) were asymptomatic, 65 (31%) had 
1 syncope of unknown origin, and 24 (11%) had to be resuscitated because of ventricular fibrillation. In 125 individuals (59%), a spontaneous type 1 ECG was recorded. In the remaining, drug challenge with a class I antiarrhythmic agent unmasked a Brugada ECG. The mean ST elevation was 2.3±1.2 mm in symptomatic patients and 1.9±1.5 mm in asymptomatic individuals (P=0.04). During a mean follow-up of 40±50 months, 4 of the 24 patients (17%) with aborted sudden cardiac death and 4 of 65 (6%) with a prior syncope had a recurrent arrhythmic event, whereas only 1 of 123 asymptomatic individuals (0.8%) had a first arrhythmic event. Four of 9 patients with arrhythmic events during follow-up were not inducible during programmed electrical stimulation. A previous history of aborted sudden death or syncope and the presence of a spontaneous type 1 ECG were predictors of adverse outcome.
Conclusions— The present study reports data on a large population of individuals with a type 1 Brugada ECG pattern with the longest follow-up reported so far. A very low incidence of severe arrhythmic events, particularly in asymptomatic individuals, was found during follow-up. In the presence of very few arrhythmic events on follow-up, programmed electrical stimulation showed very little accuracy in predicting outcome.
Key Words: death, sudden • fibrillation • electrocardiography • genetics • risk factors
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