on January 10, 2005
Published online before print January 10, 2005, doi: 10.1161/01.CIR.0000153267.21278.8D
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Submitted on June 17, 2004
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. * To whom correspondence should be addressed. E-mail: l.eckardt{at}uni-muenster.de.
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 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.
Revised on September 29, 2004
Accepted on October 11, 2004
Long-Term Prognosis of Individuals With Right Precordial ST-Segment-Elevation Brugada Syndrome
Lars Eckardt MD*,
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.
Key words: death, sudden • fibrillation • electrocardiography • genetics • risk factors
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