Long-term prognosis of individuals with right precordial ST-segment-elevation Brugada syndrome.
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.


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 > or =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.
Eckardt
Lars
L
Westfälische Wilhelms University Hospital, Department of Cardiology and Angiology, Münster, Germany. l.eckardt@uni-muenster.de
Probst
Vincent
V
Smits
Jeroen P P
JP
Bahr
Eric Schulze
ES
Wolpert
Christian
C
Schimpf
Rainer
R
Wichter
Thomas
T
Boisseau
Pierre
P
Heinecke
Achim
A
Breithardt
Günter
G
Borggrefe
Martin
M
LeMarec
Herve
H
Böcker
Dirk
D
Wilde
Arthur A M
AA
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002037:Bundle-Branch Block / Q000175:diagnosis* / Q000235:genetics / Q000503:physiopathology; D002648:Child; D004558:Electric Stimulation; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009154:Mutation; D062554:NAV1.5 Voltage-Gated Sodium Channel; D011379:Prognosis; D026941:Sodium Channel Blockers; D015222:Sodium Channels / Q000235:genetics
D062554:NAV1.5 Voltage-Gated Sodium Channel; C568320:SCN5A protein, human; D026941:Sodium Channel Blockers; D015222:Sodium Channels