(Circulation. 2008;118:e701.)
© 2008 American Heart Association, Inc.
Correspondence |
Cardiac and Vascular Sciences, St Georges University of London, London, United Kingdom
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
To the Editor:
We have read with interest the article by Juntilla et al1 describing the poor prognosis associated with the acute induction of the Brugada type 1 ECG pattern. In particular, 11 of 26 patients with drug-induced changes suffered sudden and/or resuscitated cardiac death. The majority of life-threatening cases were related to propofol infusion, whereas the rest were secondary to use of sodium channel blockers (antiarrhythmics and local anesthetics). Only 5 patients, who were asymptomatic, had been exposed to cocaine and antidepressants.
These findings, however, do not reflect the current literature, in which antidepressant overdoses appear to be the most commonly reported cause of the drug-induced Brugada ECG pattern, usually with an unremarkable event rate. For example, in a series of 95 cases of cyclic antidepressant overdoses,2 10 (10.5%) presented with the Brugada ECG, 1 of whom died of recurrent ventricular fibrillation compared with 1 death among those without the Brugada ECG. In another retrospective French study of 65 cases, 15% demonstrated the type 1 ECG pattern but without any arrhythmia.3 A larger series of approximately 400 cases of tricyclic overdoses found that only 2.3% developed the type 1 Brugada ECG pattern, again without any attendant increased risk of arrhythmia.4
To the best of our knowledge, there have been no similar systematic studies of the prevalence of the Brugada ECG pattern in patients receiving propofol and sodium channel blockers apart from 1 assessment of ajmaline by Hermida et al,5 who evaluated 1000 individuals undergoing occupational ECGs. A single spontaneous
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