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(Circulation. 2008;117:1890-1893.)
© 2008 American Heart Association, Inc.
Clinician Update |
From the Division of Cardiology, Department of Medicine, University of Oulu, Oulu, Finland (M.J.J., H.V.H.); Montreal Heart Institute and University of Montreal, Montreal, Canada (M.G., E.L., R.B.); Cardiology Department, Thorax Institute, Hospital Clinic, Barcelona, Spain (B.B., J.B.); Department of Cardiology, Academic Hospital Maastricht, Maastricht, Netherlands (K.V.); and Heart Rhythm Management Institute, UZ Brussel-VUB, Brussels, Belgium (A.S., P.B.).
Correspondence to Ramon Brugada, MD, Montreal Heart Institute, 5000 Rue Belanger, Montreal, Quebec, H1T 1C8, Canada. E-mail ramon@brugada.org
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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| Introduction and Cases |
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Approximately one fourth of the cases of Brugada syndrome are caused by loss of function mutations in the cardiac sodium channel SCN5A. Several nongenetic factors have been mentioned in the literature as possible inductors of the ECG pattern resembling Brugada syndrome.2 As such, a Brugada-type ECG may appear in some patients during
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