Skip Navigation



Europace Advance Access published online on October 29, 2009

Europace, doi:10.1093/europace/eup332
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Stirnimann, G.
Right arrow Articles by Schwick, N. G.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Stirnimann, G.
Right arrow Articles by Schwick, N. G.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.


SHORT COMMUNICATION

Brugada syndrome ECG provoked by the selective serotonin reuptake inhibitor fluvoxamine

Guido Stirnimann1, Séverine Petitprez2, Hugues Abriel2 and Nicola G. Schwick3,*

1 Institute of Clinical Pharmacology and Visceral Research, University of Bern, Bern, Switzerland; 2 Department of Clinical Research, University of Bern, Bern, Switzerland; 3 Swiss Cardiovascular Center Bern, Inselspital, University Hospital and University of Bern, CH-3010 Bern, Switzerland

A patient with an SCN5A p.W822X nonsense mutation, localized in the transmembrane region DII-S4 of the Nav1.5 sodium channel and leading to a non-expression of the mutant allele, was prescribed the selective serotonin reuptake inhibitor (SSRI) fluvoxamine (Floxyfral®), 100 mg per day. His normal baseline ECG changed to a characteristic Brugada-Type-1-ECG pattern. To investigate whether fluvoxamine may reduce the cardiac sodium current, the effect of this drug was studied on the wild-type voltage-gated cardiac sodium channel Nav1.5 stably expressed in HEK293 cells. Patch-clamp recording showed a 50% inhibition of the current at a concentration of 57.3 µM. In our patient, no arrhythmia occurred but the proarrhythmic potential of SSRI in patients with SCN5A mutations cannot be excluded. Therefore, we advise 12-lead ECG control after administering SSRI in these patients.


* Corresponding author. Tel: +41 31 632 0337, Fax: +41 31 632 1414, Email: nicola.schwick{at}insel.ch

Manuscript submitted 17 August 2009. Accepted after revision 28 September 2009.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.