Brugada syndrome ECG provoked by the selective serotonin reuptake inhibitor fluvoxamine. Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology [Europace] Journal article | | Title | Brugada syndrome ECG provoked by the selective serotonin reuptake inhibitor fluvoxamine. | | Author(s) | Stirnimann G, Petitprez S, Abriel H, Schwick NG | | Institution | 1Institute of Clinical Pharmacology and Visceral Research, University of Bern, Bern, Switzerland. | | Source | Europace 2009 Oct 29. | | Abstract | A patient with an SCN5A p.W822X nonsense mutation, localized in the transmembrane region DII-S4 of the Na(v)1.5 sodium channel and leading to a non-expression of the mutant allele, was prescribed the selective serotonin reuptake inhibitor (SSRI) fluvoxamine (Floxyfral((R))), 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 Na(v)1.5 stably expressed in HEK293 cells. Patch-clamp recording showed a 50% inhibition of the current at a concentration of 57.3 microM. 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. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 19875396 |
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