Brugada syndrome ECG provoked by the selective serotonin reuptake inhibitor fluvoxamine

Europace. 2010 Feb;12(2):282-3. doi: 10.1093/europace/eup332. Epub 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), 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.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Brugada Syndrome / chemically induced*
  • Brugada Syndrome / diagnosis
  • Depression / drug therapy
  • Electrocardiography
  • Fluvoxamine / adverse effects*
  • Fluvoxamine / therapeutic use
  • Humans
  • Male
  • Muscle Proteins / genetics
  • Mutation / genetics
  • NAV1.5 Voltage-Gated Sodium Channel
  • Serotonin Uptake Inhibitors / adverse effects*
  • Serotonin Uptake Inhibitors / therapeutic use
  • Sodium Channels / genetics

Substances

  • Muscle Proteins
  • NAV1.5 Voltage-Gated Sodium Channel
  • SCN5A protein, human
  • Serotonin Uptake Inhibitors
  • Sodium Channels
  • Fluvoxamine