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Delayed sodium channel inactivation mimics long QT syndrome 3.

Abstract
DPI 201-106 delays sodium channel inactivation. Acute administration of DPI 201-106 prolonged the QT interval, provoked spontaneous torsades de pointes in one patient, and facilitated stimulation-induced polymorphic ventricular tachyarrhythmias in two patients. Similar to the observations in animal studies, delaying sodium channel inactivation is a new form of the acquired long QT syndrome, mimicking long QT syndrome type 3.
AuthorsVolker Kühlkamp, Christian Mewis, Ralph Bosch, Ludger Seipel
JournalJournal of cardiovascular pharmacology (J Cardiovasc Pharmacol) Vol. 42 Issue 1 Pg. 113-7 (Jul 2003) ISSN: 0160-2446 [Print] United States
PMID12827035 (Publication Type: Clinical Trial, Journal Article)
Chemical References
  • Cardiotonic Agents
  • Piperazines
  • Sodium Channels
  • DPI 201-106
Topics
  • Cardiotonic Agents (administration & dosage, adverse effects)
  • Electrocardiography
  • Electrophysiology
  • Female
  • Humans
  • Infusions, Intravenous
  • Long QT Syndrome (etiology, metabolism)
  • Male
  • Piperazines (administration & dosage, adverse effects)
  • Single-Blind Method
  • Sodium Channels (drug effects, physiology)
  • Tachycardia, Ventricular (etiology, metabolism)

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