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Antiarrhythmic properties of a rapid delayed-rectifier current activator in rabbit models of acquired long QT

Thomas G Diness1, Yung-Hsin Yeh, Xiao Yan Qi

  • 1Department of Medicine and Research Center, Montreal Heart Institute and Université de Montréal, 5000 Belanger Street East, Montreal, Quebec, Canada H1T 1C8.

Cardiovascular Research
|March 28, 2008
PubMed
Abstract

Insights

A novel compound, NS1643, effectively treats long QT syndrome (LQTS) and Torsades de Pointes (TdP) arrhythmias by activating the rapid delayed-rectifier K+ current (I(Kr)). This study demonstrates NS1643

Area of Science:

  • Cardiovascular Pharmacology
  • Cardiac Electrophysiology
  • Molecular Cardiology

Background:

  • Impaired cardiac repolarization causes long QT syndrome (LQTS), increasing Torsades de Pointes (TdP) risk.
  • Current LQTS treatments are often insufficient.
  • The rapid delayed-rectifier K+ current (I(Kr)) is crucial for cardiac repolarization.

Purpose of the Study:

  • To assess the antiarrhythmic efficacy of NS1643, a novel I(Kr)-activating compound.
  • To evaluate NS1643 in rabbit models of acquired LQTS and TdP.

Main Methods:

  • Two rabbit models of acquired LQTS and TdP were used: bradycardia-induced atrioventricular block and dofetilide-induced I(Kr) inhibition.
  • NS1643 or vehicle was administered intravenously.
  • Effects on ionic currents in isolated cardiomyocytes were analyzed.

Main Results:

  • NS1643 completely abolished TdP and shortened the QT interval in bradycardic rabbits.
  • NS1643 reversed dofetilide-induced QT prolongation and suppressed ventricular tachyarrhythmias.
  • NS1643 significantly increased I(Kr) in cardiomyocytes, restoring current suppressed by bradycardia or dofetilide.

Conclusions:

  • Pharmacological activation of I(Kr) effectively reverses acquired LQTS and TdP.
  • NS1643 demonstrates potential as a therapeutic agent for LQTS.
  • I(Kr)-activating drug therapy represents a promising treatment strategy for LQTS.

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