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Atrium-specific Kir3.x determines inducibility, dynamics, and termination of fibrillation by regulating

Brian O Bingen1, Zeinab Neshati, Saïd F A Askar

  • 1Laboratory of Experimental Cardiology, Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands (B.O.B., Z.N., S.F.A.A., D.L.Y., M.J.S., A.A.V.d.V., D.A.P.); and Department of Physics and Astronomy, Ghent University, Ghent, Belgium (I.V.K., A.V.P.).

Circulation
|September 26, 2013
PubMed

Insights

Blocking atrium-specific Kir3.x channels effectively terminates atrial fibrillation by prolonging action potential duration. This study identifies Kir3.x as a promising target for new antiarrhythmic drugs.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Electrophysiology

Background:

  • Atrial fibrillation is a common arrhythmia.
  • Ventricular proarrhythmia complicates treatment.
  • Atrium-specific Kir3.x channels generate a constitutively active current (I(K,ACh-c)) after atrial remodeling.

Purpose of the Study:

  • Investigate the role of I(K,ACh-c) in atrial fibrillation induction, dynamics, and termination.
  • Evaluate the effects of I(K,ACh-c) blockade and Kir3.x downregulation on atrial fibrillation.

Main Methods:

  • Used neonatal rat atrial cardiomyocyte cultures and intact atria.
  • Induced reentry through burst pacing.
  • Treated cultures with tertiapin or used lentiviral vectors for Kcnj3/Kcnj5 shRNA.
  • Performed whole-heart mapping experiments.

Main Results:

  • Tertiapin prolonged action potential duration (APD) in atrial cultures during reentry.
  • I(K,ACh-c) blockade decreased rotor frequency and complexity.
  • Knockdown of Kcnj3 or Kcnj5 yielded similar results.
  • Blockade prevented/terminated reentry by altering APD and conduction velocity restitution slopes.
  • Reduced atrial fibrillation inducibility by over 50% after I(K,ACh-c) blockade.

Conclusions:

  • Atrium-specific Kir3.x channels control atrial fibrillation induction, dynamics, and termination.
  • Modulation of APD and restitution slopes by I(K,ACh-c) is key.
  • Kir3.x is a promising atrium-specific target for antiarrhythmic strategies.
Abstract

Keywords:
G protein-coupled inwardly rectifying potassium channelsRNA interferenceaction potentialsarrhythmiaatrial fibrillationcardiomyocytevoltage-sensitive dye imaging

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