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Longitudinal analysis of the depressive effects of intravenous amiodarone on depolarization and repolarization: a

Koichiro Yoshioka1, Mari Amino, Atsushi Matsuzaki

  • 1Department of Cardiology, Tokai University School of Medicine, 143 Shimokasuya, Isehara 259-1193, Kanagawa, Japan. ko1@is.icc.u-tokai.ac.jp

Journal of Cardiology
|December 1, 2009
PubMed

Insights

Intravenous amiodarone (AMD) effectively reduced ventricular premature contractions by altering depolarization, even with prolonged QT intervals. Its antiarrhythmic effect relies on sodium channel blockade, not just repolarization changes.

Area of Science:

  • Cardiology
  • Clinical Electrophysiology
  • Pharmacology

Background:

  • Intravenous amiodarone (AMD) is used for treating ventricular arrhythmias.
  • AMD acts by blocking sodium (Na+), calcium (Ca2+), and IKr channels, and beta receptors.

Observation:

  • A patient on chronic dialysis received AMD for non-sustained ventricular tachycardia.
  • QT prolongation was observed 5 hours after AMD administration, with QTc reaching 716 ms.
  • Ventricular premature contractions (VPCs) decreased initially but increased after AMD withdrawal.

Findings:

  • AMD's Na+-channel blocking action altered depolarization, increasing filtered QRS duration and decreasing ventricular late potentials.
  • The antiarrhythmic effect on VPCs correlated with depolarization changes, not QT prolongation or AMD blood concentration.
  • AMD's efficacy in suppressing VPCs required its Na+-channel blocking action, irrespective of QT interval prolongation.

Implications:

  • The Na+-channel blocking property of AMD is crucial for its antiarrhythmic effect in ventricular tachycardia.
  • Understanding AMD's mechanism, particularly its impact on depolarization, is vital for managing cardiac arrhythmias.
  • This case highlights the complex electrophysiological effects of AMD, especially in patients with renal impairment.

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