Longitudinal analysis of the depressive effects of intravenous amiodarone on depolarization and repolarization: A case report

Summary Intravenous amiodarone (AMD) induces multiple antiarrhythmic effects via blocking of Na + , Ca 2+ , and IKr channels, and β receptors. A patient on chronic dialysis was administered AMD for nonsustained ventricular tachycardia after successful cardiopulmonary resuscitation. QT prolongation occurred 5 h after AMD administration. AMD was withdrawn at 24 h because of prolonged QTc interval (716 ms), which persisted for a further 48 h (661 ms). Ventricular premature contraction (VPC) was significantly decreased at 7 h; however, VPC increased again after discontinuing AMD. Depolarization changes induced by the Na + -channel blocking action of AMD were analyzed. There was increasing filtered QRS-duration and duration of low-amplitude signals at voltage + -channel blocking action is required for AMD to induce the antiarrhythmic effect.