Effect of lidocaine and amiodarone on transmural heterogeneity of ventricular repolarization in isolated rabbit hearts model of sustained global ischemia

Abstract

To study the effect of of lidocaine and amiodarone on the transmural heterogeneity of ventricular repolarization in isolated rabbit hearts model of sustained global ischemia and to explore the mechanisms underlying the antiarrhythmic activity of lidocaine and amiodarone, rabbits were randomly divided into 4 groups: control group, ischemia group, lidocaine group and amiodarone group. By the monophasic action potential (MAP) recording technique, MAPs of epicardium, mid-myocardium and endocardium were simultaneously recorded across the left ventricular free wall in rabbit hearts perfused by low-flow ischemia (2.5 mL/min) in Langendorff method to study the transmural dispersion of repolarization (TDR) and arrhythmic induced by ischemia. Our results showed that TDR of three myocardial layers in ischemia group were significantly lengthened after ischemia. TDR was increased from 17.5 +/- 3.9 ms to 31.2 +/- 4.6 ms at the time that concided with the onset of sustained ventricle arrhythmic. Amiodarone could decrease TDR, but lidocaine could increase TDR at initial ischemia, and no significant difference was found at other ischemia time points. 5 cases had ventriclar arrhythmia in ischemia group (62.5%), but no case in lidocaine group (P < 0.01) and only 1 case in amiodarone group had ventrilar arrhythmia (P < 0.01). No significant difference was found between amiodarone group and lidocaine group. It is concluded that TDR of of three myocardial layers increases significantly at ischemia and it is closely associated with development of ventricular arrhythmia, and amiodarone could decrease TDR, but lidocaine could increase TDR at initial ischemia and has no effects at other ischemia time points.

Effect of Prophylactic Amiodarone Infusion on the Recurrence of Ventricular Arrhythmias in Out-of-Hospital Cardiac Arrest Survivors: A Propensity-Matched Analysis

“…Pleiotropic effects, including the improvement of cardiac metabolic efficiency after the ischemic-reperfusion period were reported to have a main role in preventing reperfusion ventricular arrhythmias, whereas an increase in transmural dispersion of repolarization was reported to be associated with development of ventricular arrhythmia in animal studies [16,17,18]. Amiodarone theoretically can prolong QTc and therapeutic hypothermia can potentiate the arrhythmogenic risk of amiodarone through QTc prolongation [19].…”