Different Effects of Amiodarone and Quinidine on the Homogeneity of Myocardial Refractoriness in Patients With Intraventricular Conduction Delay

Abstract

Background: Increases in QT and JT dispersion have been suggested as indicative of a proarrhythmic potential as a result of heterogeneity in myocardial refractoriness, the reduc tion of which by antiarrhythmic agents might be associated with a beneficial effect on the development of serious ventricular arrhythmias.

Methods: To test the hypothesis that amiodarone reduces the heter-ogeneity of ventricular refractoriness to a significantly greater extent than quinidine in patients with intraventricu lar conduction defects under treatment for ventricular arrhythmias, the corrected and uncorrected QT and JT intervals and dispersions from 12-lead surface electrocardiograms were determined in 120 patients with intraventricular conduction defects with cardiac arrhythmias before and during treatment with amiodarone (n = 60) and quinidine (n = 60).

Rcsults: Amiodarone increased QT from 403 ± 50 ms to 459 ± 47 ms (P < .001), with a sim ilar increase in the corrected QT interval (QTc) (P < .001). Amiodarone reduced QT disper sion by 40% (P < .001), whereas quinidine increased by 18% (P < .001). The net effects of both drugs were similar for QTc. Amiodarone, but not quinidine, reduced heart rate signifi cantly; amiodarone had no effect on the QRS; but quinidine increased it (P < .001). Quini dine as well as amiodarone increased the JT and JTc intervals significantly, but the effect of quinidine was quantitatively less striking. Amiodarone decreased the JT dispersion by 33% (P < .001) and JTc dispersion by 37% (P < .001). On the other hand, quinidine increased the corresponding values for JT and JTc by 18% (P < .001) and 21 % (P < .001), respectively. The overall data on QT and JT dispersions indicate an improvement in the homogeneity of myo cardial refractoriness with amiodarone treatment and the converse with quinidine treatment; this observation is consistent with a lower proarrhythmic propensity and mortality with amio darone than with quinidine. Quinidine increased the QRS interval more than amiodarone, and the data indicate that in patients with intraventricular conduction defects, the monitoring of the JT interval might more accurately reflect changes in myocardial repolarization.

Conclusions: Amiodarone and quinidine both increased the corrected and uncorrected QT and JT intervals; amiodarone decreased and quinidine increased the dispersion of these intervals, and these results suggested an improvement in the homogeneity of myocardial refractoriness as a result of amiodarone treatment and the converse as a result of quinidine treatment. Quinidine increased the QTS interval more than amiodarone, and the data indi cate that in patients with intraventricular conduction defects, the monitoring of the JT inter val might more accurately reflect changes in myocardial repolarization.