Intravenous amiodarone homogeneously prolongs ventricular repolarization in patients with life-threatening ventricular tachyarrhythmia.

BACKGROUND

The most critical adverse effects of class III drugs are marked QT prolongation and torsade de pointes. Even though intravenous amiodarone (iv-Amio) is a representative class III drug, it peculiarly inhibits both clinical ventricular tachycardia/fibrillation (VT/VF) and proarrhythmic effects. To test the hypothesis that iv-Amio homogeneously prolongs repolarization, we evaluated electrocardiographic changes before and during short-term amiodarone therapy, focusing closely on the ventricular dispersion of repolarization.

METHODS

Twenty-seven consecutive patients treated with iv-Amio for VT/VF as a first-line antiarrhythmic therapy were enrolled in this study. Twelve-lead electrocardiography was recorded before and during amiodarone therapy to evaluate the following electrocardiographic intervals: R-R, QRS, QT, QRS to T-peak (QTp), and T-peak to T-end (Tp-e; as an index of dispersion of repolarization). Repolarization indices were corrected to the heart rate by Bazett's method (QTc, c-QTp, c-Tp-e).

RESULTS

Amiodarone suppressed VT/VF in 19/27 (70%) patients without conferring any proarrhythmic effect. The QTc, c-QTp, and R-R interval were significantly prolonged during amiodarone (476±45ms vs 511±45ms, p<0.05; 338±40ms vs 364±35ms, p<0.05; 762±272ms vs 870±189ms, p<0.05; respectively), whereas the c-Tp-e and QRS durations did not change significantly (139±33ms vs 145±41ms, p=0.25; 96±20ms vs 97±21ms, p=0.33; respectively).

CONCLUSIONS

Iv-Amio homogeneously prolongs repolarization and properly inhibits original VT/VF recurrence without inducing torsade de pointes.