1999 Volume 40 Issue 4 Pages 471-475
A 33 year-old woman was referred to our hospital for further treatment of ventricular tachycardia (VT). During treatment with amiodarone (200 mg/day), clinical VT at the cycle length of 510 ms was induced. During the VT, rapid ventricular pacing was repeated at progressively shorter cycle lengths after a decrement of 10 ms steps. The VT was entrained by the rapid pacing and reproducibly terminated at a paced cycle length of 380 ms. Four weeks after reducing the amiodarone to 100 mg/day, programmed stimulation was repeated. The VT with the same morphology but with a slightly shorter cycle length of 480 ms was again induced. However, at this time, rapid pacing from the same site could not terminate VT and transient acceleration developed at a shorter paced cycle length of 260 ms. The QT (QTc) interval, effective refractory period at the pacing site and width of the paced QRS complex were similar before and after changing the amiodarone treatment. The most characteristic change of VT in the second study was a widening of the entrainment zone, which was calculated as the difference between VT cycle length and the longest pacing cycle length which interrupts VT during the entrainment (from 130 to > 220 ms), and it may be explained by the preferential shortening of the action potential duration and/or facilitation of the depressed cell to cell conduction within the reentry circuit. Amiodarone must exert a preferential action in the reentry circuit and modulate the conduction property as well as the effective refractory period. We should pay close attention to the efficacy of antitachycardia pacing during the modification of amiodarone treatment.
