The safety and efficacy of long-term amiodarone therapy were examined in 12 patients who had previously developed torsade de pointes as a complication of previous antiarrhythmic therapy. The QTc intervals were determined at the time of torsade de pointes (570 +/- 40 ms), after 7 days of amiodarone loading (490 +/- 70 ms), and after 3 months of chronic amiodarone administration (580 +/- 80 ms). Compared to a drug-free control period, QTc was significantly prolonged (P less than 0.05) at the time of torsade de pointes, after amiodarone loading, and after 3 months of amiodarone therapy. The QTc intervals at the time of torsade de pointes and after chronic amiodarone treatment were not significantly different. At 16 +/- 7 months of follow-up, all patients remained free of subsequent torsade de pointes, syncope, or sudden death. In addition, 5 of 6 patients with a history of sustained ventricular tachycardia remained free from arrhythmic recurrence despite persistence of inducible ventricular tachycardia during programmed stimulation studies done before discharge. We conclude that amiodarone can often be used safely and effectively in patients who have previously had an episode of drug-mediated torsade de pointes. Amiodarone-induced QTc prolongation, even when marked, does not predict recurrent torsade de pointes. These observations also suggest that the propensity for a drug to produce this arrhythmia is dependent on other electrophysiologic effects in addition to its ability to simply lengthen repolarization.

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Clinicians must be aware of this occult cause of device failure and more studies are needed to determine its true prevalence.

Inhibition of pacemakers due to false signals from malfunctioning pacing leads has been previously reported. Three cases are reported in which inappropriate pauses were observed shortly following implantation. In all three cases, active fixation leads with an electronically active screw and ring tip electrode were used. All leads were manufactured by Oscor Medical, St. Petersburg, Florida. In case one, models PY-61 (ventricle) and PY-51 (atrium) were used. In case two, models PY-61 were used in the ventricle and the atrium. In case three, models PY-52 were used both in the atrium and ventricle. Thresholds at the time of implantation were acceptable. In cases one and two, inappropriate pauses were noted following paced ventricular beats. In case three, inappropriate inhibition of the ventricular output was noted intermittently after some of the paced atrial beats. Spurious signals were identified as the cause of the apparent oversensing problem by using electrocardiograms with annotated telemetry information and noninvasively telemetered intracardiac electrograms. The amplitude of the spurious signals varied between 2 and 14 mV. In all cases, the problems resolved with time. A mechanism for the generation of false transients is proposed and the value of telemetered intracardiac electrograms is discussed.