Effect of amiodarone and sotalol on the defibrillation threshold in comparison to patients without antiarrhythmic drug treatment

Abstract

Aim of the study: It is generally accepted that chronic therapy with antiarrhythmic drugs might increase the defibrillation threshold at implantation of an implantable cardioverter defibrillator. A recently published animal study showed a minor effect of the class 1 antiarrhythmic drug lidocaine on the defibrillation threshold if biphasic shocks were used.

Methods and results: We therefore performed a retrospective analysis in 89 patients who received an ICD capable of monophasic (n=18) or biphasic (n=71) shocks with a transvenous lead system. In all patients the defibrillation threshold was determined according to the same step down protocol. In the 18 patients with a monophasic device the effects of chronic therapy with amiodarone (n=7) on the defibrillation threshold were evaluated in comparison to a group without antiarrhythmic treatment (n=11). In those patients receiving a biphasic device the effects of chronic therapy with amiodarone (n=29), sotalol (n=20) or no antiarrhythmic medication (n=22) on the defibrillation threshold were evaluated. The groups receiving a monophasic device did not differ in respect to age, sex, underlying cardiac disease, clinical arrhythmia (VT/VF), clinical functional status, left ventricular ejection fraction and the number of patients with additional subcutaneous electrodes. These parameters as well as the type of implanted device were not different between patient groups receiving a biphasic device. Patients on chronic amiodarone therapy receiving a monophasic device had a significantly higher defibrillation threshold (29.1 +/- 8.8 J) than patients without antiarrhythmic treatment (19.1 +/- 5.1 J, P = 0.021). The groups did not differ significantly in respect to the impedance measured at the shocking lead (P = 0.13). In three patients on chronic amiodarone an epicardiac lead system had to be implanted due to an inadequate monophasic defibrillation threshold compared to no patient without antiarrhythmic drug treatment (P = 0.043). In the patients with a biphasic device the intraoperative defibrillation threshold was not significantly different between the three study groups (P = 0.44). No patient received an epicardiac lead system. The defibrillation threshold in the amiodarone group was 15.3 +/- 7.3 J, in the sotalol group 14.4 +/- 7.2 J and in the patients without antiarrhythmic drug treatment 17 +/- 6.1 J. As well, no significant difference was seen between the groups in respect of the impedance of the high voltage electrode (P = 0.2).

Conclusion: With the use of a biphasic device in combination with a transvenous lead system the intraoperative defibrillation threshold is not significantly different between patients on chronic amiodarone in comparison to patients without antiarrhythmic drug treatment or patients on chronic oral sotalol. This is in contrast to our findings with a monophasic device.