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

Aim of the study: It is generally accepted that chronic therapy with antiar rhythmic drugs might increase the defibrillation threshold at implantation of an implantable cardioverter defibrillator. A recently published animal s tudy showed a minor effect of the class 1 antiarrhythmic drug lidocaine on the defibrillation threshold if biphasic shocks were used. Methods and resu lts: We therefore performed a retrospective analysis in 89 patients who rec eived an ICD capable of monophasic (n=18) or biphasic (n=71) shocks with a transvenous lead system. In all patients the defibrillation threshold was d etermined according to the same step down protocol. In the 18 patients with a monophasic device the effects of chronic therapy with amiodarone (n=7) o n the defibrillation threshold were evaluated in comparison to a group with out antiarrhythmic treatment (n=11). In those patients receiving a biphasic device the effects of chronic therapy with amiodarone (n=29), sotalol (n=2 0) or no antiarrhythmic medication (n=22) on the defibrillation threshold w ere evaluated. The groups receiving a monophasic device did not differ in r espect to age, sex, underlying cardiac disease, clinical arrhythmia (VT/VF) , clinical functional status, left ventricular ejection fraction and the nu mber 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 thr eshold (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 th e impedance measured at the shocking lead (P=0.13). In three patients on ch ronic amiodarone an epicardiac lead system had to be implanted due to an in adequate monophasic defibrillation threshold compared to no patient without antiarrhythmic drug treatment (P=0.043). In the patients with a biphasic d evice the intraoperative defibrillation threshold was not significantly dif ferent between the three study groups (P=0.44). No patient received an epic ardiac lead system. The defibrillation threshold in the amiodarone group wa s 15.3+/-7.3 J, in the sotalol group 14.4+/-7.2 J and in the patients witho ut antiarrhythmic drug treatment 17+/-6.1 J. As well, no significant differ ence was seen between the groups in respect of the impedance of the high vo ltage electrode (P=0.2). Conclusion: With the use of a biphasic device in c ombination with a transvenous lead system the intraoperative defibrillation threshold is not significantly different between patients on chronic amiod arone in comparison to patients without antiarrhythmic drug treatment or pa tients on chronic oral sotalol. This is in contrast to our findings with a monophasic device. (C) 1999 Elsevier Science Ireland Ltd. All rights reserv ed.