Effect of sotalol on ventricular fibrillation and defibrillation in humans

Abstract

Antiarrhythmic drugs are frequently administered to patients receiving implanted cardioverter defibrillators. Some of these drugs may decrease the efficacy of defibrillation shocks from the defibrillator. Sotalol, a drug with β-blocking and class III antiarrhythmic properties, lowers defibrillation energy requirements in experimental animals and may do so in humans. Oral sotalol 171 ± 58 mg was administered before and after device implantation in 25 patients receiving implanted defibrillators. During sotalol therapy, the lowest energy required for successful defibrillation was 5.9 ± 3.4 J (range 2–15 J). In a concurrent non-randomized comparison group of 23 patients, including 18 treated with amiodarone, the lowest successful energy was 16 ± 10 J (p <0.01). In 5 sotalol patients, ventricular fibrillation (VF) could not be induced at all (1 patient) or more than 2 or 3 times (4 patients) despite repeated 60 Hz stimulation. The induced VF had a pronounced tendency to terminate spontaneously, with the termination occurring at up to 23 seconds after the offset of 60 Hz stimulation. The cycle length of the VF was 236 ± 34 msec, significantly greater than in patients not given drug therapy (191 ± 21 msec, p <0.01). In 10 patients, but none of the controls, intracardiac electrograms during surface electrocardiograph VF were regular, monoform, and without low-amplitude diastolic activity. In addition, monophasic action potentials during apparent VF showed maintenance of distinct and normal morphology. The ventricular effective refractory period increased after sotalol (249.4 ± 19 to 278.4 ± 24 msec; p <0.03) and the maximum heart rate response to exercise was limited to 120 ± 28 beats/min. Sotalol may modify VF and may enhance defibrillation efficacy. In view of its efficacy in life-threatening ventricular arrhythmias, it appears to be particularly well suited as adjunctive therapy in patients with implanted defibrillators.