Objectives: We sought to determine the electrophysiologic actions of sotalol in the remodeled atrium of humans.
Background: In experimental studies, sotalol has limited class III action in the electrically remodeled atrium and did not prevent atrial fibrillation (AF) induction.
Methods: We determined the effective refractory periods (ERPs) at three pacing cycle lengths (400, 500, and 600 ms) in the high right atrium (HRA) and distal coronary sinus (DCS) before and after intravenous infusion of dl-sotalol in 10 patients with persistent AF who underwent internal cardioversion. The same protocols were performed in 10 control subjects in sinus rhythm.
Results: In the HRA and DCS, the atrial ERPs at different drive cycle lengths were significantly shorter in patients with AF than in control subjects (p < 0.05). In patients with AF, the atrial ERP's adaptation to rate was nearly normal in the HRA, but was poor in the DCS. In both groups, dl-sotalol significantly increased the atrial ERPs at both the HRA and DCS, as compared with baseline (p < 0.05). However, the prolongation of atrial ERPs was significantly less at a drive cycle length of 600 ms in patients with AF versus control subjects (p < 0.05). After infusion of dl-sotalol, the atrial ERP's adaptation to rate at both the HRA and DCS was poor in patients with AF, and AF was still easily inducible in the majority of them, but not in control subjects.
Conclusions: The results of the present study demonstrate that the electrophysiologic actions of dl-sotalol are significantly attenuated in the chronically remodeled human atrium, and these changes might represent a probable explanation for the low efficacy of dl-sotalol to prevent early AF recurrence after electrical cardioversion.