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The electrophysiological effects of intravenous sotalol hydrochloride (0.4 mg/kg) were assessed in 24 patients, including 13 with the Wolff-Parkinson-White syndrome, undergoing routine electrophysiological study. Fifteen to 30 minutes after sotalol administration there was a significant increase in sinus cycle length and in sinus node recovery time. There was a small increase in the AH interval, but the HV interval was unchanged. The QT and JT intervals, measured during sinus rhythm, were both increased. The atrial, ventricular, and atrioventricular nodal effective refractory periods were all prolonged, as was the atrioventricular nodal functional refractory period. In 13 patients with ventricular pre-excitation there was an increase of the accessory pathway anterograde and retrograde effective refractory periods. In 12 of these 13 sotalol was given during atrioventricular re-entrant tachycardia, resulting in termination in five. Tachycardia cycle length increased in all patients, with the major effect being in the atrioventricular direction. Though some of the effects seen in these patients are consistent with the beta adrenergic antagonist properties of sotalol, the effect on atrial, ventricular, and accessory pathway effective refractory periods and on ventricular repolarisation is not typical of that observed with other beta blockers but may be the result of lengthening of the action potential duration. These findings suggest that sotalol may be a more versatile antiarrhythmic agent than other beta receptor antagonists.

Electrophysiological effects of sotalol--just another beta blocker?