Intravenous and oral sotalol acutely prolonged the effective refractory periods of the ventricles and accessory pathways and reduced the ventricular response to atrial fibrillation.
Does sotalol prolong myocardial refractoriness and reduce ventricular response to atrial fibrillation in patients with accessory atrioventricular pathways?
Sotalol acutely prolongs myocardial refractoriness and reduces ventricular response to atrial fibrillation in patients with accessory pathways, suggesting therapeutic utility.
Sotalol, a beta adrenoceptor antagonist, was given intravenously to 15 patients with accessory atrioventricular pathways during intracardiac electrophysiological studies. Eleven patients had the Wolff-Parkinson-White syndrome and four patients had concealed left sided accessory pathways. Four patients were restudied while receiving oral sotalol. In contrast to the actions typical of beta blocking agents, intravenous sotalol prolonged the effective refractory periods of the ventricles and accessory pathways and reduced the ventricular response to atrial fibrillation in the patients with the Wolff-Parkinson-White syndrome. Similar results were obtained with oral administration. These findings support the observation that sotalol, unlike other beta blocking agents. causes acute prolongation of the myocardial action potential and suggest that this action might be of therapeutic use.
Deborah H. Bennett (1982) studied Accessory atrioventricular pathways (n=15). Sotalol was evaluated on Effective refractory periods of the ventricles and accessory pathways and ventricular response to atrial fibrillation. Intravenous and oral sotalol acutely prolonged the effective refractory periods of the ventricles and accessory pathways and reduced the ventricular response to atrial fibrillation.
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