Sotalol.

Sotalol causes noncardioselective beta-adrenergic antagonism and prolongation of repolarization of cardiac tissues (Class III electrophysiologic action). This dual pharmacologic profile confers unprecedented antiarrhythmic properties to the drug. Sotalol is highly bioavailable when administered orally in the fasting state and is mostly cleared unchanged in the urine with an apparent half-life of elimination of 15 to 17 hours. It has been found effective in the suppression of nearly all cardiac arrhythmias, with the exception of those precipitated by prolongation of ventricular repolarization. Its safety and efficacy relative to other antiarrhythmic drugs need to be examined more fully in randomized controlled trials of unselected patients. The adverse effects potentially associated with the use of sotalol are those commonly observed with beta-adrenergic blockade, as well as those resulting from excessive prolongation of the QT interval. The occurrence of torsade de pointes during treatment with sotalol may be minimized by limiting doses to no more than 640 mg/day and by strictly avoiding the development of hypokalemia.