Sotalol

SOTALOL

Sotalol has both β-adrenergic receptor-blocking (class 2) and action potential-prolonging (class 3) actions. The drug is formu-lated as a racemic mixture of D- and L-sotalol. All the β-adrenergic– blocking activity resides in the L-isomer; the D- and L-isomers share action potential prolonging actions. Beta-adrenergic– blocking action is not cardioselective and is maximal at doses below those required for action potential prolongation.

Sotalol is well absorbed orally with bioavailability of approxi-mately 100%. It is not metabolized in the liver and is not bound to plasma proteins. Excretion is predominantly by the kidneys in the unchanged form with a half-life of approximately 12 hours. Because of its relatively simple pharmacokinetics, solatol exhibits few direct drug interactions. Its most significant cardiac adverse effect is an extension of its pharmacologic action: a dose-related incidence of torsades de pointes that approaches 6% at the highest recommended daily dose. Patients with overt heart failure may experience further depression of left ventricular function during treatment with sotalol.

Sotalol is approved for the treatment of life-threatening ven-tricular arrhythmias and the maintenance of sinus rhythm in patients with atrial fibrillation. It is also approved for treatment of supraventricular and ventricular arrhythmias in the pediatric age group. Sotalol decreases the threshold for cardiac defibrillation.