Copyright © 1993 by the European Society of Cardiology.
© 1993 The European Society of Cardiology
Electrophysiologic properties of sotalol and d-sotalol. A current view
Hôpital Cardiovasculaire et Pneumologique Louis Pradel Lyon, France
Correspondence: Paul Touboul, MD, Hôpital Cardiovascularie et Pneumologique Louis Pradel, BP Lyon Monchat, 69394 Lyon Cedex 3, France
Although discovered more than two decades ago, the clinical applications of sotalol are still a matter of debate. Together with amiodarone, sotalol is considered a prototype of a new class of antiarrhythmic agents characterized by repolarization-prolonging effects (class III). Lengthening of repolarization is associated with an increase in the effective refractory period of cardiac tissues. There is no change in the maximum rate of rise during phase 0, a finding that supports the lack of sotalol effect on the fast sodium channel. The electrophysiologic action of the drug in humans provides evidence for direct cardiac effects of sotalol in addition to beta blockade. The beta-blocking properties play a major role in the sinus-rate slowing and lengthening of the atrioventricular nodal conduction time observed after sotalol administration. However, the drug also prolongs refractoriness in atria, His-Purkinje tissue, ventricular muscle and accessory atrioventricular connections. These latter changes are absent or minimal with conventional beta blockers and are likely to reflect sotalol-induced prolongation of cardiac repolarization. They result in an increase in the QT interval, an effect that is dose-dependent and more marked during chronic therapy.
The dextrorotatory isomer, d-sotalol, shares a similar electrophysiologic profile. Lengthening of repolarization in cardiac cells following d-sotalol is of the same magnitude as that produced by the levoisomer. This finding provides further evidence for a class III action of sotalol, as the dextroisomer is almost devoid of beta-blocking properties. In humans, the electrical effects of both drugs are similar. However, d-sotalol-induced changes in sinus rate and atrioventricular nodal conduction are modest. Given that the repolarization-prolonging effects of sotalol are more prominent at slow rates (reverse use-dependency), one can speculate that d-sotalol may cause less proarrhythmi
Key Words: Electrophysiology • Sotalol • d-sotalol