Sotalol: An important new antiarrhythmic

Sotalol, the most recently approved oral antiarrhythmic drug, hers a unique pharmacologic profile. Its electrophysiology is explained by nonselective beta-blocking action as well as class III antiarrhythmic activity (includin g fast-activating cardiac membrane-delayed rectifier current blockade), whi ch leeds to increases in action potential duration and refractory period th roughout the heart and in QT interval on the surface electrocardiogram. Its better hemodynamic tolerance than other beta-blockers may be a result of e nhanced inotropy associated with class III activity. Sotalol's ability to s uppress ventricular ectopy is similar to that of class I agents and better than that of standard beta-blockers. Unlike class I agents, its use in a po stin-farction trial was not associated with increased mortality rate. Thera peutically, it has shown superior efficacy for prevention of recurrent vent ricular tachycardia and ventricular fibrillation, which was the basis for i ts approval. In a randomized study, the Electrophysiologic Study Versus Ele ctrocardiographic Monitoring (ESVEM) trial, sotalol was associated with an increased in-hospital efficacy prediction rate (by Holter monitor or electr ophysiologic study), reduced long-term arrhythmic recurrence rate with supe rior tolerance, and lower mortality rate than class I ("standard") antiarrh ythmic drugs. Sotalol was 1 of 2 drugs selected for comparison with implant able defibrillators in the recent National Institutes of Health Antiarrhyth mics versus Implantable Defibrillator (AVID) study. Sotalol appears to be a preferred drug for use with implantable defibrillators; unlike some other agents (eg, amiodarone) it does not elevate and, indeed, may lower defibril lation threshold. Although unapproved for this use, sotalol is active again st atrial arrhythmias. It has shown efficacy equivalent to propafenone and quinidine in preventing atrial fibrillation recurrence, but it is better to lerated than quinidine and provides excellent rate control during recurrenc e. Sotalol's major side effects are related to beta-blockade and the risk o f torsades de pointes (acceptably small if appropriate precautions are take n). Unlike several other antiarrhythmics (eg, amiodarone), it has no pharma cokinetic drug-drug interactions, is nat metabolized, and is entirely renal ly excreted. initial dose is 80 mg twice daily, with gradual titration to 2 40 to 360 mg/day as needed. The daily dose must be reduced in renal failure . On the basis of favorable clinical trials and practice experience, sotalo l has shown a steadily growing impact on the treatment of arrhythmias durin g its 5 years of market availability, a trend that is likely to continue.