Suppressant effects of conventional beta blockers and sotalol on complex and repetitive ventricular premature complexes

Abstract

Beta-blocking drugs have been shown to reduce the overall mortality and risk of sudden cardiac death in survivors of acute myocardial infarction. It is not known whether such an effect is mediated by suppression of ventricular premature complexes (VPCs). The circadian rhythmicity of ventricular arrhythmia can also be suppressed by β-blocking drugs, and this may help reduce the risk of sudden cardiac death during the morning hours. Recent studies have also shown that β blockers can provide a safe and effective combination with class IA antiarrhythmic agents when arrhythmias cannot be controlled with class IA agents alone. Sotalol, a nonselective β antagonist, has unique electrophysiologic properties, and several studies have shown it to be more effective than conventional β blockers in suppressing ventricular arrhythmias. However, direct comparative studies of the suppression of VPCs are lacking. In a recent double-Mind, placebo-controlled, parallel study, the antiarrhythmic effects of sotalol and propranolol were compared in 172 patients with >30 VPCs/ hour. After the initial 1-week washout and 1-week placebo period, patients were randomly assigned to either 160 mg of sotalol administered twice daily (76 patients) or 40 mg of propranolol administered 3 times daily (91 patients). Those responding to therapy (decreases >75% VPCs) continued to take these closes, but nonresponders were given higher doses, 320 mg of sotalol twice daily or 80 mg of propranolol 3 times daily, respectively. The baseline mean hourly VPC count, derived from two 24-hour Holter recordings during the placebo phase, was 274 for sotalol and 255 for propranolol patients and was reduced to 54 (80% decrease) for sotalol and 104 (59% decrease) for propranolol-treated patients at 6 weeks (p < 0.002). A significantly greater percentage of patients (56%) responded to sotalol compared with those who responded to propranolol (29%) (p < 0.001). The class III antiarrhythmic activity of sotalol may account for its superiority over propranolol.