INTRAVENOUS SOTALOL FOR THE TERMINATION OF SUPRAVENTRICULAR TACHYCARDIA AND ATRIAL-FIBRILLATION AND FLUTTER - A MULTICENTER, RANDOMIZED, DOUBLE-BLIND, PLACEBO-CONTROLLED STUDY

Sotalol is an antiarrhythmic agent with combined beta-blocking and cla ss III antiarrhythmic properties. This study was designed to assess th e safety and efficacy of sotalol in terminating supraventricular tachy cardia (SVT), atrial fibrillation (AFib), and atrial flutter (AFI). Ni nety-three patients with spontaneous or induced SVT (n = 45) or AF (AF ib or AFI; n = 48) with a ventricular rate of greater than or equal to 120 beats/min were studied. In the first phase, the double-blind phas e, patients were randomly assigned to receive placebo or intravenous ( iv) sotalol, 1.0 or 1.5 mg/kg. If SVT or AF did not convert to sinus r hythm or if the ventricular rate did not slow to < 100 beats/min withi n 30 minutes, patients then entered the second phase, the open-label p hase, which also lasted 30 minutes, and were given 1.5 mg/kg iv sotalo l. In the SVT group, during the double-blind phase conversion to sinus rhythm occurred in 2 (14%) of 14 of patients who received placebo, 10 (67%) of 15 who received sotalol, 1.0 mg/kg (p < 0.05 vs placebo), an d 10 (67%) of 15 who received 1.5 mg/kg sotalol (p < 0.05 vs placebo); during the open-label phase, 1.5 mg/kg iv sotalol converted 7 (41%) o f 17 of patients. In the AF group, during the double-blind phase conve rsion to sinus rhythm occurred in 2 (14%) of 14 of patients who receiv ed placebo, 2 (11%) of 18 who received 1.0 mg/kg sotalol (p not signif icant [NS] vs placebo), and 2 (13%) of 16 who received 1.5 mg/kg sotal ol (p = NS vs placebo); in these groups, a >20% reduction of ventricul ar rate without conversion to sinus rhythm occurred in 0 (0%) of 14, 1 3 (72%) of 18 (p < 0.05 vs placebo), and 12 (75%) of 16 of patients (p < 0.05 vs placebo), respectively; during the open-label phase, 1.5 mg /kg iv sotalol converted 7 (30%) of 23 of patients. The most common ad verse events were hypotension and dyspnea. During the double-blind pha se they occurred in 10% of patients who received placebo, 9% of those who received 1.0 mg/kg iv sotalol (p = NS vs placebo), and 10% of thos e who received 1.5 mg/kg iv sotalol (p = NS vs placebo). Most of these events were mild to moderate, but all were transient and clinically m anageable. In conclusion, iv sotalol is safe and effective for acute t ermination of SVT and for acute slowing of ventricular rate during AF but not for termination of AF at doses to 1.5 mg/kg.