Oral Sotalol Research Articles

Reverse use dependence of human ventricular repolarization by chronic oral sotalol in monophasic action potential recordings

This study using MAP demonstrates the reverse use dependence of repolarization by chronic oral sotalol in the human ventricle.

Efficacy and proarrhythmia of oral sotalol in pediatric patients: J.P. Pfammatter, T. Paul, C. Lehmann, H.C. Kallfelz. Department of Pediatric Cardiology, Children's Hospital, Berne, Switzerland. J Am Coll Cardiol 1995; 26:1002–7

Efficacy and proarrhythmia of oral sotalol in pediatric patients: J.P. Pfammatter, T. Paul, C. Lehmann, H.C. Kallfelz. Department of Pediatric Cardiology, Children's Hospital, Berne, Switzerland. J Am Coll Cardiol 1995; 26:1002–7

Frequency-dependent electrophysiologic effects of d,l-sotalol and quinidine and modulation by beta-adrenergic stimulation.

Frequency-dependent electrophysiologic actions of oral quinidine and oral sotalol may be clinically important, but these properties and their modulation by beta-adrenergic sympathetic stimulation have not been determined. The frequency-dependent effects of oral quinidine (n = 17) and oral d,l-sotalol (n = 17) were determined at: (1) drug-free baseline; (2) during steady-state drug dosing; and (3) during isoproterenol infusion to patients receiving quinidine or d,l-sotalol. The monophasic APD90 and RVERP were prolonged 12% to 17% (P < 0.001) during pharmacologic therapy, and frequency-dependent effects were only observed for the RVERP during sotalol. In both drug groups, isoproterenol significantly reduced the sinus cycle length and reduced the RVERP to a greater extent at longer than at shorter paced cycle lengths. While isoproterenol fully reversed quinidine's effects on the APD90 and RVERP, sotalol-induced APD90 prolongation was reduced by only 2% to 4%, and the RVERP was unaffected. Isoproterenol attenuated the frequency-dependent effects of quinidine on QRS duration by a relatively fixed amount of 7% to 10%. Isoproterenol fully reversed quinidine-induced, but did not affect sotalol-induced prolongation in the sustained VT cycle length. (1) Over the range of examined cycle lengths, oral quinidine and d,l-sotalol did not exert frequency-dependent effects on ventricular repolarization. (2) Isoproterenol fully reversed quinidine's effects on refractoriness, repolarization, and prolongation of VT cycle length, whereas d,l-sotalol's effects were largely preserved, despite significant reductions in sinus cycle length. (3) These results suggest that beta-blockade is important in preventing reversal of antiarrhythmic drug effects by augmented sympathetic nervous system tone.

Efficacy and proarrhythmia of oral sotalol in pediatric patients

This study sought to assess the efficacy of oral sotalol for various arrhythmias in pediatric patients and to evaluate the incidence of proarrhythmia and systemic side effects. Sotalol is a beta-adrenergic blocking agent with additional class III antiarrhythmic properties. Experience in pediatric patients is limited. Data concerning the incidence of proarrhythmia in children are lacking. Seventy-one pediatric patients (mean age 7.3 years) with various supraventricular and ventricular tachyarrhythmias were treated with oral sotalol. All the patients were admitted to the hospital for initiation of sotalol therapy. Antiarrhythmic and proarrhythmic effects of sotalol were assessed by daily surface electrocardiograms (ECGs) during the in-hospital phase and by serial Holter monitoring. Sotalol was either completely (27 [66%] of 41 patients) or partially effective (11 [27%] of 41) in 38 (93%) of 41 patients with supraventricular reentrant tachycardias. In patients with atrial flutter predominantly after operation for congenital heart disease, sotalol was effective in 84% of patients (completely in 9 of 19 and partially in 7 of 19). Ventricular tachycardia was completely (3 of 11) or partially (4 of 11) controlled in 64% of children. Proarrhythmia occurred in seven patients (10%) and consisted of symptomatic bradycardia from sinoatrial block and high grade atrioventricular (AV) block, respectively, in two children; asymptomatic high grade AV block in one; torsade de pointes in one; and relevant increased ventricular ectopic activity in three. Proarrhythmia required drug discontinuation in four patients. Mean duration of treatment for all patients was 18 months (range 1 to 40). Sotalol was an effective antiarrhythmic drug for a wide range of pediatric tachyarrhythmias. The considerable number of patients with proarrhythmic effects indicates the need for initiation of treatment on an inpatient basis and close monitoring by serial Holter electrocardiography.

Comparison of sotalol with digoxin-quinidine for conversion of acute atrial fibrillation to sinus rhythm (the sotalol-digoxin-quinidine trial)

We randomized 61 patients with paroxysmal atrial fibrillation (AF) (< 48 hours from onset) to either sotalol or quinidine treatment. Conversion of rhythm was recorded by Holter monitoring. The starting 80 mg dose of sotalol was repeated at 2, 6, and 10 hours if AF persisted (heart rate >80 beats/min) and if systolic blood pressure was ≥120 mm Hg. In the quinidine group, if heart rate was >100 beats/min, it was decreased with intravenous digoxin, whereafter 200 mg of oral quinidine sulfate was given maximally 3 times, each dose 2 hours apart. Conversion of AF to sinus rhythm occurred in 17 of 33 patients (52%) taking sotalol, and in 24 of 28 patients (86%) taking quinidine (p < 0.0001). Electric cardioversion was necessary in 39% of the former and in 14% of the latter group. The mean delay from first trial drug to sinus rhythm with the trial medication was 10.2 ± 7.6 hours in the sotalol group and 4.0 ± 2.9 hours in the quinidine group (p < 0.01). Treatment was discontinued in 16 patients taking sotalol (48%) because of asymptomatic bradycardia or hypotension, and in 20 taking quinidine (71%) because of rhythm conversion. Asymptomatic wide complex tachycardia (QRS > 0.12 second) was found in 13% and 27% of patients taking sotalol and quinidine, respectively. The longest RR intervals were 6.4 and 3.8 seconds in the sotalol and quinidine groups, respectively. Oral sotalol did not appear as effective as quinidine sulfate treatment in conversion of paroxysmal AF. Both quinidine and sotalol are potentially dangerous and cannot be recommended for self-medication for acute AF outside the hospital.

Clinical implications of pleomorphic ventricular tachycardias on oral sotalol therapy

In 90 consecutive patients with coronary artery disease and sustained monomorphic ventricular tachycardia, who were treated with oral sotalol and underwent programmed stimulation to determine drug effectiveness, the influence of sotalol on induced ventricular tachycardia morphology was retrospectively examined. In 54 patients (60%) sotalol rendered the tachycardia non-inducible. However, contrary to drug-testing with class I antiarrhythmic agents, induction of multiple morphologies at baseline study did not predict failure of subsequent drug-testing with sotalol. In the remaining 36 patients (40%), in whom sotalol did not modify inducibility, 21 patients (i.e. a total of 23%) manifested at least one new morphology during electropharmacological testing on sotalol. This effect was independent of the degree of left ventricular dysfunction, infarct location and numbers of morphologies at baseline, but corresponded with drug-induced changes in refractoriness. This observation may be related to a proarrhythmic effect of sotalol. Slowing of ventricular tachycardia rate and changes in morphology may have implications in patients receiving implantable cardioverter-defibrillators or those undergoing ablative procedures.

911-36 Safety and Efficacy of Sotalol in Drug Refractory Atrial Fibrillation/Flutter

The clinical efficacy and safety of oral Sotalol in patients (pts) with refractory atrial fibrillation/flutter (AF) has not been widely examined. We evaluated 31 pts with chronic (8 pts) or paroxysmal (23 pts) AF, 20 males, mean age 61 ± 8 yrs, LV ejection fraction was &lt; 40 in 11 pts, coronary artery disease in 11 pts, cardiomyopathy in 5 pts, valvular heart disease in 3 pts, no structural heart disease in 12 pts. All pts had failed multiple 2.7 (range 1 – 4) antiarrhythmic drug trials. Oral Sotalol therapy was commenced during AF in 15 pts and in sinus rhythm in 16 pts and was titrated to maximally tolerated or effective levels. All pts underwent 24 hr Holter monitor prior to discharge. Sotalol resulted in conversion to sinus rhythm in 12 of 15 (80%) pts. 2 pts had recurrent AF. and 1 pt developed side effects while in the hospital. 28 pts were discharged on a mean dose of 220 mg daily (range 80 – 320). During followup of 8.2 mas (range 2 – 20) there were no sudden or cardiac deaths. None of the pts demonstrated proarrhythmia on Holter monitor. 4 pts (12%) had recurrence of AF. Sotalol was discontinued in 3 pts (S%) due to side effects. 22 of 31 pts (71%1 were free of recurrent AF and side effects during followup. (1) Sotalol is effective, safe and well tolerated for acute conversion of AF to sinus rhythm as well as maintenance of sinus rhythm. (2) Incidence of adverse effects including proarrhythmia is low in this pt population. (3) Effective dose of Sotalol for control of AF seems to be lower than for ventricular tachycardia.

Multicenter trial of sotalol compared with procainamide in the suppression of inducible ventricular tachycardia: A double-blind, randomized parallel evaluation

Sotalol is the prototype class III agent that combines β-blocking properties with the propensity to prolong the effective refractory period by lengthening the action potential duration. Its precise effect on the prevention of ventricular tachycardia-ventricular fibrillation (VTVF) compared to class I agents has not been evaluated in a blinded study. In a double-blind parallel-design multicenter study, the electrophysiologic and antiarrhythmic effects of intravenous and oral sotalol (n = 55) and procainamide ( n = 55) were therefore compared in patients with VTVF inducible by programmed electric stimulation. Sotalol produced a greater effect on lengthening the ventricular effective refractory period (VERP). It prevented the inducibility of VTVF in 30% versus 20% for procainamide, but this was not significantly different. In an alternate therapy group ( n = 41) of similar patients previously refractory to or intolerant of procainamide, intravenous sotalol prevented inducibility in 32%. The pooled overall sotalol efficacy rate was 31%. There was a significant relation between the increase in the VERP and the prevention of inducibility of VTVF ( n = 56; p < 0.02). VERP of ≥300 msec was critical for the prevention of VTVF inducibility. Thirteen sotalol and 6 procainamide responders from the randomized group and 30 from the nonrandomized groups completed 1 year of oral sotalol therapy follow-up. Life-table analysis of these patient in each group showed a trend in favor of sotalol; however, statistical analysis was not possible because of the small numbers of patients. Both sotalol and procainamide were well tolerated. In the randomized group there was one case of sudden death during treatment with sotalol and two cases of nonfatal torsades de pointes in the procainamide group and two in the sotalol group; in the nonrandomized alternate therapy group, there were 6 cases of nonfatal torsades de pointes. The data support the emerging role of sotalol in the control of symptomatic ventricular tachycardia and fibrillation.

Hemodynamics effects of oral sotalol during both sinus rhythm and atrial fibrillation

Objectives. This study investigated the hemodynamic effects of oral sotalol during both sinus rhythm and paroxysmal atrial fibrillation.Background. The hemodynamic effects of most antiarrhythmic drugs have been characterized in subjects during sinus rhythm. However, there are no data concerning these effects on the paroxysmal tachyarrhythmias.Methods. In 17 patients with paroxysmal atrial fibrillation and without heart failure (aged 62 ± 11 years, ejection fraction 51 ±4%), an etctrophysiologic-hemodynamic study was performed twice. In the first study, hemodynamic variables were evaluated both during sinus rhythm and after the induction of atrial fibrillation. Sotalol (160 or 240 mg/day) was administered for 6 to 7 days and the study was then repeated with the same methods.Results. The drug significantly diminished heart rate during both sinus rhythm and atrial fibrillation. During sinus rhythm, sotalol did not change systemic pressures and significantly increased left and right ventricular end-diastolic, left and right atrial and pulmonary pressures. Cardiac index decreased, whereas stroke volume was unchanged after the drug. Ejection fraction and left ventricular end-diastolic and end-systolic volumes evaluated by echocardiography were unchanged after sotalol. During atrial fibrillation, the drug had less evident effects on cardiac function. Left ventricular end-diastolic, left atrial and pulmonary pressures did not increase significantly.Conclusions. The hemodynamic changes induced by oral sotalol appear to be mainly related to an involvement of ventricular distensibility; this effect is less evident during atrial fibrilation than during sinus rhythm. In patients with paroxysmal atrial fibrillation without heart failure treated with oral sotalol, a recurrence of the tachyarrhythmia is hemodynamically well tolerated.

Effect of oral sotalol on systemic hemodynamics and programmed electrical stimulation in patients with ventricular arrhythmias and structural heart disease

We explored the central hemodynamic responses to oral sotalol during dose titration in patients with ventricular arrhythmias who underwent programmed ventricular stimulation. Twelve patients were included in the study, 9 with a history of sustained ventricular tachyarrhythmias (6 postmyocardial infarction and 3 with cardiomyopathy) and 3 with a history of nonsustained ventricular tachycardia postmyocardial infarction. Left ventricular ejection fractions were <45% in 10 patients, and <35% in 5; the mean ejection fraction was 37% (range 20–51%). Sotalol prevented the induction of ventricular tachycardia in each of 3 patients wtth nonsustained ventricular tachycardia and in 6 of 9 wtth sustained ventricular tachycardia at baseline study. At peak action (2 hours) after sotalol loading (mean dose, 167 mg orally twice daily), the hemodynamic effects included bradycardia, decreased cardiac index, increased left ventricular filling pressure and systemic vascular resistance, and no change in stroke volume or stroke work index. One patient was not continued on sotalol, owing to an excessive increase in the pulmonary capillary wedge pressure, despite the lack of symptomatic heart failure. Congestive heart failure in association with marked bradycardia developed in another patient, who had suppression of inducible ventricular tachycardia after sotalol loading; this patient was managed wtth a reduction in the dose of sotalol and a regimen of digoxin and furosemide, and has been well compensated and without a recurrence of sustained ventricular tachycardia for more than 4 years. Ventricular tachycardia has been controlled wtth sotalol, without hemodynamic deterioration, in 6 of these patients. The evidence supports the idea that, despite its β-adrenergic blocking effects, sotalol can be used, albeit with some caution, even in patients with compromised left ventricular systolic function.

Safety and efficacy of oral sotalol for sustained ventricular tachyarrhythmias refractory to other antiarrhythmic agents

The safety and efficacy of oral sotatol were evaluated in 481 patients with drug-refractory sustained ventricular tachyarrhythmias (VT) In an open-label multicenter study. After drug-free baseline evaluations, therapy was initiated at 80 mg every 12 hours, with upward dose titrations of 160 mg/day being allowed at intervals of 72 hours to a maximum dose of 480 mg every 12 hours. Efficacy determinations were made by either programmed electrical stimulation (PES) or Holter monitoring responses. Of the 481 patients enrolled, 473 underwent acute-phase titration. Of the 269 patients assessable by PES, 94 (34.9%) exhibited complete response (suppression of inducible VT), with an additional 67 patients (24.9%) exhibiting partial response. Of the 109 patients assessable by Holter monitoring, 43 (39.4%) exhibited a complete response. There were no significant differences between responders and nonresponders with regard to left ventricular ejection fraction. Although response rates tended to improve as the sotatol dose was increased to 640 mg/day, efficacy was most commonly achieved at a sotalol dose of 320 mg/day. Sotalol was discontinued because of adverse effects in 42 (8.9%) of the acute-phase patients. The most common adverse effect was proarrhythmia, which was observed in 23 patients (4.9%). Proarrhythmia took the form of torsades de pointes in 12 patients and an increase in VT episodes in 11. In 3 acute-phase patients (0.6%), sotalol was discontinued because of the emergence of congestive heart failure. A total of 286 patients entered the long-term phase. Life-table estimates of the proportion of patients who remained free of recurrence of arrhythmia at 12, 18, and 27 months were 0.76,0.72, and 0.66, respectively. There were no significant differences in time to recurrence of arrhythmia as related to PES response, Hotter monitor response, baseline left ventricular ejection fraction, or history of congestive heart failure. Among the 70 patients (24.5%) in whom there was recurrence of arrhythmia, sudden death occurred in 17 and sustained VT in 41. Sotalol was discontinued owing to presumed adverse effects in 21 (7.3%) of the long-term patients, including 8 with proarrhythmia; proarrhythmia consisted of torsades de pointes in 3 patients and increased episodes of VT in 5. These findings suggest that sotalol is an effective drug for the long-term treatment of patients with drug-refractory sustained VT. Proarrhythmia was observed in only 6.4% of the study population and tended to occur during the acute titration phase. The need to discontinue therapy because of congestive heart failure was uncommon. The risk of recurrence of arrhythmia appeared to be unrelated to response to PES or ambulatory monitoring, type of heart disease, or extent of toft ventricular dysfunction.

Effect of sotalol on ventricular fibrillation and defibrillation in humans

Antiarrhythmic drugs are frequently administered to patients receiving implanted cardioverter defibrillators. Some of these drugs may decrease the efficacy of defibrillation shocks from the defibrillator. Sotalol, a drug with β-blocking and class III antiarrhythmic properties, lowers defibrillation energy requirements in experimental animals and may do so in humans. Oral sotalol 171 ± 58 mg was administered before and after device implantation in 25 patients receiving implanted defibrillators. During sotalol therapy, the lowest energy required for successful defibrillation was 5.9 ± 3.4 J (range 2–15 J). In a concurrent non-randomized comparison group of 23 patients, including 18 treated with amiodarone, the lowest successful energy was 16 ± 10 J (p <0.01). In 5 sotalol patients, ventricular fibrillation (VF) could not be induced at all (1 patient) or more than 2 or 3 times (4 patients) despite repeated 60 Hz stimulation. The induced VF had a pronounced tendency to terminate spontaneously, with the termination occurring at up to 23 seconds after the offset of 60 Hz stimulation. The cycle length of the VF was 236 ± 34 msec, significantly greater than in patients not given drug therapy (191 ± 21 msec, p <0.01). In 10 patients, but none of the controls, intracardiac electrograms during surface electrocardiograph VF were regular, monoform, and without low-amplitude diastolic activity. In addition, monophasic action potentials during apparent VF showed maintenance of distinct and normal morphology. The ventricular effective refractory period increased after sotalol (249.4 ± 19 to 278.4 ± 24 msec; p <0.03) and the maximum heart rate response to exercise was limited to 120 ± 28 beats/min. Sotalol may modify VF and may enhance defibrillation efficacy. In view of its efficacy in life-threatening ventricular arrhythmias, it appears to be particularly well suited as adjunctive therapy in patients with implanted defibrillators.

Oral Sotalol Reduces the Incidence of Atrial Fibrillation after Coronary Artery Bypass Surgery

Episodes of atrial fibrillation or flutter frequently complicate the postoperative course after coronary bypass surgery. A hundred and one patients undergoing coronary artery bypass surgery were randomized to oral pre- and postoperative treatment with sotalol, a non-selective beta-blocking agent with class-III antiarrhythmic properties (50 patients), or to half the preoperative beta-blocking dose according to the routine of the department (51 patients). Thus, there was no equipotency regarding beta blockade in the two groups. The incidence of atrial fibrillation was 10% in the sotalol group and 29% in the comparison group, p = 0.028. In 10% of the sotalol patients the dose had to be reduced or stopped compared to in none the group given routine treatment. The patients who developed atrial fibrillation were older, but otherwise there was no statistically significant difference between the two groups. Sotalol was effective in reducing the incidence of atrial fibrillation. However, careful titration of the optimal dose should be performed in order to avoid side effects of the beta blockade.

Usefulness of oral sotalol for the treatment of junctional ectopic tachycardia

An infant with junctional ectopic tachycardia diagnosed at three weeks of age was treated with oral sotalol. At the first echocardiogram the shortening fraction was decreased. After one day of treatment the ventricular rate decreased from 230 to 130 beats per minute. Five months later sinus rhythm was restored, shortening fraction was normal and sotalol was withdrawn without relapse.

Effectiveness of oral sotalol for treatment of pediatric arrhythmias

Sotalol is a β blocker with class III activity. Few investigators have reported its use in pediatric patients. From August 1985 to May 1990, 66 patients (mean age 8.7 years; range 9 days to 24 years), including 14 infants aged <3 months, were treated with oral sotalol alone (n = 46) or in association with digoxin (n = 20). Supraventricular reentrant tachycardia was present in 38 patients (20 with documented preexcitation), atrial flutter in 10 and atrial ectopic tachycardia in 7. Three patients had other types of supraventricular tachycardia. Tachycardia was of ventricular origin in 6 patients and both of supraventricular and ventricular origin in the remaining 2. Mean dose of oral sotalol was 135 mg/m 2/day given in 2 doses. Congenital heart disease was present in 28 patients, 14 with previous cardiac surgery, mostly at the atrial level. Prior treatment with 1 or more antiarrhythmic agent had been unsuccessful in 83% of patients. Mean duration of treatment was 13.3 months (range 2 months to 5 years). Overall, treatment was successful in 79% of cases. Highest rate of success was observed in patients with supraventricular reentrant tachycardia with or without preexcitation (89%) and in those with atrial ectopic tachycardia (85.5%). Atrial flutter could be controlled in 60% of cases. Sotalol seemed less effective in ventricular tachycardia with a complete control of the arrhythmia being achieved in only 17%; however, it decreased the number of runs of ventricular tachycardia and the number of ventricular premature complexes in 50% of patients. There were no adverse effects in 89% of patients. Two patients with previous sick sinus syndrome had worsening of their bradycardia necessitating implantation of a pacemaker in 1. Sotalol is a very effective drug for the treatment of the various Pediatric arrhythmias, in particular supraventricular arrhythmias, without significant adverse effects.

Efficacy of intravenous sotalol for suppressing inducibility of supraventricular tachycardias at rest and during isometric exercise

The efficacy of intravenous sotalol (1 mg/kg) for suppressing inducibility of supraventricular tachycardias (SVT) with different electrophysiologic mechanisms was studied in 30 consecutive patients referred for an electrophysiologic study because of paroxysmal SVT. Orthodromic SVT using accessory atrioventricular (AV) connection was inducible in 14 patients, AV nodal reentrant SVT in 8, and intraatrial SVT in 8 before administration of sotalol. Isometric handgrip exercise facilitated the inducibility of SVT in 8 patients who were noninducible at rest. After intravenous sotalol, 7 of 14 patients (50%) with orthodromic SVT, 8 of 8 (100%) with AV nodal reentrant SVT, and 8 of 8 (100%) with intraatrial reentrant SVT became noninducible into sustained SVT. Isometric exercise facilitated the inducibility of only 3 nonsustained SVT runs after sotalol infusion, and exercise did not reverse the prolongation of refractory periods of the atrium, AV node, accessory pathway and ventricle caused by sotalol. During a mean follow-up period of 18 ± 7 months, none of the 14 patients who remained noninducible into sustained SVT during the stress test after intravenous sotalol and tolerated long-term oral sotalol therapy had recurrence of symptomatic SVT. Thus, sotalol is efficacious for suppressing SVT with AV nodal or intraatrial reentrant mechanism, but less efficacious in patients with accessory AV pathway. The β-blocking and cellular antiarrhythmic effects of sotalol are not significantly reversed by exercise.

Efficacy and electrophysiologic effects of oral sotalol in patients with sustained ventricular tachycardia caused by coronary artery disease

The efficacy of oral sotalol in preventing sustained ventricular tachycardia induction by invasive electrophysiological testing was assessed in 22 patients (60 ± 9 years) with prior myocardial intarction. Programmed stimulation consisted of two basic drives followed by up to three extrastimuli at two right ventricular sites. At baseline, sustained monomorphic ventricular tachycardia was inducible in all patients. With sotalol (360 ± 172 mg/day), it was no longer inducible in 10 patients; in 12 others, it remained inducible and its cycle length was only minimally prolonged (322 ± 42 to 345 ± 44 msec, p < 0.05). Sotalol markedly prolonged sinus cycle length, uncorrected QT interval, and right ventricular effective and functional refractory periods, but had little effect on ventricular conduction time either in sinus rhythm or with right ventricular pacing. There was no significant difference in drug dose or in electrophysiologic effect of drug that related to efficacy, nor was there any correlation between drug-induced prolongation of ventricular tachycardia cycle length and its effects. Six patients received oral sotalol over the long term without spontaneous recurrence of ventricular tachycardia (follow-up: 23 ± 18 months). These results demonstrate that sotalol is effective (45%) against sustained ventricular tachycardia induction at moderate doses and is well tolerated over a long term in the setting of remote myocardial infarction. However, its electrophysiologic effects as measured at invasive testing are not predictive of efficacy against ventricular tachycardia induction.

Efficacy and Safety of Oral Sotalol in Early Infancy

Sotalol, a nonselective beta blocking agent with additional Class III activity has been shown to be extremely effective in the treatment of supraventricular tachycardias in adults and children. Little information is available on its use in infants. From August, 1985 to April, 1990, 18 infants, 2 months of age or less, were treated with oral sotalol for supraventricular arrhythmias. Their age ranged from a few hours to 2 months, mean 5 weeks, at the start of treatment. Weights were between 2.58-5 kg, mean 3.9 kg and dosage 2-4 mg/kg/24 hrs given in two equal doses, 12 hourly. Sixteen infants had structurally normal hearts, one had multiple cardiac rhabdomyomas, and one was postoperative Mustard procedure for transposition of the great arteries. Thirteen of 18 infants had reentrant forms of supraventricular tachycardia, six of these had overt preexcitation. Two infants had chaotic atrial tachycardia, two atrial flutter, and one with ectopic atrial tachycardia. Previous antiarrhythmic therapy had been unsuccessful in 12 patients. All infants, except one with chaotic atrial tachycardia, were successfully controlled with sotalol. Ten infants discontinued therapy between the ages of 7 and 18 months as it was felt to be no longer necessary. Mean duration of treatment was 12.8 months. Three had recurrences of their arrhythmia and were again successfully controlled by sotalol. Mild sinus bradycardia occurred in all infants. No other side effects were noted. Sotalol is an effective, safe drug for the treatment of supraventricular tachycardias in early infancy.

Long term efficacy and tolerance of oral sotalol in patients with drug-refractory ventricular arrhythmias

Long term efficacy and tolerance of oral sotalol in patients with drug-refractory ventricular arrhythmias

Efficacy of oral sotalol in reentrant ventricular tachycardia

Oral sotalol was given to 64 patients (78% postinfarction) with recurrent, reentrant ventricular tachycardia (VT) during an average follow-up period of 19.7 months. Fifty-nine (92%) patients had previously experienced recurrent ventricular tachycardia, in spite of having received an average of three conventional antiarrhythmic drugs (13 had previously failed on other Class III drugs). The nature and mechanism of the VT was proved with electrophysiologic testing (EPS), and the chronic sotalol dosage was determined by repeated EPS at 3- to 4-day intervals until the VT was no longer inducible. Sotalol failed in five patients and was discontinued in six patients because of severe side effects (three proarrhythmic effects, including two with torsades de pointes)--a total of 18%. Sotalol was successful alone in 42 patients (65%) and in combination with another antiarrhythmic drug in 11 patients (18%). The average dose of sotalol required for success was 589 mg; 658 mg was the mean daily dose when given alone and 486 mg when given in combination. Side effects were common and were due mainly to the beta-blocking effects of sotalol. Dual chamber pacing was required by 11 patients because of poorly tolerated bradycardia, and 14 patients remained symptomatic from worsening of the cardiac failure in spite of pacing, increased diuretics, or vasodilator therapy. The average drug dosage was the same for symptomatic (680 mg) and asymptomatic (627 mg) patients. Sotalol is a valuable antiarrhythmic drug for reentrant ventricular tachycardia. High doses are needed, and at these doses the beta-blocking activity is responsible for most of the side effects.