Wolff-Parkinson-White syndrome in children: electrophysiologic and pharmacologic characteristics.

Intracardiac electrophysiologic studies were performed on 28 infants and children, ages 1 month to 18 years, with the Wolff-Parkinson-White syndrome to try to determine 1) the electrophysiologic characteristics of the accessory connection and 2) the mechanisms of associated supraventricular dysrhythmias. Although the antegrade refractory periods of the normal conduction system were shorter than those found in adults, those of the accessory connection were slightly longer. Reciprocating supraventricular tachycardia (SVT), which had been a clinical problem in 26 of 28, could be induced in the laboratory in all 26 subjects. The mechanism involved reentry with antegrade conduction through the atrioventricular (AV) node and retrograde through the accessory connection in 22. Eleven of these 22 had a wide QRS during tachycardia due to a bundle branch block. Three other subjects had wide QRS tachycardia, but the mechanism involved antegrade conduction through the accessory connection and retrograde through the AV node. The other patient had AV node reentry tachycardia. Two patients did not have clinical SVT, and in these two, SVT could not be induced. Neither patient had retrograde conduction through the accessory connection. The site of the accessory connection could be identified in 26 subjects by the sequence of retrograde activation of the atrium during SVT or ventricular pacing. Digitalis shortened the refractory period of the accessory connection in five of the eight patients studied.     

Atrioventricular nodal reentrant tachycardia: studies on upper and lower 'common pathways'

Electrophysiologic studies were performed in 28 patients with documented atrioventricular (AV) nodal reentrant supraventricular tachycardia (SVT) to investigate the presence of AV nodal tissue situated between the tachycardia circuit and both the atrium (upper common pathway, UCP) and the His bundle (lower common pathway, LCP). All patients demonstrated a 1:1 AV relationship during SVT. The study protocol consisted of atrial then ventricular pacing at the SVT cycle length. UCPs were manifested in eight of 28 (29%) patients by either antegrade AV Wenckebach (six patients) or a paced atrium-His (AH) interval exceeding the AH in SVT (two patients, differences 5 and 9 msec). LCPs were manifested in 21 of 28 (75%) patients by either retrograde Wenckebach periodicity (two patients) or a paced HA interval exceeding the HA in SVT (19 patients, mean difference 25 +/- 20 msec). By these criteria, eight patients (29%) had evidence for both UCPs and LCPs. UCPs were more likely than LCPs to be manifested by Wenckebach criteria (p less than .05). Thus the AV nodal reentrant SVT circuit appears to be intranodal and is frequently surrounded by AV nodal tissue (UCP and LCP), antegrade and retrograde conduction properties of these common pathways are discordant in some cases, and conduction properties of UCP tissue differ from those of LCP tissue. These findings may have relevance in that the UCP or LCP may limit the ability of premature extrastimuli to penetrate the circuit to initiate or terminate AV nodal SVT.     

Electrophysiologic effect of intravenous propafenone in supraventricular tachycardia]

The electrophysiologic effects of intravenous propafenone were studied in twenty six patients with supraventricular tachycardias. Ten patients (38%) with intranodal reentrance tachycardia common type, and sixteen patients (62%) atrioventricular orthodromic reentrance tachycardia. Propafenone (2 mg/kg intravenously) given over ten minutes period caused termination of the intranodal reentrance tachycardia in 60% of the cases and 50% to the patients with atrioventricular reentrance tachycardia. The antiarrhythmic effects observed are related to the slowing of the conduction velocity and to the prolongation of the refractoriness in the AV node and accessory pathways preventing the reentrance mechanism. The reinduction of the tachycardia was possible in 46% of the patients. This effects was more significative in the group with accessory pathways (50%), and 40% of the patients with intranodal reentrance. The supraventricular tachycardia was inducible by programmed electrical stimulation in 46% of the patients. None of the patients developed side effects to the administration of the propafenone.     

Treatment of supraventricular and paroxysmal ventricular tachycardia with bepridil

Bepridil is a molecule which, apart from its anti-anginal properties, also has antiarrhythmic effects due to its calcium antagonist action which depresses antero and retrograde AV conduction in the physiological pathways. Conduction in accessory AV pathways is also depressed to a lesser and more variable extent. It also has an anti-ventricular arrhythmic action probably due to an associated membrane-stabilising effect. This drug was used intravenously to treat attacks of reciprocating supra-ventricular tachycardia (SVT) (60 p. 100 conversion to sinus rhythm: 6 out of 10 cases of intra-nodal reentry, 6 out of 10 cases of reentry via an accessory pathway) and also in ventricular tachycardia (VT) (7 conversions in 15 patients within 2 to 9 minutes). It was impossible to induce attacks of SVT after administering the drug in about a third of patients; better results were obtained in intra-nodal SVT (5 cases of effective prevention out of 10) than in SVT involving an accessory pathway (1 case out of 10). It was not possible to reinitiate VT after treatment in 3 out of 6 cases (very aggressive pacing methods, a long QT interval and accelerated idio-ventricular rhythm were responsible for the failures). Oral therapy (400 to 800 mg, usually 600 mg daily in 3 doses) prevented any recurrence of SVT in over half the patients (prevention of intranodal SVT: 80 p. 100; prevention of SVT involving an accessory pathway: 13 p. 100) and in 4 out of 6 patients with VT. Provocative pacing studies after intravenous or oral bepridil provide a good indication of long-term efficacy. The drug is generally well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)     

Supraventricular tachycardia in patients without overt preexcitation

In this article, the authors discuss the features and differential diagnosis of supraventricular tachycardia with a regular ventricular rate that occurs in patients without overt preexcitation during sinus rhythm. In the authors' experience, the two most common mechanisms of these tachycardias are reentry within the atrioventricular node (AV nodal reentry) and atrioventricular reentry using a concealed accessory pathway for retrograde conduction and the AV node/His-Purkinje system for antegrade conduction (AV reentry). Sinus nodal reentry, intra-atrial reentry, automatic atrial tachycardia, and nonparoxysmal junctional tachycardia account for the remaining episodes of regular supraventricular tachycardia. Therapy for AV and AV nodal reentry is also discussed.     

Wolff-Parkinson-White syndrome with orthodromic supraventricular tachycardia associated with a "hyper-conductor" atrio-ventricular node. A therapeutic challenge

One case of Wolff-Parkinson-White Syndrome with paroxysmal supraventricular tachycardia related to orthodromic atrioventricular reentry using an accessory pathway for retrograde conduction an a rapidly conducting AV node for anterograde conduction is present. The pharmacological therapy with Digoxin, Propranolol, Quinidine, Disopyramide and Propafenone was not effective. An electrophysiologic study showed a reciprocating tachycardia induced by spontaneous ventricular beats. Both the effective refractory period of the AV node and the anterograde effective refractory period of the accessory pathway were minor or equal to 220 msec which made the control of the arrhythmia difficult. Amiodarone was able to suppress the premature ventricular beats, depress conduction and prolong refractoriness in both, the AV node and accessory pathway to prevent recurrences of atrioventricular reentry. In this patient a false positive test with ajmaline was documented. The electrophysiologic study showed the association of Wolff-Parkinson-White Syndrome with an enhanced atrioventricular nodal-conduction and allowed the selection of an appropriate antiarrhythmic agent.     

Pirmenol in termination of paroxysmal supraventricular tachycardia

An assessment was made of the effect of pirmenol in the termination of paroxysmal supraventricular tachycardia (SVT). Sinus rhythm was restored by intravenous administration in 11 of 17 patients during a spontaneous attack. Another 8 patients were studied electrophysiologically. Pirmenol terminated an induced SVT in 3 of 5 patients having an atrioventricular (AV) intranodal re-entry mechanism but in none of 3 patients having an atrioventricular bypass tract as one re-entrant limb. The overall success in restoring sinus rhythm was 14 of 25 patients (56%). The drug was hemodynamically well tolerated even in cases of continued SVT. Pirmenol increased the atrial effective refractory period and had no obvious effect on AH and HV intervals. The functional refractory period of the AV node was decreased, probably by an anticholinergic effect. The effective and functional refractory periods of retrograde atrioventricular conduction via the AV node and bypass tract were increased in some patients. The mechanism terminating the AV intranodal SVT was a block in the retrograde part of the dual AV nodal pathway, a typical antiarrhythmic Class I effect.     

Usefulness of programmed stimulation in predicting efficacy of propafenone in long-term antiarrhythmic therapy for paroxysmal supraventricular tachycardia

The electrophysiologic effects of intravenous (i.v.) and oral propafenone were evaluated in 14 patients with Wolff-Parkinson-White syndrome and in 10 patients with atrioventricular (AV) nodal reentrant tachycardia. The effective refractory periods of the right atrium and the AV node increased after both preparations. In patients with Wolff-Parkinson-White syndrome, i.v. propafenone blocked anterograde accessory pathway conduction in 2 patients and retrograde conduction in 1; during oral therapy, accessory pathway conduction block occurred in 2 additional patients. The mean cycle length of the supraventricular tachycardia (SVT) increased from 338 +/- 60 ms to 387 +/- 56 ms (p less than 0.05) after i.v. application, and from 336 +/- 65 ms to 367 +/- 65 ms (p less than 0.05) during oral propafenone. The shortest pacing interval maintaining a 1:1 AV conduction increased from 325 +/- 65 ms to 368 +/- 81 ms (p less than 0.05) after i.v. infusion, and from 333 +/- 57 ms to 369 +/- 75 ms (p less than 0.05) during oral therapy. There was no difference in the electrophysiologic effects between i.v. and oral propafenone. The induction of SVT was prevented by i.v. propafenone in 10 of 20 patients and in 4 additional patients with oral propafenone. During follow-up, 6 of 7 patients, whose SVT could not be initiated by electrophysiologic drug testing, remained free from recurrences, whereas 5 of 7 patients with inducible tachycardia had recurrences of SVT. Thus, in patients with SVT, propafenone prolonged accessory pathway and AV nodal conduction and had a beneficial effect on circus movement tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Double-blind study of intravenous propafenone for paroxysmal supraventricular reentrant tachycardia

Propafenone was administered during electrophysiologic testing to determine its efficacy and safety for terminating and preventing reinduction of paroxysmal supraventricular reentrant tachycardia. Four men and 10 women (mean age 50 years, range 28 to 69) were studied. Five patients had Wolff-Parkinson-White syndrome with orthodromic atrioventricular (AV) reentrant tachycardia, three had a concealed accessory pathway with AV reentrant tachycardia and six had tachycardia due to reentry within the AV node. In the five patients with Wolff-Parkinson-White syndrome, propafenone terminated reentrant tachycardia in three (the tachycardia was reinducible in one) and had no effect in two. In the three patients with a concealed accessory pathway, propafenone terminated reentrant tachycardia in all three and prevented reinduction of the tachycardia in two. In the six patients with tachycardia due to reentry within the AV node, propafenone terminated and prevented reinduction of reentrant tachycardia. Propafenone had no effect on blood pressure, heart rate, PA interval, AV node refractoriness or rate of reentrant tachycardia. Propafenone significantly (p less than 0.05) prolonged the AH, HV, QRS and ventriculoatrial intervals and decreased the AV node Wenckebach rate. Of the nine patients receiving long-term oral propafenone therapy, eight had a reduction of at least 90% in reentrant tachycardia during a mean follow-up period of 14.5 months (range 11 to 22); all eight patients had had noninducible reentrant tachycardia after intravenous propafenone. One patient had increased frequency of reentrant tachycardia; this patient had had inducible reentrant tachycardia after intravenous propafenone. In conclusion, intravenously administered propafenone terminated reentrant tachycardia in 85% of patients and prevented reinduction in 71%, with no adverse hemodynamic effects.     

Differential electrophysiologic properties of decremental retrograde pathways in long RP' tachycardia

Long RP' supraventricular tachycardias (SVT) often demonstrate both slow and decremental conduction properties in the retrograde pathway of the reentrant circuit. The electrophysiologic properties of these pathways are poorly understood. We studied 10 patients with long RP' SVT (RP'/RR, 0.52 to 0.71); five had the unusual form of atrioventricular nodal reentry (fast-slow) and five patients had accessory AV pathways with slow, decremental retrograde conduction properties. During SVT, the effects of intravenous adenosine (37.5 to 150 micrograms/kg), which increases potassium current (iK) in supraventricular tissue and hyperpolarizes membrane potential toward Ek (-90 mV), and the response to slow-inward channel blockade with verapamil (0.10 to 0.20 mg/kg iv) were evaluated. Adenosine and verapamil has similar effects in the presence of fast-slow AV nodal reentry since both agents terminated SVT by producing block in the retrograde slow AV nodal pathway. In contrast, adenosine and verapamil had differential effects on retrograde conduction in decremental accessory pathways. Adenosine terminated all episodes of SVT in the retrograde decremental pathway, whereas verapamil had a direct effect on this tissue in only two of five patients. Decremental retrograde accessory pathways can therefore demonstrate at least two types of electrophysiologic responses. Pathways that respond only to adenosine-induced hyperpolarizing K+ current likely comprise depressed fast-Na+ channel tissue, i.e., partially depolarized (greater than -60 to -70 mV) atrial tissue. In contrast, decremental accessory pathways that respond to both modulation of the slow-inward calcium current and K+ conductance have pharmacologic properties similar to those of the AV node and may represent more completely depolarized atrial fibers with resting membrane potentials of -60 mV or less.     

Efficacy of propafenone in Wolff-Parkinson-White syndrome: electrophysiologic findings and long-term follow-up

The efficacy and safety of intravenous propafenone was studied in 10 patients with Wolff-Parkinson-White syndrome and in 2 patients with a concealed accessory pathway. During electrophysiologic study, the effect of propafenone on the effective refractory period of the accessory pathway was determined, as well as its effect during orthodromic atrioventricular (AV) reentrant tachycardia and atrial fibrillation. Propafenone caused significant increases in the accessory pathway refractory period, both in the anterograde direction (290 +/- 19 versus 474 +/- 50 ms, p less than 0.05) and in the retrograde direction (238 +/- 15 versus 408 +/- 44 ms, p less than 0.05). Complete anterograde accessory pathway conduction block occurred in four patients. Sustained AV reentrant tachycardia was inducible in 11 patients before administration of propafenone. Drug infusion during AV reentrant tachycardia promptly terminated arrhythmia in 10 of these 11 patients and caused slowing of AV reentrant tachycardia in the remaining patient. Before propafenone, sustained atrial fibrillation was inducible in six patients and nonsustained atrial fibrillation in four patients. After propafenone, no patient had inducible sustained atrial fibrillation. Furthermore, propafenone caused a marked decrease in peak ventricular rate during atrial fibrillation. Eight patients have been treated with oral propafenone and followed up for 12 +/- 2 months. All have remained virtually free of recurrent arrhythmia and none has developed significant side effects. Propafenone is a very promising agent for emergency intravenous therapy as well as long-term oral therapy in patients with Wolff-Parkinson-White syndrome.     

Three types of atrioventricular reciprocating tachycardia using bilateral accessory pathways in a patient with Wolff-Parkinson-White syndrome

Electrophysiologic studies were performed on a patient with Wolff-Parkinson-White syndrome and recurrent supraventricular tachycardia. Bilateral accessory pathways capable of antegrade and retrograde conduction and three different types of atrioventricular (AV) reciprocating tachycardia were demonstrated. One type of narrow QRS tachycardia used the normal AV pathway for antegrade conduction and the left-sided accessory pathway for retrograde conduction. Two types of wide QRS tachycardia (one with right bundle branch block and one with left bundle branch block) used both accessory pathways for antegrade and retrograde conduction, respectively, and were independent of the normal AV pathway. The data showed that bilateral accessory pathways have different electrophysiologic properties and participate in three different types of AV reciprocating tachycardia.     

Effects of intravenous flecainide acetate in patients with concealed atrioventricular pathway with supraventricular tachycardia]

The acute efficacy and electrophysiologic effects of intravenous flecainide acetate (1.5 mg/kg) on 10 patients with concealed AV pathway with supraventricular tachycardia (SVT) by esophageal programmed electrical stimulation were evaluated. The results showed that: (1) the drug has marked depressing effects on the retrograde accessory pathway conduction and minimal effects on the antegrade AV nodal conduction; (2) there were no effects on the patients with normal sinus node function; (3) the drug has little side effects during the studies; (4) flecainide terminated induced SVT in 9 of 10 cases (90%), and prevented induced SVT in 7 of 9 cases (78%).     

小儿室上性心动过速的食管心电生理分型及演变

目的 :探讨小儿室上性心动过速 (SVT)的类型及其电生理特征 ,以及食管起搏对小儿SVT的干预作用。方法 :对 4 7例 8个月～ 15岁有SVT发作史的患儿进行了食管心电生理研究。结果 :4 7例SVT经食管心房调搏 (TEAP)确定分型 4 2例 (89.4 % ) ,其中旁路折返 2 8例 (6 6 .7% ) ,房室结内折返 10例 (2 3.8% ) ,心房内折返l例 ,窦房结折返l例 ,心房自律性增高 2例 ;不能定型 5例 (10 .6 % )。结论 :小儿SVT近 95 %为折返机制所致 ,以旁路折返最常见 ,其次为房室结内折返 ,与成人报道不同 ,可能与小儿传导系统发育规律以及旁路电生理特性发生演变有关     

Treatment of paroxysmal reentrant supraventricular tachycardia with flecainide acetate

The electrophysiologic effects and therapeutic efficacy of intravenous and oral flecainide were studied in 15 patients with spontaneous and inducible sustained paroxysmal supraventricular tachycardia (SVT). Twelve patients had atrioventricular (AV) reentrance using an accessory pathway for retrograde conduction and 3 had AV nodal reentrance. Fourteen patients received intravenous flecainide (2 mg/kg body weight over 15 minutes) during an initial electrophysiologic study. Nine patients were restudied during oral flecainide administration (200 to 400 mg/day). After intravenous or oral flecainide therapy, reentrant SVT was noninducible in 6 patients with AV reentrance and in the 3 with AV nodal reentrance. In these 9 patients, intravenous flecainide prevented induction of reentrant SVT by depressing conduction over the retrograde limb of the reentry circuits. In the 6 patients with inducible sustained AV reentrant SVT before and after flecainide therapy, the cycle length of tachycardia increased significantly, mainly as the result of an increase in ventriculoatrial conduction time. There was concordance between the intravenous and the oral effects of flecainide on the mechanism of the SVT. Twelve patients continued oral flecainide treatment for a mean of 16 months (range 5 to 28). Tachycardia recurred in 3 of 4 patients whose arrhythmia remained inducible after flecainide therapy and in 1 of 8 patients whose SVT was suppressed. It is concluded that flecainide is an effective and convenient antiarrhythmic agent to treat patients who have AV nodal or AV reentrant SVT.     

Successful sequential radiofrequency catheter ablation of anatomically discrete antegrade and retrograde accessory pathway conduction in the Wolff-Parkinson-White syndrome.

Histopathologically, accessory atrioventricular (AV) pathways comprise tiny strands of working myocardium that traverse the AV groove and link between the atrial and ventricular myocardium. Antegrade and retrograde conduction in bidirectional accessory pathways have generally been considered to occur along the same fibers. This report details the successful catheter ablation of a left free wall accessory pathway with radiofrequency energy. Antegrade and retrograde conduction of the pathway were abolished sequentially by separate episodes of energy delivered at anatomically discrete though closely adjacent sites along the mitral annulus. This finding raises the interesting possibility of anatomic "compartmentalization" of antegrade and retrograde conduction along an accessory pathway.     

Electrophysiologic properties of cibenzoline in Wolff-Parkinson-White syndrome and atrioventricular nodal reentry tachycardia

The electrophysiologic effects of the new class-1 antiarrhythmic drug cibenzoline (1.5 mg/kg within 10 min, followed by an infusion of 0.5 mg for 30 min) were investigated in six patients with atrioventricular (av) nodal reentrant tachycardia and nine patients with atrioventricular tachycardia. Sinus cycle length, sinus node recovery time, effective refractory period (ERP) of the atrium and the ventricle as well as the ERP of the av node were not significantly affected by cibenzoline. Retrograde conduction via the av node was prevented by cibenzoline in 6/15 patients, retrograde ERP was increased in 4/15 patients and in 5/15 patients determination of the retrograde ERP of the AV node was impossible. Intranodal conduction time (AH-interval) and infranodal conduction time (HV-interval) was increased from 96 +/- 27 ms to 117 +/- 40 ms (p less than 0.01) and 36 +/- 12 ms to 62 +/- 12 ms (p less than 0.01), respectively. In four patients with antegrade conduction along the accessory pathway no antegrade conduction was seen after the application of cibenzoline. Retrograde ERP of the accessory pathway was increased in two patients, it was unchanged in three patients, and no retrograde conduction along the accessory pathway was seen in four patients. AV nodal reentrant tachycardia was not inducible, after cibenzoline in 4/6 patients and in 5/9 patients with AV reentrant tachycardia. If tachycardia remained inducible, an increase in tachycardia cycle length from 333 +/- 46 ms to 402 +/- 24 ms was observed (p less than 0.01). In conclusion the electrophysiologic effects of cibenzoline make it a suitable drug for the treatment of av nodal reentrant tachycardia and atrioventricular tachycardia.     

Usefulness of the pre-excitation index to determine the mechanism of supraventricular paroxysmal tachycardia and the location of the anomalous pathway

To evaluate the preexcitation index in determinate the mechanism of paroxysmal supraventricular tachycardia and localize accessory pathway, fifty nine patients with clinical and electrocardiographic supraventricular tachycardia were analyzed. There were thirty eight patients (64.4%) with orthodromic AV reentry using an accessory pathway for retrograde conduction and 21 patients (35.6%) with typical AV nodal reentrant tachycardia. Preexcitation of the atrium during tachycardia by premature ventricular complex at a time when anterograde His bundle activation was present in 30 o 38 (79%) patients with AV reentry while only 8 of 21 (38%) patients with AV nodal reentry demonstrated preexcitation during tachycardia. There was no significant difference between left and right accessory pathways and in mean tachycardia cycle length between the two groups. However, atrioventricular reentry demonstrated atrial preexcitation during tachycardia more frequently than AV nodal reentry. In conclusion, our findings show that the preexcitation index is a useful method for determinate the mechanism of supraventricular tachycardia and to localize accessory pathways.     

Use of intracardiac recordings to determine the site of drug action in paroxysmal supraventricular tachycardia

Paroxysmal supraventricular tachycardia most often results from atrioventricular (AV) reentry using an accessory AV pathway (Wolff-Parkinson-White syndrome) or reentry within the region of the AV node. In AV reentry, using an accessory pathway, suppression of the tachycardia may be achieved by depressing either anterograde AV nodal conduction or retrograde accessory pathway conduction. Intracardiac recordings and programmed electrical stimulation have established that β-adrenergic antagonists and calcium channel blockers principally affect AV nodal conduction (anterograde limb of the reentrant circuit), whereas class IA and IC agents principally affect the accessory AV pathway (retrograde limb). Pharmacologic therapy has been more effective when directed at the limb in which conduction is most marginal at the tachycardia rate (weak limb). In individual patients, intracardiac recordings and programmed electrical stimulation can be used to identify the weak limb, indicating the class of agents most likely to be effective. Specialized techniques allowing direct recording of accessory pathway activation suggest that limitations in accessory pathway conduction may be explained by anatomic impediments. Conduction is most limited at the atrial interface of the accessory pathway in some patients, whereas in others the ventricular interface may be the limiting factor. Class IA and IC agents appear to have the greatest effect at sites where conduction is most tenuous, i.e., at the anatomic impediments.

Similar considerations apply to AV nodal reentry. Anterograde slow AV nodal pathway conduction is most often depressed by digitalis preparations, β-adrenergic antagonists, and calcium channel blockers, whereas retrograde fast AV nodal pathway conduction is more often depressed by class IA and IC agents. Intracardiac recordings and programmed electrical stimulation can also be used in these patients to identify the weak limb and direct pharmacologic therapy. Direct catheter recordings of AV nodal conduction remain elusive, limiting knowledge of the different conduction properties of the anterograde and retrograde limbs and the site(s) of drug action. Studies in progress, comparing the retrograde AV nodal conduction time during tachycardia with that during ventricular pacing at the same rate, suggest that the His bundle may be incorporated in the reentrant circuit in some patients. It appears that verapamil more readily depresses retrograde fast pathway conduction in these patients than in those in whom the His bundle does not form part of the reentrant circuit, but the reasons for this are unknown.     

Effects of intravenous sotalol in patients with atrioventricular accessory pathways

Effects of intravenous injection of 0.6 mg/kg sotalol, a beta-blocking agent with additional class III properties, were studied by means of electrophysiologic techniques in 14 patients, seven with the Wolff-Parkinson-White syndrome and seven with concealed atrioventricular (AV) accessory pathways. Sotalol brought about a significant increase in the retrograde effective refractory period of the anomalous pathway, whereas changes in the antegrade effective refractory period were more variable. In five of nine patients with electrically induced reciprocating tachycardia sotalol prevented the initiation of sustained reentry. In most cases the suppression of the circus movement was the result of the development of AV nodal block. Thus our data support the use of sotalol for the treatment of tachycardias incorporating anomalous AV conduction pathways.