Electrophysiologic effects and clinical efficacy of flecainide in children with recurrent paroxysmal supraventricular tachycardia

The electrophysiologic effects of intravenous flecainide were evaluated in 16 patients aged 9 +/- 4 years: 15 with recurrent paroxysmal supraventricular tachycardia (SVT) and 1 with overt accessory pathway and history of syncope. Eleven patients had an accessory pathway; it was concealed in 2, overt in 9 and in 10 of these patients an orthodromic atrioventricular reentrant tachycardia was induced. Five patients without accessory pathway had an atrioventricular nodal reentrant tachycardia. After intravenous flecainide (1.5 mg/kg) the effective refractory period of the atrium and ventricle increased significantly; the anterograde and retrograde effective refractory periods of the atrioventricular node did not. Flecainide blocked retrograde conduction in the accessory pathway in 4 patients (effective refractory period 245 +/- 41 ms) and anterograde conduction in 8 of 9 patients (effective refractory period 284 +/- 57 ms). The mean cycle length of orthodromic reciprocating tachycardia and atrioventricular nodal reentrant tachycardia increased significantly. After flecainide tachycardia was noninducible in 6 patients with orthodromic reciprocating tachycardia and in 1 with atrioventricular nodal reentrant tachycardia. It was inducible but nonsustained (less than or equal to 30 seconds) in 1 patient with orthodromic reciprocating tachycardia and in 3 with atrioventricular nodal reentrant tachycardia. Fifteen patients continued oral flecainide treatment for 19 +/- 11 months.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiological effects and clinical efficacy of propafenone in children with recurrent paroxysmal supraventricular tachycardia

Twenty-four patients aged 10.1 +/- 4.5 (mean +/- SD) years with recurrent paroxysmal supraventricular tachycardia underwent an electrophysiological study. Eleven patients had an overt and seven had a concealed accessory connection; six patients had no accessory connection. An orthodromic reciprocating tachycardia was inducible in 17 of 18 patients with an accessory connection, and an atrioventricular nodal reentrant tachycardia was inducible in four of six patients without accessory connection. After administration of propafenone, the sinus cycle length decreased. Intra-arterial, intranodal, and His-ventricle intervals and QRS duration increased. The atrial and ventricular effective refractory periods and anterograde and retrograde effective refractory periods of the atrioventricular node increased. The cycle length at which nodal second-degree block occurred increased. Of 18 patients with accessory connection, propafenone prolonged retrograde conduction in all, blocked anterograde conduction in five, and prolonged it in six. The drug terminated the orthodromic reciprocating tachycardia in all 17 patients and the atrioventricular nodal reentrant tachycardia in three of four patients. In three of four patients with atrioventricular nodal reentrant tachycardia and in 15 of 17 patients with orthodromic reciprocating tachycardia, the tachycardia was no longer inducible or nonsustained after propafenone. A follow-up of 26 +/- 10 months revealed that the drug when orally administered to all patients prevented recurrences of tachycardia in 15 of 18 patients with and in four of six patients without accessory connection. The results of short-term drug testing with propafenone predict the response to long-term oral therapy with this drug.     

Electrophysiologic and clinical effects of flecainide for recurrent paroxysmal supraventricular tachycardia

The antiarrhythmic effects of flecainide acetate were evaluated in 9 patients with paroxysmal atrioventricular (AV) nodal tachycardia and 17 patients with AV tachycardia. An electrophysiologic study was performed before and after intravenous flecainide acetate, 2 mg/kg body weight, was infused over 15 minutes and was followed by a maintenance infusion of 1.6 mg/kg given over 1 hour to 26 patients and during oral treatment to 15. Treatment with oral flecainide acetate was continued for 14 +/- 5 months. Intravenous flecainide acetate terminated AV nodal tachycardia by blocking the retrograde fast pathway conduction in 7 of 7 patients and AV tachycardia by blocking retrograde conduction in the extranodal pathway in 10 of 10 patients. AV nodal tachycardia and AV tachycardia were noninducible in 8 of 9 patients (90%, p less than 0.001) and 11 of 17 patients (65%, p less than 0.001), respectively. Long-term treatment with oral flecainide acetate suppressed AV nodal tachycardia and AV tachycardia in 8 of 9 patients (90%, p less than 0.001) and 11 of 17 patients (65%, p less than 0.001), respectively. A favorable outcome was associated with block in the accessory pathway after intravenous flecainide acetate and noninducibility during oral treatment. Recurrences preferentially occurred in the younger patients. Flecainide acetate is effective in the acute and long-term management of paroxysmal supraventricular reentry tachycardia by suppressing conduction through the retrograde fast limb of the tachycardia circuit. The clinical effect can be predicted by electrophysiologic testing.     

Intravenous and oral encainide: electrophysiological effects in patients with paroxysmal reciprocating supraventricular tachycardia

The electrophysiologic effects of encainide (E) after acute i.v. (1 mg/kg in 60') and oral administration (75 to 150 mg/die for 48-72 h) were evaluated in 10 pts with PSVT (5 men and 5 women, mean age 48 +/- 15 years). The mechanism of PSVT was related to a reentry through an accessory A-V pathway in 6 cases while in the other 4 the reentry was confined in the A-V node. PA, AH and HV intervals lengthened from 42.8 +/- 5.1, 77.8 +/- 19.7 and 38.3 +/- 6.6 msec to 50 +/- 13.5, 91.7 +/- 22.9 and 49.4 +/- 12.9 and to 48.3 +/- 7.1, 94.4 +/- 33.9 and 44.4 +/- 9.2 msec, after i.v. and oral E respectively. Atrial and ventricular refractory periods showed slight not significant variations. Wenckebach point lengthened from 316 +/- 28 msec to 354 +/- 32 and to 359 +/- 45 msec, after i.v. and oral E respectively. Tachycardia cycle length was 358 +/- 32 msec in basal conditions. After i.v. E tachycardia was inducible only in 6 cases, with a mean cycle length of 403 +/- 48 msec. After oral E tachycardia was reproduced only in 3 patients with a mean cycle length of 433 +/- 85 msec. Nine patients were treated chronically with E, at a mean dose of 89 +/- 36 mg/day. After a follow-up of 18 +/- 8 months, tachycardia recurred but with a marked reduction of the attacks, in 3 patients; only 3 patients complained of side effects (blurred vision). Thus E is highly effective in the prevention of PSVT; the drug seems well tolerated thanks to the low dosage required for the control of PSVT.     

Electrophysiologic effects and clinical efficacy of propafenone in pediatric patients with paroxysmal supraventricular reentrant tachycardia

Twenty patients (pts) with recurrent paroxysmal supraventricular tachycardia (PSVT), 12 female and 8 male, aged 9.8 +/- 4.7 years, underwent an electrophysiologic study (EPS) in order to assess the effects of propafenone (Pf) administered intravenously (1.5 mg/Kg in 3'). Thirteen pts (Group I) had an accessory pathway (AP) which was concealed in 5 and overt in 8 and in 12 of them an orthodromic atrioventricular reentrant tachycardia (ORT) was induced. In 5 of 7 pts (Group II) without AP an idio-nodal reentrant tachycardia (AVNRT) was induced. After Pf the sinus cycle length decreased significantly from 668 +/- 165 to 612 +/- 109 msec and PA, AH, HV intervals and QRS duration increased significantly from 35 +/- 11, 71 +/- 18, 34 +/- 6 and 73 +/- 12 to 43 +/- 11, 87 +/- 15, 39 +/- 9 and 85 +/- 10 msec respectively. The atrial and ventricular effective refractory period (ERP) increased from 216 +/- 18 and 211 +/- 19 to 227 +/- 21 and 217 +/- 21 msec respectively. The anterograde and retrograde nodal ERP and anterograde and retrograde Wenckebach point increased from 240 +/- 48, 227 +/- 28, 278 +/- 37 and 287 +/- 38 to 270 +/- 58, 330 +/- 32, 340 +/- 59 and 408 +/- 37 msec respectively. Pf terminated the tachycardia (T) in all 12 pts of Group I after prolongation of the cycle length which increased from 299 +/- 46 to 383 +/- 69 msec.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Electrophysiological characteristics and catheter ablation in patients with paroxysmal supraventricular tachycardia and paroxysmal atrial fibrillation

Introduction: Paroxysmal supraventricular tachycardia (PSVT) is often associated with paroxysmal atrial fibrillation (AF). However, the relationship between PSVT and AF is still unclear. The aim of this study was to investigate the clinical and electrophysiological characteristics in patients with PSVT and AF, and to demonstrate the origin of the AF before the radiofrequency (RF) ablation of AF.
Methods and Results: Four hundred and two consecutive patients with paroxysmal AF (338 had a pure PV foci and 64 had a non-PV foci) that underwent RF ablation were included. Twenty-one patients (10 females; mean age 47 ± 18 years) with both PSVT and AF were divided into two groups. Group 1 consisted of 14 patients with inducible atrioventricular nodal reentrant tachycardia (AVNRT) and AF. Group 2 consisted of seven patients with Wolff-Parkinson-White (WPW) syndrome and AF. Patients with non-PV foci of AF had a higher incidence of AVNRT than those with PV foci (11% vs. 2%, P = 0.003). Patients with AF and atypical AVNRT had a higher incidence of AF ectopy from the superior vena cava (SVC) than those with AF and typical AVNRT (86% vs. 14%, P = 0.03). Group 1 patients had smaller left atrial (LA) diameter (36 ± 3 vs. 41 ± 3 mm, P = 0.004) and higher incidence of an SVC origin of AF (50% vs. 0%, P = 0.047) than did those in Group 2.
Conclusion: The SVC AF has a close relationship with AVNRT. The effect of atrial vulnerability and remodeling may differ between AVNRT and WPW syndrome.     

Electrophysiological effects of nicainoprol in patients with paroxysmal supraventricular tachycardias

The electrophysiological effects of nicainoprol, a new class I antiarrhythmic drug, were evaluated in 29 patients with supraventricular reentrant tachycardias, due to accessory pathways in 15 and dual atrioventricular nodal pathways in 14 patients. Nicainoprol was administered intravenously as a bolus followed by continuous infusion of 1.5 mg/kg in two and of 2 mg/kg in 27 patients over one hour. Nicainoprol was given as a bolus of 1.5-2 mg/kg during sinus rhythm in 11 patients or during induced supraventricular tachycardia in 18. The drug successfully terminated the tachycardia in 17 patients due to block in the retrograde tachycardia limb in 15 and the antegrade limb in 2 patients. Prolongation of the cycle length preceded the termination in each case. In one case, the termination could not be achieved despite the administration of 3 mg/kg. The sinus cycle length, heart rate corrected QT interval as well as right atrial and right ventricular effective refractory periods remained unchanged. In contrast, the intranodal and infranodal conduction times, as well as QRS duration, were prolonged significantly. In patients with dual atrioventricular nodal pathways, there was a significant (P less than 0.05) increase of the effective refractory periods of the anterograde slow pathways. The changes of the anterograde fast pathways, however, did not reach significance level. More pronounced effects were found on effective refractory periods of the retrograde pathways, which were blocked in 4 patients and significantly (P less than 0.05) prolonged in the remainder. Similarly, in patients with accessory pathways the effect on the retrograde conduction was more marked with complete block in 5 patients and significant prolongation of effective refractory periods and shortest paced cycle lengths in the remainder.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiological mechanisms of the effect of allapinin in patients with paroxysmal supraventricular tachycardia

An intracardiac electrophysiological study was undertaken to examine 15 patients with paroxysmal supraventricular tachycardias. Allapinin intravenously given in a dose of 0.4 mg/kg, was tested for effects. The agent was demonstrated to cause a substantial inhibition of rapid retrograde pathway function in atrioventricular nodal tachycardia and abnormal antero- and retrograde pathway function. This is the major aspect of the drug's action that prevents the development of episodes of paroxysmal supraventricular tachycardias. The agent fails to virtually affect the function of the atrioventricular node in the anterograde direction in the two types of the tachycardia. Thus, allapinin has the mechanism of action that is typical of quinidine-like drugs used in supraventricular tachycardias.     

Paediatric use of flecainide in supraventricular tachycardia: clinical efficacy and pharmacokinetics.

Twenty three children with recurrent supraventricular tachycardia were treated with flecainide. Twenty one of these received intravenous treatment during an attack (2 mg/kg over 10 minutes). The tachycardia was terminated in 17. After an intravenous bolus of flecainide, blood samples were drawn at regular intervals for analysis of flecainide concentration over 48 hours. Pharmacokinetic variables were calculated--median terminal half life 7.5 hours, median volume of distribution 6.2 l/kg, and median plasma clearance 7.2 ml/min/kg. There was a significant correlation between half life and age. Twenty of the children received long term treatment with an oral preparation of flecainide to prevent further attacks. Twelve had no further attacks and 16 were considered to have good control. Two children suffered potentially serious arrhythmogenic effects soon after the start of oral treatment and flecainide had to be stopped. During oral treatment regular blood samples were drawn and plasma concentrations were analysed to assess the therapeutic range. This did not differ substantially from that proposed in adults (400-800 micrograms/l). Eight children were electively withdrawn from oral flecainide to see whether they really needed it. Blood samples for measurement of flecainide concentration were drawn after their last oral dose. Pharmacokinetic variables were calculated: time to maximum concentration 2 hours, median terminal half life 7.9 hours. For the combined data from patients receiving intravenous and oral treatment there was a significant correlation between elimination half life and age. An intravenous dose of 2 mg/kg over at least 10 minutes and an initial oral dose of 6 mg/kg/day in three divided doses is recommended. Treatment should be started in hospital so that children in whom the drug may be arrhythmogenic can be identified and plasma concentrations measured to identify patients in whom lack of efficacy is caused by underdosage.     

Acute and chronic effects of verapamil in patients with paroxysmal supraventricular tachycardia

Efficacy of acute intravenous verapamil, 10 mg, and chronic oral verapamil, 320 mg, daily were studied electrophysiologically in 15 patients with paroxysmal supraventricular tachycardia (PSVT). Plasma verapamil concentrations were measured concurrently. Both intravenous and oral verapamil significantly increased the AV node conduction time, the cycle length producing a Wenckebach period, and the refractory period of the AV node. These changes were reflected in changes in plasma verapamil concentration. The echo zone and the supraventricular tachycardia (SVT) zone markedly narrowed after administration of both intravenous and chronic oral verapamil. Verapamil's efficacy was found to be related to the type of SVT. For instance, verapamil was more effective in SVT due to AV nodal re-entry than in SVT due to concealed accessory pathway. Fourteen patients were followed from 3 to 31 months and all except one were well controlled. In conclusion, verapamil was effective in prophylaxis of paroxysmal SVT.     

Effects of atenolol in patients with reciprocating supraventricular tachycardia

We studied 12 patients with crisis of paroxysmal reciprocating supraventricular tachycardia before and after intravenous injection of 5 mg of atenolol. The patients were then followed for periods ranging from 6 to 50 months (median 34 months). During this time, they received oral atenolol therapy, at 200 mg for the first two weeks, and 100 mg daily thereafter. Tachycardia was due to reciprocation within the atrioventricular node in 9 patients, and to pre-excitation in 3 patients. Atenolol slowed the sinus rate, prolonged the atrioventricular conduction time, and increased the atrial cycle length at which atrioventricular nodal Wenckebach phenomenon occurred. During the tachycardia, atenolol increased the tachycardia During the tachycardia, atenolol increased the tachycardia cycle length, due to prolongation of the intranodal atrioventricular conduction time. Of the 11 patients who were observed for the full period, 7 had no further episodes of arrhythmia. One patient (with left-sided pre-excitation) failed to respond to any antiarrhythmic medication, one patient remained free of symptoms for two years, but received an atrial pacemaker for control of the tachycardia at the end of this period. Two patients (one with dual atrioventricular nodal pathways, and one with concealed left-sided pre-excitation) await other treatment for their tachycardia, after remaining free of symptoms for one and two years, respectively. These findings suggest that atenolol is an effective beta blocker for use in controlling arrhythmias in patients with reciprocating supraventricular tachycardia, for use in once daily dosage, and is a medication largely free of side effects.     

Incidence of symptomatic tachycardia in untreated patients with paroxysmal supraventricular tachycardia

The purpose of this article is to investigate the occurrence of symptomatic paroxysmal supraventricular tachycardia (PSVT) in untreated patients and to assess factors that influenced its occurrence. We studied 34 patients with this arrhythmia during an observation period in which they received no antiarrhythmic drug therapy for up to 90 days. Recurrence of PSVT was documented by telephone transmission of the electrocardiogram. Each patient was allowed to have exactly one episode of tachycardia before being removed from the study. We measured how long patients remained free of their tachycardia (the tachycardia-free period) and heart rate during tachycardia. Twenty-nine of the 34 patients had an attack of symptomatic tachycardia within the 90-day observation period. The proportion of patients who had not had any symptomatic PSVT by each day of follow-up was calculated using the Kaplan-Meier method as follows: 75% by day 3, 50% by day 19, 25% by day 36, and 17% by day 90. Patients with any other heart or lung disease had significantly shorter tachycardia-free periods. The mean heart rate during spontaneous tachycardia was 203.5 +/- 34.9 beats per minute (range, 142 to 288 beats per minute). Patients with longer tachycardia-free periods had significantly faster heart rates during tachycardia.     

Use of digoxin in patients with paroxysmal supraventricular tachycardia

The effectiveness and electrophysiologic mechanisms of antiarrhythmic effect of digoxin were examined in 27 patients with paroxysmal atrioventricular nodal reciprocal tachycardia (PAVNRT) and supraventricular tachycardia (SVT) due to latent complementary conductive pathways, i. e. latent Wolff-Parkinson-White (WPW) syndrome. To assess antiarrhythmic action of digoxin, transesophageal pacing and plasma digoxin radioimmonoassays were used. Preventive antiarrhythmic efficiency of digoxin was 53% in PAVNRT patients, and 25% in SVT patients with latent WPW syndrome. Antegrade atrioventricular conduction block seems to be the mechanism of oral digoxin preventive effect. There was no relationship between antiarrhythmic efficiency of digoxin and its plasma level.     

临床路径用于行射频消融术的阵发性室上性心动过速患者的效果评价

目的评价我院临床路径对行射频消融术的阵发性室上性心动过速患者的效果。方法：回顾分析140例行射频消融术的阵发性室上性心动过速患者,将其分为路径组和对照组,比较两组患者的平均住院日、住院总费用、医患满意度等指标的差异。结果：路径组在平均住院日、住院总费用均显著低于对照组（P〈0-05）,而在医患满意度方面均显著高于对照组（P〈0-05）。结论：对行射频消融术的阵发性室上性心动过速患者实施临床路径,可显著缩短住院日,降低住院费用,提高临床疗效和医患满意度。     

Evaluation of psychopathology in patients with paroxysmal supraventricular tachycardia

BACKGROUND: A higher prevalence of anxiety- and depression-related symptoms are expected in patients with at least one somatic disease and who are on medications compared with the general population. OBJECTIVES: To determine if patients with paroxysmal supraventricular tachycardia (PSVT) show a higher prevalence of anxiety and depressive symptoms compared with a control population. The induction of depressive symptoms by beta-blockers or calcium channel blockers was also evaluated. METHODS: Twenty-five patients (17 women, eight men) with documented PSVT (atrioventricular re-entrant tachycardia or atrioventricular nodal re-entrant tachycardia) were evaluated by a battery of questionnaires and inventories, which provide information about the presence of symptoms of anxiety and/or depression. All patients were examined by a psychiatrist and completed the following five scales: Symptom Checklist-90, Hamilton Anxiety Scale, Hamilton Depression Rating Scale, Zung's Self-Rating Depression Scale and Beck Self-Assessment Depression Scale. RESULTS AND CONCLUSIONS: The majority of the evaluations (Hamilton Anxiety Scale, Beck Self-Assessment Depression Scale, Zung's Self-Rating Depression Scale), did not show a higher incidence of severe symptoms of depression in the group of patients with PSVT. However, the Hamilton Depression Rating Scale rated the symptoms of depression as significant, but the score was low enough to be considered nonsignificant. According to the Symptom Checklist-90, men perceived the presence of the cardiological disease more intensively and more negatively than women (P=0.1). Psychiatric history and therapy with psychopharmacological agents were comparable in both groups. It was noted that patients had sporadic contacts with a psychiatrist or a psychologist, but this was not directly associated with PSVT.     

Intravenous diltiazem in patients with paroxysmal re-entrant supraventricular tachycardia

The electrophysiologic effects and efficacy of diltiazem were evaluated with programmed electrical stimulation of the heart in 12 patients with supraventricular re-entrant tachycardia (five with atrioventricular nodal tachycardia and seven with circus movement tachycardia the accessory pathway being concealed in 4). Diltiazem was infused over 1 minute at the dose of 0.25 mg/kg and the electrophysiologic parameters were evaluated at 5 and 30 minutes. Diltiazem prolonged the AH interval from 83.5 +/- 58 to 99 +/- 55 msec (P less than 0.05), effective and functional refractory periods of atrioventricular node from 244 +/- 40 to 268 +/- 56 msec (P less than 0.05) and from 432 +/- 124 to 468 +/- 130 msec (P less than 0.005) respectively, lowered the atrial pacing rate inducing second-degree atrioventricular block from 159 +/- 32 to 134 +/- 33 beats/min (P less than 0.005) and decreased systolic and diastolic blood pressure from 143.5 +/- 33 to 132.5 +/- 22 mm Hg (P less than 0.05) and from 90 +/- 15 to 82.5 +/- 9 (P less than 0.05), respectively. Diltiazem prevented the reinduction of the tachycardia in 4 of 5 patients with atrioventricular nodal tachycardia and in 4 of 7 with circus movement tachycardia. The mechanism of action of diltiazem consisted of depression of conduction in atrioventricular node in anterograde fashion while there were no effects on refractoriness of the accessory pathway. The drug was well tolerated with no adverse effects. Diltiazem, therefore, appears an effective and safe drug in the acute treatment of re-entrant supraventricular tachycardia.     

Epinephrine-induced reversal of verapamil's electrophysiologic and therapeutic effects in patients with paroxysmal supraventricular tachycardia

The purpose of our study was to determine whether an infusion of epinephrine reverses the electrophysiologic effects of verapamil and whether reversal of verapamil's effects on the induction of paroxysmal supraventricular tachycardia (PSVT) by epinephrine during electropharmacologic testing is predictive of stress-related recurrences of PSVT during long-term treatment with verapamil. The infusion rates of epinephrine used in this study were 25 and 50 ng/kg/min, which previously have been demonstrated to result in plasma epinephrine concentrations in the range that occurs during a variety of stresses in humans. The subjects of this study were 17 patients with recurrent PSVT who underwent an electrophysiologic study in the control state and after at least 2 days of treatment with 240-480 mg/day verapamil. After assessing the response to verapamil, epinephrine was infused and testing was repeated. Verapamil significantly slowed atrioventricular conduction and prolonged refractoriness in the atrium and atrioventricular node. The effects of the two infusion rates of epinephrine were generally similar in magnitude and, therefore, the results were pooled. Epinephrine partially or completely reversed all of verapamil's electrophysiologic effects. Verapamil suppressed the induction of sustained PSVT in 15 patients. Epinephrine facilitated the induction of PSVT in seven of these 15 patients. All 15 patients were treated on a long-term basis with verapamil. The eight patients in whom epinephrine did not facilitate the induction of PSVT had no recurrences of PSVT during 9-18 months of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)