Clinical,electrocardiographic and electrophysiologic observations in patients with paroxysmal supraventricular tachycardia

Seventy-nine patients without ventricular preexcitation but with documented paroxysmal supraventricular tachycardia were analyzed. Electrophysiologic studies suggested atrioventricular (A-V) nodal reentrance in 50 patients, reentrance utilizing a concealed extranodal pathway in 9, sinus or atrial reentrance in 7 and ectopic automatic tachycardia in 3. A definite mechanism of tachycardia could not be defined In 10 patients (including 7 whose tachycardia was not inducible). The three largest groups with inducible tachycardias were compared in regard to age, presence of organic heart disease, rate of tachycardia, functional bundle branch block during tachycardia and relation of the P wave and QRS complex during tachycardia. A-V nodal reentrance was characterized by a narrow QRS complex and a P wave occurring simultaneously with the QRS complex during tachycardia. Reentrance utilizing a concealed extranodal pathway was characterized by young age, absence of organic heart disease, fast heart rate, presence of bundle branch block during tachycardia and a P wave following the QRS complex during tachycardia. Sinoatrial reentrance was characterized by frequent organic heart disease, a narrow QRS complex and a P wave in front of the QRS complex during tachycardia.In conclusion, a mechanism of paroxysmal supraventricular tachycardia could be defined in most patients. Observations of clinical and electrocardiographic features in these patients should allow prediction of the mechanism of the tachycardia.     

Slow pathway ablation in children with documented reentrant supraventricular tachycardia not inducible during invasive electrophysiologic study

Radiofrequency catheter ablation (RFA) has become the procedure of choice for permanent therapy of atrioventricular nodal reentrant tachycardia (AVNRT). This report presents our experience with atrio-ventricular node (AVN) modification in patients with documented narrow complex reentrant SVT, but no evidence for an accessory pathway, and no inducible tachyarrhythmia during invasive electrophysiology (EP) study. METHODS: The study population consists of nine children, age range 6-13 years (median 9) with previously documented SVT who had no tachyarrhythmia inducible during EP study (at baseline and following isoprenaline infusion). Eight of the 9 EP studies were performed under general anesthesia, and one under conscious sedation. An accessory pathway was excluded in all patients by appropriate atrial and ventricular extrastimulus pacing techniques. Eight of the nine patients had dual AV nodal physiology, and one had single AV nodal echo beats. The slow AV nodal pathway was empirically ablated, by applying RF lesions in the right inferoseptal AV groove, achieving catheter tip temperature of 50 degrees C. The appearance of an accelerated junctional rhythm during RF application was deemed to denote a successful application site. AV conduction during RF application was confirmed by incremental atrial pacing. The catheter position, and its relation to the compact AV node was constantly monitored using the LocaLisa navigation system. The end-point was absence of dual AVN physiology, and/or AV nodal echo beats. RESULTS: Successful slow pathway ablation was achieved in all patients. One patient appeared to have two separate slow pathways with different locations and two AH-jumps, which were both successfully ablated. None of the patients had evidence of temporary or permanent AV block at follow-up (median duration 9 months, range 4 to 36 months); none has had recurrence of symptoms or documented tachyarrhythmia. CONCLUSIONS: In children with structurally normal hearts, a previously documented SVT, absence of an accessory pathway and noninducibility of SVT during EP study, empirical slow pathway ablation appears to be justified.     

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)     

Invasive electrophysiologic evaluation of patients with supraventricular tachycardia

This article describes the clinical and technical aspects of invasive electrophysiology studies in patients with supraventricular tachycardia. The methods and interpretation of programmed stimulation and pharmacologic interventions during sinus rhythm and supraventricular tachycardia are discussed.     

Comparison of the electrophysiologic effects of intravenous and oral verapamil in patients with paroxysmal supraventricular tachycardia

The electrophysiologic effects of intravenous verapamil (a bolus dose of 0.15 mg/kg body weight followed by infusion of 0.005 mg/kg per min) were compared with those of oral verapamil (80 mg every 6 hours for 48 hours) in eight patients who had paroxysmal Supraventricular tachycardia. The mechanism of tachycardia was atrioventricular (A-V) nodal reentry in four patients and A-V reentry utilizing an accessory pathway for retrograde conduction in the remaining four. The electrophysiologic effects of oral and intravenous verapamil were similar. Both preparations significantly prolonged anterograde effective and functional refractory periods of the A-V node (p < 0.001). Both significantly increased the shortest pacing cycle length maintaining 1:1 anterograde conduction over the A-V node (p < 0.001). Retrograde conduction over the A-V node was greatly prolonged with verapamil in one patient but was unaffected in the others. There was no significant effect on sinoatrial conduction time, sinus nodal recovery time or atrial or ventricular refractoriness. Both preparations prevented induction of tachycardia in six patients none of whom had recurrence of sustained tachycardia while receiving long-term oral therapy (5 to 10 months). Neither preparation had a significant effect in two patients and this predicted failure of long-term oral therapy in one of these patients.The results of acute drug testing with intravenous verapamil can be extrapolated to predict the electrophysiologic results and response to long-term therapy with oral verapamil.     

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.     

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.     

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.     

Effectiveness and electrophysiologic action of amiodarone in controlling attacks of supraventricular paroxysmal tachycardia

The study was undertaken to examine 21 patients with episodes of recurrent ventricular paroxysmal tachycardia. The latter were arrested by amiodarone intravenously injected in a dose of 5 mg/kg. The episode was stopped in 9 (45%) cases, i.e. in 6 (60%) cases with atrioventricular junction tachycardia and 3 (30%), involving accessory conduction tracts. Amiodarone-induced deterioration was observed in the atrioventricular conduction (in the anterograde one in most cases) and that along the accessory conduction tracts. In all the cases, the episode was abolished due to the anterograde block of impulse conduction along the atrioventricular node. There was an amiodarone-induced small decrease in the function of automatism in the sinus node.     

Study of thyroid function in patients with paroxysmal supraventricular tachycardia

Twenty-nine patients with paroxysmal supraventricular tachycardias of different origins and clinical pattern were investigated to detect latent thyroid disorders; hyperthyroidism was diagnosed in 2 of those, and hypothyroidism, in 4. Functional thyroid disorders were more common in patients with mitral prolapse and supraventricular tachycardias due to additional conductive pathways (the Wolff-Parkinson-White syndrome) and paroxysmal nodal reciprocal tachycardia, particularly if they were resistant to antiarrhythmic treatment and/or had aggravated thyroid history. It is suggested that thyroid dysfunction is just a triggering factor of arrhythmia since thyrostatic and replacement therapy eliminate paroxysms of tachycardia, while organic pathology of the heart and its conductive network remains unaffected.     

Nadolol and supraventricular tachycardia: an electrophysiologic study

To assess antiarrhythmic efficacy of oral nadolol, 15 patients with recurrent supraventricular tachycardia were studied. Eight patients had atrioventricular (AV) nodal reentrant tachycardia and seven had AV reciprocating tachycardia involving an accessory AV pathway. Electrophysiologic studies were performed before and after intravenous infusion of propranolol (0.20 mg/kg), and were repeated 5 to 8 days after oral nadolol therapy at a daily dose of 80 to 160 mg. Both intravenous propranolol and oral nadolol induced significant prolongation of the sinus cycle length from 741 +/- 73 ms to 834 +/- 97 and 1,029 +/- 95 ms, respectively (p less than 0.001 and p less than 0.0001, respectively). Both intravenous propranolol and oral nadolol depressed AV nodal but not accessory AV pathway conduction, and shifted the dual AV nodal pathway conduction curves (A1A2, A2H2; A1A2, H1H2) upward and to the right by prolonging the conduction time and increasing the refractory period. Ten patients (seven with AV nodal reentry and three with AV reciprocation) who responded to intravenous propranolol also responded to oral nadolol with loss of the inducibility of sustained tachycardia; the remaining five patients (one with AV nodal reentry and four with AV reciprocation) who did not respond to intravenous propranolol also failed to respond to oral nadolol with persistence of the inducibility of sustained tachycardia. Thus, in conclusion, intravenous propranolol testing predicts the therapeutic efficacy of oral nadolol therapy and oral nadolol in once-daily doses may be used for long-term prophylaxis of recurrent supraventricular tachycardia.     

食管电生理诊断阵发性室上性心动过速

目的探讨食管电生理诊断阵发性室上性心动过速(paroxysmal supraventricular tachycardia,PSVT)及分型的准确性。方法收集经食管电生理和心内电生理检查并行射频消融治疗的PSVT42例,将两种电生理对PSVT的诊断及分型进行比较,用X2检验,以P<0.05为差异有统计学意义。结果两种电生理检查诊断房室结双径路、慢快型房室结折返性心动过速、常见的顺向型房室折返性心动过速差异无显著性,食管电生理对房室旁路的粗略定位准确性较高,但对快慢型房室结折返性心动过速、慢房室旁路参予的房室折返性心动过速与房性心动过速不易辨别。结论食管电生理诊断常见类型的PSVT与心内电生理有相似的价值,且具有无创、简便、费用低等优点;但对不常见或复杂的PSVT不易辨别。     

室上性心动过速中旁道折返的少见现象

报告阵发性室上性心动过速（PSVT）电生理检查中发现的几种少见的旁道电生理特性。例1为一左侧隐匿性房室旁道参与的房室折返性心动过速,其心室扫描示旁道逆向有效不应期260ms,但520－390ms时无逆向传导功能。例2为一慢－慢型房室交接区折返性心动过速,同时存在一条右侧隐匿性房室旁道作为旁观者。例3为一宽QRS波群心动过速,其体表心电图呈典型马海姆纤维型预激综合征,电生理揭示存在左侧房室隐匿性旁道和束室旁道两条附加旁道,前者为心动过速的逆传支,后者与房室结－希室束同为顺传支。对上述几种少见的电生理现象临床意义进行讨论。     

Serial electrophysiologic studies of the effects of oral diltiazem on paroxysmal supraventricular tachycardia

In 16 patients with paroxysmal supraventricular tachycardia, electrophysiologic studies were done before and serially at hourly intervals for eight hours after the third oral dose of 90 mg diltiazem given every eight hours. Diltiazem increased both the longest atrial paced cycle length producing type 1 atrioventricular block and the effective refractory period of the atrioventricular conducting system at all measurements. Before diltiazem, all 16 patients had induction of sustained tachycardia. After diltiazem, sustained tachycardia could not be induced in ten patients at any measurements; in these patients, either echo or nonsustained tachycardia was induced. In the remaining six patients, sustained tachycardia was induced, particularly after six hours. Follow-up observations in 12 patients receiving the same dosage of oral diltiazem for 6 +/- 2 months (mean +/- SD), showed that of the eight patients in whom electrophysiologic testing induced either echo or nonsustained tachycardia, six were asymptomatic and two experienced transient palpitation. Of the other four patients with induction of sustained tachycardia, three had transient palpitation and one had occasional attacks of sustained tachycardia requiring modification of therapy. Thus, oral diltiazem increases atrioventricular nodal refractoriness, with an effect lasting up to eight hours. It is an effective agent for the prophylaxis of paroxysmal supraventricular tachycardia.     

Atrioventricular conduction patterns in patients with paroxysmal supraventricular tachycardia.

Atrioventricular conduction patterns suggestive of dual A-V nodal pathways have been reported in patients with and without a history of paroxysmal A-V nodal re-entrant tachycardia (PSVT). The purpose of this study was to determine whether significant association exists between this conduction pattern and the occurrence of PSVT in man. The pattern of A-V conduction was evaluated at similar pacing rates in 13 patients with documented PSVT and 135 patients with PSVT. Patients without PSVT were divided into groups with normal PR intervals (106 patients), PR intervals of 120 msec. or less (12 patients), and PR intervals of 200 msec. or greater (17 patients). Evidence of dual A-V nodal pathways was found in seven of 13 patients with PSVT and nine of 135 patients without PSVT, including eight of 106 patients with normal PR intervals, none of 12 patients with short PR intervals, and one of 17 patients with PR intervals of 200 msec. or greater. The incidence of dual A-V nodal pathways was significantly greater (P less than 0.01) in patients with PSVT when compared with all other groups. In two of four patients with PSVT, propranolol was found to unmask evidence of dual pathways; no evidence of dual pathways was produced by propranolol in 23 patients without PSVT. The data show that the pattern of dual A-V nodal pathways is common only in patients with PSVT and is significantly less frequent in patients without PSVT regardless of the presence of short or long PR intervals. The results of this study establish a strong association between this conduction pattern and the occurrence of PSVT in man.