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.     

Electrophysiological properties of atrial fibrillation with WPW syndrome and the role of procainamide in conversion

Fifty one patients with recurrent episodes of atrial fibrillation associated with WPW syndrome were studied by pre-operative clinical electrophysiogical testing. The results showed that: these patients had an markedly prolonged intra-atrial conduction time (PA intervals: 42.22 +/- 10.93 ms) than the patients only with attack of atrioventricular reentry tachycardia (AVRT) (PA intervals: 17.21 +/- 9.68ms, P less than 0.001). The attack of atrial fibrillation related to an markedly prolonged atrial vulnerable phase and the retrograde conduction of accessory pathway (AP). The clinical results of atrial fibrillation were decided by the antegrade effective refractory period (AERP) of AP. When the shortest R-R (V-V) intervals during attack of atrial fibrillation was shorter than 180ms, the atrial fibrillation spontaneously turned to the ventricular fibrillation. The conversion of atrial fibrillation to sinus rhythm showed that procainamide not only prolonged AERP of AP, which were 248.57 +/- 15.74ms and 388.57 +/- 63.9 ms (P less than 0.001) respectively before and after intravenous procainamide infusion, but also prolonged intra-atrial conduction time significantly, the PA interval before and after intravenous procainamide infusion were 42.22 +/- 10.93 ms and 57.14 +/- 11.12 ms (P less than 0.025) respectively.     

Effects of atropine on induction and maintenance of atrioventricular nodal reentrant tachycardia.

The electrophysiologic effects of atropine were studied in 14 patients with dual atrioventricular (AV) nodal pathways and recurrent paroxysmal supraventricular tachycardia (PSVT). During PSVT, all patients used a slow pathway (SP) for antegrade and fast pathway (FP) for retrograde conduction. Atropine enhanced both SP antegrade and FP retrograde conduction, shown by a decrease in paced cycle lengths (atrial and ventricular) producing AV and ventriculoatrial block. Five patients had induction of sustained PSVT before and after atropine. Seven patients failed to induce or sustain PSVT before atropine, because of retrograde FP refractoriness. All seven had induction of sustained PSVT after atropine due to facilitation of FP retrograde conduction. Two patients had only single atrial echoes before atropine, reflecting SP antegrade refractoriness. After atropine, sustained PSVT was inducible in one, and nonsustained in the other, PSVT cycle length could be compared in seven patients before and after atropine and decreased from 383 +/- 25 to 336 +/- 17 (p less than 0.05). Thus, in patients with dual AV nodal pathways, atropine facilitated SP antegrade and FP retrograde conduction, shortened cycle length of PSVT and potentiated ability to sustain PSVT.     

Radiofrequency Ablation of a Concealed Nodoventricular Mahaim Fiber Guided by a Discrete Potential

INTRODUCTION: We present the case of a 17-year-old woman who underwent an electrophysiological study and radiofrequency (RF) ablation of supraventricular tachycardia refractory to medical treatment. Two right-sided, concealed, nondecremental atrioventricular accessory pathways (AV-APs) involved in orthodromic circus movement tachycardias were identified. After RF ablation of both AV-APs, evidence of bidirectional dual AV nodal conduction was demonstrated and regular narrow complex tachycardia was induced. METHODS AND RESULTS: During the tachycardia, retrograde slow and fast AV nodal pathway conduction with second-degree ventriculoatrial (VA) block and VA dissociation were observed. During the tachycardia with second-degree VA block, ventricular extrastimuli elicited during His-bundle refractoriness advanced the next His potential or terminated the tachycardia. Mapping the right atrial mid-septal region, a distinct high-frequency activation P potential was recorded in a discrete area, two thirds of the way from the His bundle toward the os of the coronary sinus. Detailed electrophysiologic testing with the recordable P potential demonstrated that the tachycardia utilized a concealed nodoventricular AP arising from the proximal slow AV nodal pathway. CONCLUSION: The tachycardia with slow 1:1 VA conduction could be reset by ventricular extrastimuli elicited during His-bundle refractoriness advancing the subsequent activation P potential and atrial activation. RF ablation guided by recording of the activation P potential resulted in elimination of both the slow AV nodal pathway and the nodoventricular connection with preservation of the normal AV conduction system.     

Circadian variations in the electrical properties of the human heart assessed by sequential bedside electrophysiologic testing

To assess the variability of the currently used electrophysiologic parameters and their possible circadian rhythm, sequential bedside electrophysiologic testing was performed during a 24-hour period, at intervals of 1 to 2 hours, in 12 patients who had normal atrioventricular (AV) conduction times and normal sinus node function. The coefficients of variation during the 24-hour period were: +/- 10.4% for the R-R interval, +/- 10.6% for the sinus node recovery time (SRT) at atrial pacing of 100 bpm, +/- 32.5% for the corrected SRT, +/- 15.1% for the ventriculoatrial (VA) effective refractory period (ERP), +/- 8.3% for the AV nodal ERP, +/- 5.7% for the AH interval, +/- 5.2% for the HV interval, +/- 5.5% for the atrial ERP, +/- 3.3% for the right ventricular ERP, +/- 2.8% for the QT interval, +/- 4% for the VA interval, and +/- 3.4% for the retrograde Kent bundle ERP. Between 12:00 midnight and 7:00 AM, there was significant lengthening of: the sinus node rate (p less than 0.0005), the SRT at atrial paced rates of 100 and 120 bpm (p less than 0.025), the QT interval duration (p less than 0.025), and the ERP of the atria (p less than 0.025), AV node (p less than 0.01), and right ventricle (p less than 0.05). Thus conventional electrophysiologic parameters are subject to daily variability and, like sinus node function, AV nodal and myocardial refractoriness follow a circadian rhythm with an acrophase between 12:00 midnight and 7:00 AM. In addition, prolonged bedside recording of the His bundle potential can be reliably obtained.     

Sequential dual chamber extrastimulation: A novel pacing maneuver to identify the presence of a slowly conducting concealed accessory pathway

BACKGROUND: Transient VA block can be created in the AV node (AVN) when an atrial extrastimulus is delivered at the AVN effective refractory period (ERP) due to anterograde concealed conduction. OBJECTIVE: We hypothesized that ventricular stimulation during pacing-induced AVN refractoriness could identify concealed accessory pathways (APs) that remain hidden with standard maneuvers. METHODS: Patients undergoing electrophysiological study for supraventricular tachycardia were screened for presence of an AP using standard pacing maneuvers and/or V pacing during adenosine infusion. The dual-chamber sequential extrastimulation maneuver consisted of an 8-beat drive train of simultaneous AV pacing at 600 msec, followed by an A2 delivered at AVN ERP, followed by a V2 delivered at the drive train cycle length (600 msec). Repeat drives were then performed with decrements of 10 msec for V2 until VA block was seen. Retrograde AVN and AP ERP were recorded with standard (V1, V2) and dual-chamber extrastimulation (A1/V1, A2, V2). Patients with an AP identified with standard pacing, manifest pre-excitation, or A ERP < AVN ERP were excluded. RESULTS: Fourteen patients with and 19 patients without an AP were studied. In all patients with an AP, exclusive VA conduction over the AP, without fusion, was seen with the described pacing maneuver. In patients without an AP, retrograde AV nodal ERP was extended by a mean of 138 +/- 46 msec (range 50 to 210 msec) with the A2. Anterograde concealed conduction into the AP was also seen in some patients who showed AP conduction during standard V1V2 pacing (mean retrograde extension of ERP 12 +/- 8 msec, range 0 to 20 msec). CONCLUSION: Dual-chamber sequential extrastimulation is a useful maneuver for identifying slowly conducting APs not revealed with standard pacing maneuvers because of an ERP and conduction time similar to the AVN. The maneuver uses anterograde concealed conduction to prolong AVN refractoriness much more than that of a concealed AP, thereby allowing the AP to become manifest with the V2.     

Electrophysiologic effects of lorcainide (R 15889) in man

The electrophysiological effects of lorcainide (R 15 899) were studied in 15 patients. Atrioventricular conduction was analysed by His bundle recording and cardiac refractory periods were determined by the extra stimulus method. The assessment of sino atrial function was performed by measuring sinus node recovery times and sino atrial conduction times. The electrophysiological data was recorded before and 10 minutes after a slow intravenous injection of 1,5 mg/Kg of lorcainide followed by a continuous infusion at 0,02 mg/Kg/min. The following results were obtained; 1) The HV interval increased in all cases (average : II ms) 2) The QRS and QT intervals were significantly prolonged 3) Lorcainide produced a slowing of conduction and an increase in the refractory periods at atrial level 4) AV nodal conduction was unaffected 5) The sinus rate slightly increased. There were no significant changes in sinus node recovery time or sino atrial conduction. It must be concluded that, in man, lorcainide produces electrophysiological effects of antiarrhythmic agents of the quinidine type.     

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.     

Radiofrequency catheter ablation of two accessory pathways with different unidirectional conduction properties

Simultaneous occurrence of narrow and broad QRS complex tachycardias in patients with WPW syndrome usually indicates a macroreentry in an orthodromic atrioventricular reentry-tachycardia using the AV node as antegrade and the accessory pathway as retrograde conduction and vice versa in an antidromic circuit. We report on a 32-year-old woman with WPW syndrome presenting with both a narrow and a broad QRS complex tachycardia using two accessory pathways with different unidirectional conduction properties in combination of an exclusively antegrade conducting AV node. This case report describes conventional mapping techniques and ablation of this unusual entity of a WPW syndrome.     

Electrophysiologic effects of diprafenone in supraventricular and ventricular tachycardia

The electrophysiologic effects of diprafenone were evaluated in 31 patients (9 X AV nodal reentrant tachycardia, 9 X Wolff-Parkinson-White syndrome, 4 X paroxysmal atrial fibrillation, 10 X recurrent ventricular tachycardia). Electrophysiologic studies were performed before and after intravenous infusion of 1.5 mg/kg body weight diprafenone in a period of 10 minutes. Diprafenone prolonged the mean RR interval during sinus rhythm from 690 +/- 109 ms to 789 +/- 93 ms and the maximal sinus node recovery time from 1081 +/- 216 ms to 1300 +/- 398 ms (p less than 0.001). The effective refractory period of the right atrium increased from 195 +/- 22 ms to 210 +/- 28 ms (p less than 0.01) and of the right ventricle from 220 +/- 20 ms to 235 +/- 20 ms (p less than 0.001). Diprafenone produced a prolongation of the antegrade effective refractory period of the AV node from 260 +/- 35 ms to 294 +/- 39 ms (p less than 0.01) and of the retrograde effective refractory period from 265 +/- 76 ms to 400 +/- 130 ms (p less than 0.001). The effective refractory periods of the Kent bundle increased: antegrade from 299 +/- 45 ms to 413 +/- 133 ms, retrograde from 252 +/- 33 ms to 286 +/- 169 ms (p less than 0.05). Suppression of inducibility was observed in 12 of 17 patients with supraventricular reentrant tachycardia, in 5 of 8 patients with atrial fibrillation and in 7 of 10 patients with recurrent ventricular tachycardia. The rate of supraventricular tachycardias decreased under the influence of the substance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Patient with atrioventricular node reentrant tachycardia with eccentric retrograde left-sided activation: treatment with radiofrequency catheter ablation

We describe a patient with supraventricular tachycardia with triple atrioventricular (AV) node pathway physiology. A discontinuous curve was present in the antegrade AV nodal function curves. During right ventricular pacing, the earliest retrograde atrial activation was recorded at the left-sided coronary sinus electrode. The retrograde ventricular-atrial interval was long and had decremental conduction. We induced a slow-slow AV node reentrant tachycardia (AVNRT) with eccentric retrograde left-sided activation. After slow pathway ablation, dual AV nodal pathway physiology was present. AVNRT with eccentric retrograde left-sided activation is relatively rare, and our findings suggest that eccentric retrograde left-sided atrial inputs consist partially of a slow pathway and disappear with slow pathway ablation.     

Conduction properties of the antegrade fast and slow AV nodal pathways associated with AV nodal reentrant tachycardia.

To elucidate differences in conduction properties among the normal atrioventricular (AV) node and the antegrade fast and slow dual AV nodal pathways (DAVNPW), AV nodal conduction curves were analyzed quantitatively in 38 patients. Eighteen patients had antegrade DAVNPW with AV nodal reentrant tachycardia (AVNRT) (dual pathways group) and the remaining 20 had smooth AV nodal conduction curves, without evidence of AV nodal dysfunction (control group). The effective refractory period (ERP) of the antegrade fast pathway was longer than that of the normal AV node (at both basic cycle lengths of 700 and 500 msec, p less than 0.01). Although the atrial premature beats were delayed by a longer ERP in the fast pathway, there was no significant difference in the degree of prolongation of AV nodal conduction time related to shortening of the coupling interval (i.e., ratio of A2H2 increment to A1A2 decrement) between these two pathways. On the other hand, the ERP of the antegrade slow pathway was similar to that of the normal AV node. The degree of prolongation of AV nodal conduction time (relative to the shortening of the coupling interval) was greater in the antegrade slow pathway than in the normal AV node. In conclusion, these findings suggest that in DAVNPW with AVNRT: (1) the antegrade fast pathway is similar to the AV node and its conduction properties are unlikely to be better than those of the normal AV node and (2) the antegrade slow pathway has quantitatively poorer conduction properties than the normal AV node, since it has a greater degree of decremental conduction.     

Cibenzoline: electrophysiologic effects of a new class I anti-arrhythmia agents in supraventricular tachycardia

Cibenzoline, an imidazoline derivate, is a new class 1 antiarrhythmic agent. The electrophysiologic effects and antiarrhythmic properties of cibenzoline (100 mg i.v.) were evaluated in 22 patients with paroxysmal supraventricular tachycardia: 12x Wolff-Parkinson-White Syndrome, 9x AV nodal reentrant tachycardia, 1x atrial tachycardia. Cibenzoline shortened the sinus cycle length from 742 +/- 103 ms to 661 +/- 87 ms (p less than 0.001) and the sinus node recovery time from 1026 +/- 106 ms to 926 +/- 135 ms (p less than 0.001). The substance lengthened the AH interval from 93 +/- 19 ms to 112 +/- 24 ms (p less than 0.001) and the HV interval from 42 +/- 12 ms to 61 +/- 14 ms (p less than 0.001). The effective refractory periods of the atrium and right ventricle did not change significantly, but the effective refractory period of the AV node in antegrade (269 +/- 42 ms vs 278 +/- 46 ms; p less than 0.05) and retrograde direction (281 +/- 57 ms vs 413 +/- 124 ms; p less than 0.001) increased markedly. Cibenzoline prolonged the effective refractory period of the accessory pathway in retrograde direction from 263 +/- 41 ms to 428 +/- 101 ms (p less than 0.001). The effective refractory period of the antegrade accessory pathway did not change. During atrial stimulation inducibility of the reentrant tachycardia was suppressed in 14 of 22 patients and the inducibility of atrial fibrillation in 7 of 12 patients. The RR interval of the reentrant tachycardia was prolonged from 353 +/- 57 ms to 420 +/- 57 ms (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Radiofrequency catheter ablation of two accessory pathways with different unidirectional conduction properties

Summary Simultaneous occurrence of narrow and broad QRS complex tachycardias in patients with WPW syndrome usually indicates a macroreentry in an orthodromic atrioventricular reentry-tachycardia using the AV node as antegrade and the accessory pathway as retrograde conduction and vice versa in an antidromic circuit. We report on a 32-year-old woman with WPW syndrome presenting with both a narrow and a broad QRS complex tachycardia using two accessory pathways with different unidirectional conduction properties in combination of an exclusively antegrade conducting AV node. This case report describes conventional mapping techniques and ablation of this unusual entity of a WPW syndrome.     

Electrophysiological effects of lorcainide in sinoatrial disease and in Wolff-Parkinson-White syndrome

The influence of lorcainide on sinus node function and intracardiacconduction was studied in 34 patients, including seven patientswith sinoatrial disease and 14 patients with Wolff-Parkinson-Whitesyndrome. Programmed cardiac stimulation and His bundle electrographywere undertaken. Lorcainide, 2 mg/kg body weight, was givenintravenously over a period of 10 min. In normal subjects, aslight increase of sinus rate was observed; lorcainide did notchange corrected sinus node recovery time (CSNRT) and sinoatrialconduction time (SACT), calculated by use of the premature stimulustechnique. In sinoatrial disease, however, three out of sevenpatients demon-strated a decrease of heart rate due to sinusnode exit block, and CSNRT was markedly prolonged under theinfluence of the drug. Sinus node entrance block to prematureatrial beats was observed in two controls and two patients withsinoatrial disease. Spontaneous sinus node exit block developedin two patients with sinoatrial dysfunction after administrationof lorcainide. Refractory periods of the right atrium, rightventricle and conduction through the A V node (AH intervals)were unaffected by lorcainide, while HQ, QRS and QT intervalswere prolonged. In Wolff-Parkinson-White syndrome, antegradeconduction via the accessory pathway was blocked in six outof 12 patients. After lorcainide, refractory periods of theaccessory pathway increased in both the antegrade and retrogradedirection. The ventricular rate during reciprocating tachycardiaand during atrial fibril-lation was decreased by lorcainide.The results identify slowing of intraventricular conductionas the main action oflorcainide. In sinoatrial disease, lorcainidemay aggravate sinus node dysfunction.     

Electrophysiologic effects of intravenous metoprolol

We evaluated the electrophysiologic effects of intravenous metoprolol, a selective beta-1-blocking agent, in 12 patients. Electrophysiologic parameters were measured during the control period, immediately following, and 4 to 6 hours after infusion of 0.15 mg/kg. Metoprolol serum concentration was serially measured in 6 of the 12 patients. Immediately after metoprolol infusion, the sinus cycle length increased by 20% from 738 +/- 166 msec to 885 +/- 181 msec (p less than 0.01), AH interval during sinus rhythm increased by 34% from 83 +/- 27 msec to 112 +/- 37 msec (p less than 0.01), and antegrade atrioventricular (AV) nodal Wenckebach cycle length increased by 20% from 360 +/- 188 msec to 432 +/- 199 msec (p less than 0.01). Sinus node recovery time and sinoatrial conduction time did not become abnormally prolonged in any patient. His-Purkinje conduction was unaltered. High atrial and ventricular refractory periods were modestly increased (less than 15 msec); the increase in refractoriness reached statistical significance when repeat measurements were made at 4 to 6 hours. No adverse effects were noted. Metoprolol serum concentration at the time of peak measured electrophysiologic effect was 54.6 +/- 15.2 ng/ml. We conclude that at this dose, intravenous metoprolol significantly prolongs sinus cycle length and AV nodal conduction, may modestly increase atrial and ventricular refractoriness, and appears to have electrophysiologic potency similar to propranolol. It is well tolerated following intravenous administration and may be of particular value in the acute treatment of supraventricular tachycardia when beta-receptor selectivity is desired.     

Antiarrhythmic and proarrhythmic properties of diazepam demonstrated by electrophysiological study in humans

We evaluated the electrophysiological parameters before and after the intravenous infusion of diazepam (0.2 mg/kg) in 20 cardiac patients to investigate the drug's antiarrhythmic effect. Diazepam did not significantly change the arterial pressure. After the intravenous infusion of diazepam, the sinus cycle length significantly shortened from 847 +/- 132 to 747 +/- 155 ms (p less than 0.01). No significant change in the maximal sinus node recovery time was noted. The AH interval at the atrial pacing length of 600 ms shortened significantly from 140 +/- 40 to 127 +/- 39 ms (p less than 0.05). However, there was no significant change after the administration of diazepam in the longest atrial pacing rate associated with Wenckebach conduction in the atrioventricular (AV) node, effective and functional refractory periods of the AV node, HV interval, and QRS width during ventricular pacing at the cycle length of 600 ms. The atrial and ventricular effective refractory periods remained unchanged after the administration of diazepam. Six of the eight patients who showed dual AV nodal refractory period curves in the control study did not demonstrate them after diazepam administration by increasing the atrial or AV node effective refractory period. Thus, diazepam showed significant electrophysiological effects of the heart including shortening of the sinus cycle length, improvement in AV node conduction, and no significant effect on the His-Purkinje or intraventricular conduction and refractoriness of the atrium, AV node and ventricle. On the other hand, diazepam may influence the inducibility of supraventricular reentrant tachycardia incorporating the AV node.     

Effects of verapamil on supraventricular tachycardia in patients with overt and concealed Wolff-Parkinson-White syndrome

Verapamil (0.15 mg/kg) intravenously, was administered to 19 patients with recurrent supraventricular tachycardia (SVT) undergoing electrophysiological evaluation. Twelve patients had overt Wolff-Parkinson-White (WPW) syndrome and seven patients had concealed accessory pathways conducting in the retrograde direction only. Verapamil had a significant effect in delaying conduction and prolonging refractoriness in the atrioventricular (AV) node, but no significant actions on any of the other cardiac tissues that formed the tachycardia circuit in these patients. In particular, it had no significant effects on anterograde or retrograde bypass conduction or refractoriness. Sustained SVT was initiated in 15 patients, and was terminated within 60 to 105 seconds of a 30-second injection of verapamil in 13 patients. Cycle length alternation during SVT was seen in six patients prior to reversion, and spontaneous ventricular complexes (VPCs) were observed following verapamil administration in five patients. Two patients with apparently normal sinus node function showed prolongation of their sinus node recovery times immediately following reversion of SVT by verapamil. Echo zones were assessed before and after verapamil, and sustained or self-terminating SVT could still be induced after the drug in 13 of the 15 patients who had sustained SVT beforehand. It was concluded that intravenous verapamil was effective in terminating sustained SVT in the majority of patients with overt or concealed WPW and that, despite a potential for sinus node depression and the initiation of VPCs, it had no clinically significant side effects. The ability to reinitiate SVT following its administration suggests the need for immediate follow-up with maintenance drug therapy.     

Atrial fibrillation and atrial vulnerability in the Wolff-Parkinson-White syndrome

To explore the etiology of paroxysmal atrial fibrillation (AF) in the Wolff-Parkinson-White (WPW) syndrome, we examined the rates of AF episodes and performed electrophysiologic studies in 58 patients with WPW syndrome. They were classified into three patient groups depending on the property of antegrade conduction over accessory pathways: manifest WPW, intermittent WPW, and concealed WPW. Atrial vulnerability was defined as the inducibility of AF or repetitive atrial responses. The three groups were: 24 patients in manifest WPW, aged 42 +/- 15 yrs, 38% with AF; 12 patients in intermittent WPW, aged 40 +/- 15 yrs, 25% with AF; 22 patients in concealed WPW, aged 44 +/- 16 yrs, 9% with AF. There were no significant differences in the mean age between the groups. The incidences of atrial vulnerability detected in electrophysiologic studies in each group were 54%, 42%, and 27% respectively. The incidence of AF was well correlated with that of atrial vulnerability (p less than 0.01). The effective refractory periods (ERP) of the atrium and the retrograde ERP of the accessory pathway did not differ significantly between the three groups. Atrial conduction delay was more prominent in manifest WPW than in concealed WPW. The incidence of AF and atrial vulnerability was highest in the manifest WPW group, intermediate in the intermittent WPW group, and lowest in those patients with concealed WPW. The difference in incidence between the manifest WPW group and the concealed WPW group was significant (p less than 0.05). Therefore, the property of antegrade conduction over accessory pathways may be related to the genesis of AF in the WPW syndrome.     

A clinical study of induction rate of atrioventricular reciprocating tachycardia in WPW syndrome]

The differences in induction rate of atrioventricular reciprocating tachycardia (AVRT) were analyzed in 76 consecutive patients of WPW syndrome with tachycardia attack, confirmed by either ECG or history, and who underwent electrophysiological study. AVRT was induced by programed electrical stimulation in 72% of patients with manifest WPW syndrome, in 77% of patients with intermittent WPW syndrome, and in 96% of patients with concealed WPW syndrome, respectively. There was a significant difference in induction rate between manifest WPW syndrome and concealed WPW syndrome (p less than 0.05). Induction rate of AVRT in patients with accessory pathway (AP) located in the ventricular septum was significantly lower (50%) than in patients with AP located in the left ventricle (88%) and in the right ventricle (72%) (p less than 0.05). Ventricular atrial conduction was found in only 56% of patients with AP located in the ventricular septum, while it was found in 94% of patients with AP located in the left ventricle, and in 100% of patients with AP located in the right ventricle (p less than 0.05). There were no significant differences in antegrade effective refractory periods of atrioventricular node and AP between patients with and without inducible AVRT. There was also no significant difference in the retrograde effective refractory periods of AP between patients with or without inducible AVRT. We concluded that the induction rate of AVRT would be affected by the location of AP and the mode of delta wave appearance in the surface electrocardiogram.