Significance of pacing cycle lengths in manifest entrainment of orthodromic circus movement tachycardia by ventricular pacing

The physiology of entrainment of orthodromic circus movement tachycardia (CMT) was studied using ventricular pacing during 18 episodes of induced CMT in 7 patients with atrioventricular (AV) accessory pathways. The first paced impulse was delivered as late as possible in the tachycardia cycle (mean 88 +/- 5% of the spontaneous cycle length [CL]). Entrainment was demonstrated by the following criteria: 1:1 retrograde conduction via the accessory pathway; capture of atrial, ventricular and His bundle electrograms at the pacing rate; and resumption of tachycardia at its previous rate after cessation of pacing. The number of ventricular paced impulses ranged from 5 to 14 (mean 8 +/- 3), and entrainment occurred in 2 to 7 paced cycles (mean 4 +/- 2). Orthodromic activation of a major part of the reentry circuit (manifest entrainment) was demonstrated during 9 episodes by the occurrence of His bundle electrogram preceding the first CMT QRS at the time anticipated from the last paced beat. In the 9 other episodes, persistent retrograde His bundle activation and AV nodal penetration by each paced impulse caused a delay (mean 79 +/- 25 ms) in activation of the His bundle preceding the first CMT QRS after the last paced beat. The mean pacing CL achieving manifest entrainment was 92 +/- 3% of the tachycardia CL, compared with 84 +/- 3% for retrograde AV nodal penetration (p less than 0.01). In conclusion, manifest entrainment of orthodromic CMT can be demonstrated by ventricular pacing at very long CLs; shorter CLs may cause CMT termination due to retrograde AV nodal penetration.     

Transient entrainment and interruption of atrioventricular node tachycardia

The possibility of transiently entraining and interrupting the common type of atrioventricular (AV) node tachycardia (anterograde slow, retrograde fast AV node pathway) was studied using atrial and ventricular pacing in 18 patients with paroxysmal AV node tachycardia. Transient entrainment occurred in all patients. During atrial pacing, localized block in the AV node for one beat followed by anterograde conduction over the fast pathway was observed in three patients. During ventricular pacing, localized block for one beat followed by retrograde conduction over the slow pathway was not observed in any patient. Neither atrial nor ventricular fusion beats were observed during entrainment. These observations indicate in a way not previously shown that reentry involving two functionally dissociated pathways in the AV node is the underlying mechanism of paroxysmal AV node tachycardia. The inability to demonstrate atrial or ventricular fusion beats during entrainment suggests a true intranodal location of the reentrant circuit. Finally, the ability to transiently entrain intranodal tachycardia demonstrates that this electrophysiologic phenomenon is not exclusively limited to macroreentrant circuits.     

Termination of circus movement tachycardia utilizing an accessory atrioventricular pathway by retrograde concealed penetration of the atrioventricular node through the bundle branch system: A mechanism of tachycardia termination in Wolff-Parkinson-White syndrome

A 30 year old woman with Wolff-Parkinson-White syndrome underwent electrophysiologic study for investigation of circus movement tachycardia utilizing the accessory pathway for retrograde conduction. The accessory pathway was located on the right side. Episodes of circus movement tachycardia with left and right bundle branch block were induced. Some episodes of circus movement tachycardia with left bundle branch block terminated spontaneously. Two episodes of spontaneous termination at the level of the atrioventricular (A-V) node were preceded by prolongation of the H-V interval causing delay in atrial activation. This delayed atrial cycle was then followed paradoxically by spontaneous termination of the tachycardia in the A-V node. A similar phenomenon could be demonstrated reproducibly with single echo beats induced by coronary sinus extrastimuli. It appears that retrograde concealed penetration of the A-V node through the bundle branch system during anterograde left bundle branch block is the most likely mechanism for this phenomenon.     

Entrainment of atrioventricular nodal reentrant tachycardias during overdrive pacing from high right atrium and coronary sinus: With special reference to atrioventricular dissociation and 2:1 retrograde block during tachycardias

Entrainment was attempted during electrophysiologic evaluation of 8 patients with atrioventricular (AV) nodal reentrant tachycardia. Entrainment could be performed while pacing from the high right atrium in 35 of 35 episodes, from proximal coronary sinus in 9 of 21 episodes and from distal coronary sinus in 10 of 20 episodes. The minimal rates required were 8 to 40 beats/min faster than those of the tachycardias. That the atria (as defined in electrophysiologic studies) were not a necessary component of the reentry circuit was suggested by the occurrence, during tachycardia, of short episodes of AV dissociation and of 1 episode of 2:1 retrograde block. For the tachycardia to be interrupted, the pacing rate usually had to be slightly faster than that required to entrain, as well as sufficiently rapid to produce anterograde block of an atrial impulse in the slow AV nodal pathway. Moreover, termination of tachycardia apparently was a function of the pacing site. In some episodes, either because of a proximity effect or because of a preferential input into the upper common pathway, coronary sinus pacing terminated the tachycardia at slower rates or with fewer stimuli than high right atrial pacing. Thus, patients with drug-resistant AV nodal reentrant tachycardias may benefit from recently introduced pacing techniques for termination of tachycardia through entrainment.     

Clinical efficacy and electrophysiologic effects of intravenous and oral encainide in patients with accessory atrioventricular pathways and supraventricular arrhythmias

The electrophysiologic effects and clinical efficacy of intravenous (i.v.) and oral encainide were studied in 13 patients with accessory atrioventricular (AV) pathways (7 overt, 1 intermittent and 5 concealed) and drug-resistant Supraventricular arrhythmias (5 paroxysmal atrial fibrillation, 1 atrial tachycardia and 7 with orthodromic circus movement tachycardia). Previously, therapy had failed with a mean of 3 conventional antiarrhythmic agents. In 5 patients, amiodarone administration had also been unsuccessful. All patients underwent programmed electrical stimulation of the heart before and after 1.5 mg/kg of i.v. encainide. Seven patients were restudied during oral encainide therapy (mean 155.8 ± 54.2 mg/day) 3 days to 6 weeks (average 21 days) later. Anterograde conduction over the accessory AV pathway blocked in 4 of 7 patients after i.v. encainide. Oral encainide blocked anterograde conduction over the accessory pathway or prolonged the refractory period of the accessory pathway in 3 of 4 patients. This change in anterograde conduction was independent of the predrug value for the anterograde refractory period of the accessory AV pathway. Intravenous and oral encainide had minimal effects on retrograde conduction over the accessory AV pathway. The clinical effect of oral encainide was studied in 12 patients. Four patients responded to oral encainide and have been free of arrhythmia or side effects for 2 to 20 months (average 10.5). Encainide failed to prevent the clinical arrhythmia in 2 patients. In 4 patients with atrial arrhythmias, circus movement tachycardia developed during oral encainide therapy. In 1 patient the frequency of circus movement tachycardia increased with oral encainide treatment. Five of the previous 7 patients also suffered from central nervous system side effects, and in 1 patient serious central nervous system effects led to withdrawal of encainide. In conclusion, encainide has a marked effect on anterograde conduction and a minimal effect on retrograde conduction over the accessory AV pathway. Oral encainide was effective in controlling Supraventricular arrhythmia in 4 of 12 of this selected group of patients with accessory AV pathways. Failure to control the initial arrhythmia, facilitation of circus movement tachycardia and central nervous system side effects led to discontinuation of oral encainide in the other patients.     

Pacing and right atrial ventricular dissociation in auricular stimulation in reciprocal tachycardia using an accessory pathway

The effects of right atrial (RA) and coronary sinus (CS) stimulation have been studied in 13 patients with circus movement tachycardia (CMT). Tachycardia entrainment has occurred in all patients during RA pacing and in 11/13 during CS pacing, for a pacing rate 10 to 31 beats faster than the tachycardia rate. During RA pacing, short episodes of right atrial ventricular dissociation (6/13 patients) occurred but not during CS pacing. This can be explained by the anatomical proximity of the CS to the AV node (AVN) or by postulating two separate lateral inputs in the upper part of the AVN. Tachycardia entrainment is a criteria in favor of a reentry mechanism. It delineates a ranges of frequency between tachycardia rate and the slowest possible atrial stimulation rate capable of tachycardia termination which may be benefit for patients with drug resistant CMT, for whom antitachycardia pacemaker is envisaged.     

Subthreshold atrial pacing in patients with a left-sided accessory pathway: an effective new method for terminating reciprocating tachycardia

This study investigated the possibility of terminating reciprocating atrioventricular (AV) tachycardia using subthreshold atrial pacing. Ten patients with a left-sided accessory pathway and sustained AV tachycardia underwent subthreshold atrial pacing from the coronary sinus site closest to insertion of the accessory pathway. In seven of these patients, the tachycardia could be reliably terminated with subthreshold atrial overdrive pacing. When pacing at a cycle length of 80 +/- 23% of the tachycardia cycle length, the minimal subthreshold current that was effective in tachycardia termination was 64 +/- 14% of threshold current and the maximal ineffective current was 49 +/- 17% of threshold (p less than 0.05). In all cases, the tachycardia was terminated by one or two instances of atrial capture that resulted in a premature atrial impulse (20 +/- 4% advancement of the atrial cycle) that blocked the AV node limb of the tachycardia. Anterograde conduction over the accessory pathway never occurred, either during the tachycardia or during subthreshold pacing after a return to normal sinus rhythm. No instances of atrial fibrillation were provoked by subthreshold pacing. Possible explanations for the intermittent atrial capture with critically placed subthreshold impulses include supernormal atrial conduction or summation of impulses at the atrial insertion site of the accessory pathway. It is concluded that subthreshold pacing is effective in selected patients with AV tachycardia due to an accessory pathway. Furthermore, because neither atrial fibrillation nor anterograde conduction over the accessory pathway is seen with subthreshold pacing, this modality may hold significant promise for permanent antitachycardia pacing in these patients.     

Linking phenomenon during atrial stimulation with accessory pathways

Linking is an electrophysiologic phenomenon in which each successive impulse entering a macroreentry circuit propagates preferentially along 1 limb because of the functional impedance to conduction in the contralateral limb produced by the previous impulse. Electrophysiologic studies were performed in 12 patients with a bidirectionally conducting accessory pathway. Linking was analyzed while 1:1 atrioventricular conduction took place through the normal pathway. When atrial pacing (at the same cycle length) could be initiated during sinus rhythm in patients with rapidly conducting accessory pathways, linking was dynamically maintained by repetitive local refractoriness (interference). When it could be initiated during the usual type of orthodromic circus movement tachycardia, linking was sustained by actual impulse collision, the underlying mechanism having also been called entrainment. When it could be initiated during sinus rhythm in a patient with a slowly conducting accessory pathway, linking was maintained by impulse collision, but the underlying mechanism could not be called entrainment because stimulation had not been started during tachycardia. This study showed that 2 terms--linking and entrainment--may be applied to the same mechanism and, conversely, that the same name could not be used in reference to the same mechanism when pacing was initiated under different circumstances. However, using the proposed conceptual formulation for linking, it is apparent that seemingly diverse mechanisms associated with macroreentry circuits involving accessory pathways are, in fact, variations on a common electrophysiologic theme.     

Activation mapping of reentry around an anatomic barrier in the canine atrium. Observations during entrainment and termination

We determined total right atrial activation sequences during entrainment and termination of flutter induced in dogs with a surgically induced atrial lesion. This type of atrial flutter is due to circus movement of an impulse around the tricuspid valve orifice. We recorded simultaneously from 96 bipolar intracavity electrodes in the right atrium of the isolated, perfused heart. By constructing isochronal maps, we demonstrated the pattern of atrial activation during atrial pacing protocols that either entrained or entrained and then terminated the reentrant rhythm. We show that during pacing the antidromic wavefront from the paced impulse (An) collides with the orthodromic wavefront from the previous paced impulse (On-1). During entrainment, the site of collision of the orthodromic and antidromic wavefronts was constant during pacing at a fixed rate but shifted in the antidromic direction as the pacing rate increased. Furthermore, the last paced beat was entrained only up to the site of collision of the previous paced beat. During one period of entrainment, termination of the reentrant arrhythmia occurred because On-1 blocked in the reentrant pathway due to refractory tissue left by On-2. However, subsequent An did not collide directly with On as was expected, but rather On blocked by an interaction with tissue left refractory by An. Because On was blocked, no reentry occurred when pacing ended.     

Characteristics of entrainment during autodecremental atrial and ventricular stimulation

The entrainment characteristics of orthodromic circus movement tachycardias occurring during autodecremental atrial and ventricular stimulation were studied in 9 patients with manifest Wolff-Parkinson-White syndrome. The phenomenon occurred in 34 of 38 episodes of tachycardia during autodecremental atrial stimulation. It was not seen in 4 episodes because the first impulse penetrating the circuit terminated the arrhythmia. Invariably, the HH and VV intervals were not equal to, but longer than, the stimulus-stimulus intervals, thus not fulfilling the definition of "classic" (constant cycle length) entrainment postulated by Okumura et al. Furthermore, the first 2 of the 3 diagnostic criteria were not demonstrated and the third only could be demonstrated in 7 episodes. Tachycardia termination was achieved in all 38 episodes. Entrainment occurred during autodecremental ventricular stimulation in 79 of 80 episodes, with the AA and H-H- intervals (when visible) being equal to the corresponding paced cycle lengths. Moreover, the intervals between the last paced ventricular beat and the first ventricular beat of the resumed tachycardia were invariably longer than the last stimulus-stimulus intervals. These characteristics were those which Okumura et al attributed to "concealed" entrainment. Tachycardia termination was achieved in 77 of 80 episodes. In summary: (1) autodecremental atrial pacing produced a specific form of entrainment that did not fulfill the "classic" definition of Okumura et al; (2) autodecremental ventricular pacing consistently produced "concealed" entrainment; and (3) autodecremental stimulation was very effective in terminating 115 of 118 (98%) of episodes of circus movement tachycardias.     

Observations on the antidromic type of circus movement tachycardia in the Wolff-Parkinson-White syndrome

In the differential diagnosis of tachycardias showing a wide QRS complex and having a 1 to 1 relation between ventricular and atrial events, a supraventricular tachycardia with anterograde conduction over an accessory pathway and retrograde conduction by way of the specific conduction system must be considered. Five patients showing this type of circus movement tachycardia were studied by programmed electrical stimulation of the heart. Sudden changes in the tachycardia cycle length were observed in these patients that were based on changes in the VH interval. This finding suggested a change in the reentrant circuit with anterograde conduction over the accessory pathway but retrograde conduction sometimes occurring over the right bundle branch and at other times over one of the two divisions of the left bundle branch system. Characteristically, the tachycardia cycle length changed suddenly depending on the bundle branch used in retrograde direction. In one patient, an important difference was also observed between the anterograde effective refractory period of the accessory bypass (280 ms) and the shortest RR interval between preexcited QRS complexes during atrial fibrillation (measuring 190 ms). It is postulated that the short RR intervals during atrial fibrillation in the Wolff-Parkinson-White syndrome could result from bundle branch reentry after activation of the ventricles over the accessory pathway.     

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.     

Linking by collision initiated in the absence of preexisting reentrant tachycardia

Dynamic functional block in 1 limb of a reentrant circuit ("linking") can be maintained by either repetitive interference or collision of successive impulses entering the circuit. Occurrence of linking by collision during attempted overdrive pacing of reentrant tachycardias accounts for the entrainment phenomenon. To investigate whether linking by collision can be initiated in the absence of preexisting tachycardia, a human reentrant circuit model was studied. The model consisted of the atrioventricular node and His-Purkinje system as anterograde limb and an electronic stimulator that served as "retrograde limb" by initiating a paced atrial impulse at a predetermined ventriculoatrial interval following each sensed ventricular depolarization. In 3 patients with intact ventriculoatrial conduction, "reentrant tachycardia" was initiated by a ventricular extra-stimulus (V2), which retrogradely blocked bilaterally below the His bundle. When this same V2 was followed, instead, by a paced V2V2 train at a cycle length equal to the programmed ventriculoatrial interval of the "tachycardia," it could be shown that each beat of the train not only "traversed" the simulated "retrograde limb" but also retrogradely collided with a prior circulating impulse in the anterograde limb of the circuit, thereby constituting linking by collision at a supra-Hisian level with inability of even a single "reentrant cycle" to be completed; "tachycardia" became manifest only after termination of the V2V2 train. The findings suggest the existence of a unique mechanism for initiation of certain clinical reentrant tachycardias during incremental pacing.     

Initiation of atrioventricular nodal reentrant tachycardia in patients with discontinuous anterograde atrioventricular nodal conduction curves with and without documented supraventricular tachycardia: Observations on the role of a discontinuous retrograde conduction curve

To evaluate factors playing a role in initiation of atrioventricular (AV) nodal reentrant tachycardia utilizing anterogradely a slow and retrogradely a fast conducting AV nodal pathway, 38 patients having no accessory pathways and showing discontinuous anterograde AV nodal conduction curves during atrial stimulation were studied. Twenty-two patients (group A) underwent an electrophysiologic investigation because of recurrent paroxysmal supraventricular tachycardia (SVT) that had been electrocardiographically documented before the study. Sixteen patients (group B) underwent the study because of a history of palpitations (15 patients) or recurrent ventricular tachycardia (one patient); in none of them had SVT ever been electrocardiographically documented before the investigation. Twenty-one of the 22 patients of group A demonstrated continuous retrograde conduction curves during ventricular stimulation. In 20 tachycardia was initiated by either a single atrial premature beat (18 patients) or by two atrial premature beats. Fifteen of the 16 patients of group B had discontinuous retrograde conduction curves during ventricular stimulation, with a long refractory period of their retrograde fast pathway. Tachycardia was initiated by multiple atrial premature beats in one patient. Thirteen out of the remaining 15 patients received atropine. Thereafter tachycardia could be initiated in three patients by a single atrial premature beat, by two atrial premature beats in one patient, and by incremental atrial pacing in another patient. In the remaining eight patients tachycardia could not be initiated. Our observations indicate that the pattern of ventriculoatrial conduction found during ventricular stimulation is a marker for ease of initiation of AV nodal tachycardia in patients with discontinuous anterograde AV nodal conduction curves.     

Exposure of concealed right bundle branch block in Wolff-Parkinson-White type B by pacing from the vicinity of the A-V node.

In two infants with Wolff-Parkinson-White type B, right bundle branch block was concealed during sinus rhythm and pacing from close to the atrial entrance of the right-sided accessory pathway. However, pacing from the vicinity of the A-V node, the A-V node itself, and the His bundle exposed the right bundle branch block by producing exclusive ventricular activation through the normal, A-V nodal His-Purkinje pathway. In addition, pacing from close to the A-V node also resulted in fusion beats characterized by absence of delta waves with (pseudo) normal QRS complexes and short H-V intervals. False patterns of tachycardia-dependent and bradycardia-dependent block in the accessory pathway also occurred. These dynamic phenomena were attributed to the (peri-A-V nodal) pacing-related, relatively early arrival of excitation at the ventricles through the normal pathways coexisting with delayed arrival of excitation via the accessory pathway. The latter in turn was due to the longer intra-atrial conduction time from paced (peri-A-V nodal) site to atrial entrance of the accessory pathway.     

Verapamil effects in AV node reentry tachycardia with intermittent supra-Hisian AV block

The electrophysiologic details of two patients with atrioventricular (AV) node reentry tachycardia with intermittent 2:1 supra-Hisian block are presented. Both patients had clear evidence for atrial arrhythmias as well, emphasizing the need for a careful diagnostic analysis. Evidence supporting a diagnosis of AV node reentry tachycardia included: (1) short ventriculoatrial (VA) coupling intervals, (2) normal retrograde sequence of atrial activation, (3) dependence on critical AV node conduction times for initiation of tachycardia by atrial pacing, (4) ability to pace and capture the atria or ventricles without interrupting the tachycardia, and (5) fixed VA coupling intervals despite changes in tachycardia cycle length. Ten milligrams of verapamil was administered during sustained supraventricular tachycardia with 1:1 AV conduction, but despite prompt termination of tachycardia in both cases, 2:1 AV block was not induced. Atrial echoes could still be induced after verapamil, and diagnostic features (3) and (5) were particularly evident after the drug. Further analysis confirmed that verapamil did not have any observable effects on the likely site for supra-Hisian block—that is, the “final common pathway” of the AV node. This would support a contention that verapamil may have a selective effect on tissues within the confines of the AV node.     

Electrophysiologic mechanisms of orthodromic tachycardia initiation during ventricular pacing in the Wolff-Parkinson-White syndrome

Orthodromic tachycardia is the most common arrhythmia in patients with Wolff-Parkinson-White syndrome. It is often initiated during incremental ventricular pacing that requires the onset of retrograde block along the normal pathway (that is, atrioventricular [AV] node-His-Purkinje system) with concomitant retrograde atrial activation by way of the accessory pathway. However, the site of retrograde block, that is, the AV node versus the His-Purkinje system, during incremental ventricular pacing and, hence, the mechanism of orthodromic tachycardia initiation have not been systematically elucidated. The mechanisms of orthodromic tachycardia induction were studied in 17 patients with Wolff-Parkinson-White syndrome using a specially designed pacing protocol. A beat by beat analysis indicated that the retrograde His-Purkinje system block was the most common initiating mechanism of orthodromic tachycardia in 14 of the 17 cases. In two cases, AV node block preceded the onset of orthodromic tachycardia, whereas the data in the remaining case suggested that both mechanisms were operative but at different pacing cycle lengths. The orthodromic tachycardia induction with His-Purkinje system block occurred within the first two cycles in most cases. When orthodromic tachycardia initiation was delayed beyond the first two cycles of the ventricular train it represented either a 2:1 block in the His-Purkinje system; a linking phenomenon in the His-Purkinje system; or a block in the AV node. These data have methodologic, mechanistic and therapeutic implications for patients with the Wolff-Parkinson-White syndrome.     

Atrioventricular sequential pacing: differential effect on retrograde conduction related to level of impulse collision

Patients with DDD pacemakers who have intact retrograde conduction are known to be at risk of developing ventricular and "endless loop" tachycardia. To address this problem, a pacing protocol was designed in which V2A2 conduction was assessed in 16 patients during ventricular pacing alone (standard method) and during paced atrioventricular (AV) sequential drive (AV sequential method); the results were then compared. In eight of 16 patients who had intact retrograde conduction with both methods (group 1), the V2A2 intervals were significantly shorter (by 60 to 340 msec) with the AV sequential method. In the remaining eight patients, who demonstrated V2A2 block with the standard method, no V2A2 block occurred with the AV sequential method. In this study, two sets of AV intervals were programmed to produce collision of the two impulses (atrial and ventricular), either in the AV node or the His-Purkinje system (HPS). The site of V2A2 facilitation was related to the site of impulse collision. These results can be explained by earlier excitation by the atrial impulse (of AV node and/or HPS) during AV sequential pacing. However, in some cases it was evident that antegrade propagation of the atrial impulse was responsible for subsequent facilitation. The data suggest that assessment of retrograde conduction in candidates for DDD pacemakers can be made most accurately by the AV sequential method.     

Reliability of retrograde atrial activation patterns during ventricular pacing for localizing accessory pathways

Definitive localization of accessory pathways is based on atrial activation patterns during orthodromic supraventricular tachycardia when retrograde conduction occurs exclusively through the accessory pathway. In some patients, supraventricular tachycardia cannot be induced or is deleterious. To determine whether accessory pathway sites can be identified accurately during ventricular pacing, retrograde atrial activation was assessed during orthodromic supraventricular tachycardia and ventricular pacing at multiple cycle lengths in 41 patients with a single accessory pathway. To obviate retrograde fusion due to concomitant conduction through the normal atrioventricular (AV) conduction system that may obscure the location of the accessory pathway, the difference in conduction time from the site of earliest atrial activation to the His bundle atrial electrogram (delta A-SVT) was measured during orthodromic supraventricular tachycardia and compared with values observed during ventricular pacing (delta A-VP). Characteristic values for the delta A-SVT interval were identified for left lateral (66 +/- 17 ms), left posterior (50 +/- 8 ms), posteroseptal (33 +/- 7 ms), right free wall (22 +/- 15 ms) and anteroseptal (0 +/- 0 ms) accessory pathway sites. During ventricular pacing, the site with the earliest atrial electrogram was used to define the accessory pathway location only if the maximal value of the delta A-VP interval over the range of cycle lengths assessed was comparable with the value of the delta A-SVT interval characteristic of that region. Values of the delta A-SVT interval correlated closely with the maximal values of the delta A-VP interval (r = 0.91). With this approach, 40 (98%) of 41 accessory pathway sites were identified correctly during ventricular pacing.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of flecainide on electrophysiological properties of accessory pathways in the Wolff-Parkinson-White syndrome

The effect of flecainide in 12 patients with the Wolff-Parkinson-Whitesyndrome was analyzed with respect to the anterograde and retrogradeconduction properties of the accessory pathway, the modes ofinitiation and termination of circus movement tachycardias,and the ventricular response during induced atrial fibrillation.The principal effect of this drug was to depress both anterogradeand retrograde conduction of the accessory pathway. In 8/9 casescircus movement tachycardia was terminated by prolongation ofthe retrograde effective refractory period of the accessorypathway. Flecainide increased the shortest and the mean cyclelength during induced atrial fibrillation. It is concluded thatthe drug may be of potential benefit in patients with paroxysmalsupraventricular tachycardias in patients with the Wolff-Parkinson-Whitesyndrome.