Conductive Property of the Zone of Slow Conduction of Reentrant Ventricular Tachycardia and Its Relation to Pacing Induced Terminability

In order to assess the functional characteristics of the zone of slow conduction of reentrunt VT, rapid pacing was performed to entrain VT. The orthodromic conduction time was measured as the interval between the stimulus and the orthodromically captured electrogram recorded distal to the zone of slow conduction, hut not precisely at the exit point, and its response to rapid pacing was evaluated. In 32 of 33 consecutive patients, rapid pacing was performed to entrain VT. Of these, rapid pacing was repeated in 28 patients at 3–10 cycle lengths in steps of 10 msec before VT was terminated, or rapid pacing produced an acceleration of the rate. A pacing induced prolongation of the orthodromic conduction time (slowed conduction) was observed in 16 (57.1%) patients and in another 12 (42.9%) patients, the conduction time was constant. The pacing induced termination was observed in 93.8% of VT with slowed conduction and in 50% of VT with constant conduction, and the difference was significant (P < 0.05). There was no difference in the cycle length of VT or the shortest paced cycle length between VT with and without slowed conduction. The zone of slow conduction in human VT showed different conductive properties and VT with slowed conduction was associated with an easier and safer terminability with rapid pacing. The fact might be useful in selecting patients for antitachycardia pacing.     

Frequency Dependent Shortening of Conduction Time through the Reentrant Pathway during Transient Entrainment of Ventricular Tachycardia

In a patient with nonischemic ventricular tachycardia (VT), VT was entrained and the conduction time from the pacing site to the entrained local electrogram showed a rate dependent shortening and its degree affected by the pacing site. The QRS complex, which was entrained by the last pacing stimulus, was constant and identical to that of VT and no rate dependent facilitated conduction was observed when the heart was paced at similar paced cycle lengths during sinus rhythm. As the mechanism of the shortening of the conduction time through the reentrant circuit, a shift of the entrance seems most likely.     

Identification of the Slow Conduction Zone in Idiopathic Left Ventricular Tachycardia

The mechanism of verapamil sensitive idiopathic left ventricular tachycardia (ILVT) is considered to be reentry. However, the nature of the reentry circuit, including the location of the slow conduction zone, is unclear. We sought the local electrical activity that would reflect slow conduction by precise mapping around the tachycardia exit (TE) in nine patients with ILVT (mean age, 28 ± 10 years) undergoing radiofrequency catheter ablation (RFCA). The TE was defined as the earliest discrete spiky potential (SP) recorded during the tachycardia, or as a complete configuration-matched pacemap 12-lead electrocardiogram (ECG). In all patients, the TE was located at the mid or inferior distal portion of the septum. The SP at the TE preceded the surface QRS by 20 ± 9 ms. The pacemap score at the TE was 11.4 ± 0.6 points. In three patients, fractionated potentials (FP) were recorded during the tachycardia. The onset of the FP preceded the surface QRS by 47 ± 8 ms and was earlier than the SP at the TE (P < 0.01). The sites where an FP was detectable were restricted to a small area, and were at a distance of 14 ±4 mm from the TE. The direction of the FP site from the TE was more basal in two patients and inferior in one, Pacemap ECGs at the sites with an FP showed poor matching (9 ± 1 points), presumably because of predominant capture of the local ventricular muscle rather than an electrically isolated reentry circuit. Successful RFCA was achieved at the site of the FP in all three patients in which one was recorded, and at the TE in the other six patients. The FP, which has been shown to reflect the slow conduction of the ventricular tachycardia circuit in structural heart disease, was also detected in ILVT in the present study, and it is likely to reflect electrical excitation of the distal rim of the slow conduction zone.     

Procainamide Induced Change of the Width of the Zone of Entrainment and its Relation to the Inducibility of Reentrant Ventricular Tachycardia

Procainamide depresses conduction velocity and prolongs refractoriness in myocardium responsible for reentrant VT, but the mechanism by which the induction of VT is suppressed after procainamide administration remains to be determined. In the present study, the relationship between electrophysiological parameters and the noninducibility of VT was assessed during procainamide therapy with a special reference to the change of an excitable gap. Clinically documented monomorphic sustained VT was induced in 30 patients and, utilizing the phenomenon of transient entrainment. the zone of entrainment was measured as the difference between the cycle length of VTand the longest paced cycle length interrupting VT (block cycle length) which was determined as the paced cycle length decreased in steps of 10 ms, and used as an index of the excitable gap. The effective refractory period was measured at the pacing site and the paced QBS duration was used as an index of the global conduction time in the ventricle. The cycle length of VT, the block cycle length, and the width of the zone of entrainment were determined and compared between the responders and nonresponders. In 15 patients, these parameters were determined at the intermediate dose and related to subsequent noninducibility at the final dose. At the final doses of procainamide, VT was suppressed in 8 (26.7%) of 30 patients. However, the cycle length of VT, the block cycle length, and the width of the zone of entrainment were unable to predict the drug efficacy, i.e., noninducibility. The change in the effective refractory period at the pacing site or the width of the paced QRS duration was not different between the responders and nonresponders. Among the variables, only the width of the zone of entrainment showed a significant narrowing in the responders at the intermediate dose of procainamide, and it was smaller than that of the nonresponders. The significant narrowing of the width of the zone of entrainment was associated with the subsequent noninducibility of VT at the final dose. The present study showed that the baseline cycle length of VT, the block cycle length, the drug induced change of the effective refractory period, or the paced QRS duration was not a predictor of the noninducibility after procainamide administration. However, a significant narrowing of the width of the zone of entrainment at the intermediate dose was associated with the noninducibility of VT at the final dose.     

Demonstration of Entrainment and Presence of Slow Conduction During Ventricular Tachycardia in Arrhythmogenic Right Ventricular Dysplasia

During VT in two cases with arrhythmogenic right ventricular dysplasia, entrainment criteria, constant fusion beats except for the last entrainment beat, progressive fusion, and a localized conduction block associated with interruption of VT, were demon strated with rapid ventricular pacing performed during VT. Furthermore, a long conduction interval was present during entrainment from the pacing site to the earliest activation site during VT. indicating the presence of a slow conduction area. VT in these cases was, thus, due to reentry with an area of slow conduction within the circuit.     

Double Response of the Ventricle During Transient Entrainment in a Common Atrioventricular Nodal Reentrant Tachycardia

We report a patient with slow-fast atrioventricuiar (AV)nodal reentrant tachycardia, in which double ventricuJar response was demonstrated during rapid pacing at cycle length of 300 msec or less from the high right atrium. The determinants of double ventricular response during transient entrainment in the present case were: (1)a crucial conduction delay in the slow pathway; (2)the collision between the activation via the antegrade fast pathway (antidromically)of the last paced beat and the activation via the antegrade slow pathway (orthodromically)of the previous paced beat, instead of the unidirectional block in the slow pathway; and (3)the enhanced AV nodal conduction over the antegrade fast pathway.     

Radiofrequency Catheter Ablation of the Slow Reentrant Pathway of Sustained Ventricular Tachycardia

The article reports the cases of two patients with severe coronary artery disease and associated recurrent sustained ventricular tachycardia successfully treated with radiofrequency catheter ablation. In the first patient, two different types of ventricular tachycardia (one incessant) were eliminated. In all procedures, an area of slow conduction critical for tachycardia maintenance was localized by endocardial mapping techniques. Radiofrequency energy delivered to this area could permanently modify the anatomical substrate of the arrhythmia. After single follow-ups of 19, 14, and 13 months regarding the arrhythmic entities, the patients are well and free from spontaneous recurrences.     

Significance of Ventricular Pacing Site in Manifest Entrainment During Orthodromic Atrioventricular Reentrant Tachycardia with Left-Sided Accessory Pathway

We examined entrainment by ventricular pacing in six patients during orthodromic atrioventricular reentrant tachycardia (AVRT) utilizing a left-sided lateral accessory pathway. Constant fusion and progressive fusion were demonstrated in all patients by left ventricular pacing during tachycardia, but in none of the patients by right ventricular pacing. When left ventricular pacing was performed during AVRT, the antidromic wave front from the pacing impulse (n) collided with the orthodromic wave front of the previous pacing beat (n - 1) within the ventricle, therefore, constant fusion and progressive fusion were demonstrated in the surface electrocardiographic QRS complexes. On the other hand, when right ventricular pacing was performed during orthodromic AVRT, the antidromic wave front from the pacing impulse (n) collided with the orthodromic wave front of the previous paced beat (n - 1) within the normal atrioventricular pathway, and constant fusion and progressive fusion were therefore not demonstrated. These phenomena were explained by the relationship of the ventricular pacing site and the reentrant circuit. This study demonstrates the importance of the pacing site in manifest entrainment of orthodromic AVRT during ventricular pacing.     

Reentrant Ventricular Arrhythmias in the Late Myocardial Infarction Period: 14. Mechanisms of Resetting, Entrainment, Acceleration, or Termination of Reentrant Tachycardia by Programmed Electrical Stimulation

The mechanisms of resetting, entrainment, acceleration, or termination of reentrant ventricular tachycardia by programmed electrical stimulation were studied in the canine post-infarction model. In this model, reentrant circuits were localized in the epicardial layer overlying the infarction and were accessible to detailed mapping by multiplexer techniques. The reentrant circuit has a characteristic figure-eight configuration in the form of two circulating wavefronts around arcs of functional conduction block that coalesce into a slow common reentrant wavefront. Termination of reentrant tachycardia occurred when a stimulated wavefront arrived earlier to a strategically located area in the proximal portion of the zone of slow conduction, before refractoriness expired distally, resulting in conduction block. The three factors that determined if the stimulated wavefront could reach this zone in time for conduction block were: the cycle length of stimulation; the number of stimulated beats; and the site of stimulation. The most optimal situation for stimulated termination of reentry was a critically coupled single stimulus applied to the ischemic zone close to the proximal side of the zone of slow conduction that captured locally and conducted prematurely to the strategic zone for conduction block. When a single stimulated wavefront failed to terminate reentry, one or more subsequent wavefronts succeeded. However, the stimulated train had to be terminated following the beat that interrupted reentry. Otherwise, a subsequent stimulated beat could reinitiate the same reentrant circuit or induce a different circuit. The new circuit could have a shorter revolution time, resulting in tachycardia acceleration, and occasionally degeneration into ventricular fibrillation. Overdrive termination of reentry required both a critical cycle length of stimulation and a critical number of beats in a stimulated train. Otherwise, the stimulated train could establish a new balance of refractoriness and conduction velocity in the reentrant pathway. This could perpetuate the reentrant process at the shorter cycle length of the stimulated train and spontaneous reentry would resume on termination of the train (entrainment). The study provides better understanding of the mechanisms of action of programmed electrical stimulation on reentrant ventricular tachycardia.     

Entrainment Onset in a Pacemaker Model of Reentrant Ventricular Tachycardia: Insight into Localization of Critical Elements of a Reentrant Circuit

We investigated entrainment in a pacemaker model of reentrant ventricular tachycardia (VT) created in the intact dog heart using a VAT pacemaker with both electrodes on the ventricular epicardium. This produced an incessant wide QRS tachycardia originating from the pacing site with a cycle length equal to the conduction time between the sensing and pacing site plus the pacemaker AV delay. The conduction time between entrainment sites and the critical elements of the reentrant pathway (sensing and pacing sites) was determined by pacing at a comparable cycle length during sinus rhythm. Entrainment was achieved in 12 tachycardias with pacing at 1-4 sites at cycle lengths 10-100 msec shorter than tachycardia and confirmed by constant QRS fusion, progressive QRS fusion, and coupling of the first nonpaced QRS or intracardiac electrogram at the entraining cycle length. By least squares regression, the timing of entrainment onset (first reset of pacing or sensing site electrogram) measured by the prematurity of the local electrogram at the entraining site was highly correlated to the shortest conduction time between the entraining site and the circuit (F value of 84.7 and R = 0.752 [P less than 0.001]). Therefore, the timing of entrainment onset maybe useful in predicting the conduction time from the entraining site to critical elements of a reentrant circuit and may assist in localization of the reentrant pathway.     

Entrainment of Ventricular Tachycardia in Arrhythmogenic Right Ventricular Tachycardia

In two patients with arrhythrnogenic right ventricular dysplasia (ARVDJ, sustained ventricular tachycardia (VT) was induced by programmed stimulations during serial drug testings. One patient had five and the other had two VT morphologies, and the sites of origin were determined by endocardial catheter mappings. When overdrive pacing was performed, constant fusion in the QflS complex was observed in the two patients. Constant fusion of a different degree was also observed at different paced cycle lengths. Both patients had dilated right ventricles and wall-motion abnormality, and the diagnosis of ARVD was further confirmed by the specimen resected at the site of origin of VT. Therefore, VT in ARVD can be entrained and reentry is the most likely mechanism of such VT.     

Termination of Ventricular Tachycardia by Nonpropagated Local Depolarization: Further Observations on Entrainment of Ventricular Tachycardia from an Area of Slow Conduction

A 60-year-old woman with a large left ventricular apical aneurysm underwent preoperative catheter mapping of ventricular tachycardia. A zone of slow conduction with marked decremental conductive properties was identified between the left ventricular aneurysmal pouch and the right ventricular septum. Pacing from the right ventricular septum produced a QRS on the surface electrocardiogram of the same morphology as that of spontaneous ventricular tachycardia, while pacing from the left ventricular aneurysm caused tachycardia entrainment without fusion. Termination of ventricular tachycardia invariably occurred in association with an unpropagated left ventricular capture, followed by a change in ventricular activation to an opposite direction. This case provides a direct demonstration of reentrant ventricular tachycardia termination by orthodromic block in a zone of slow conduction.     

Radiofrequency Catheter Ablation of Accessory Pathways During Entrainment of AV Reentrant Tachycardia

Radiofrequency ablation of accessory pathways must sometimes be done during orthodromic atrioventricular reentrant tachycardia when manifest anterograde accessory pathway conduction is absent or retrograde fusion obscures accessory pathway location during ventricular pacing. Unfortunately, abrupt heart rate slowing upon radiofrequency induced termination of atrioventricular reentrant tachycardia often causes catheter dislodgment. We report our experience in circumventing this problem during radiofrequency ablation by using entrainment of atrioventricular reentrant tachycardia. The latter maintains retrograde activation pattern over the accessory pathway while preventing abrupt ventricular rate change. Eight patients (4 men and 4 women, mean age 37.3 ± 17.9) with eleven left-sided accessory pathways were included. Ablation during entrainment was used as the first approach in three patients with concealed accessory pathways and one patient with a bidirectional accessory pathway. In another four patients, ablation during entrainment was used after technical difficulties in ablating during tachycardia. Only 1–3 radiofrequency applications were required to eliminate the accessory pathway using the entrainment technique. The catheter remained stable when accessory pathway conduction was interrupted by radiofrequency current. In conclusion, entrainment of atrioventricular reentrant tachycardia during radiofrequency application is useful for maintaining catheter position for accessory pathway ablation during atrioventricular reentrant tachycardia.     

Pleomorphic Ventricular Tachycardia: Demonstration of Conduction Reversal Within the Reentry Circuit

A case is presented of a patient with incessant venfricular tacbycardia of left bundle branch block morphology. Endocardial mapping revealed the site of earliest activation during tachycardia to be the proximal right ventricular septum. Pacing at this site elicited the clinical tachycardia, whereas pacing at the proximal left ventricular septum induced a right bundle branch block morphology identical to that of a previously recorded spontaneous ventricuiar tachycardia. Electrophysiological evidence is given that both types of tachycardia originate from a single reentry circuit located in the proximal ventricular septum in which the reentrant wavefront may travel either orthodromically (during spontaneous tachycardia and right ventricular pacing) or antidromically (during left ventricular pacing).     

Transient Entrainment and Interruption of Ventricular Tachycardia

The effects on spontaneously occurring ventricular tachycardia of rapidly pacing the right ventricle at rates faster than the rate of the ventricular tachycardia were studied during 10 episodes in seven patients. In three episodes, ventricular pacing interrupted the ventricular tachycardia at the initial pacing rate (111%, 114%, and 119% of the ventricular tachycardia rate, respectively). In seven episodes, the initial pacing rate failed to interrupt the ventricular tachycardia. In six of those seven episodes, the ventricular tachycardia was transiently entrained to the faster pacing rates. In one of those seven episodes, transient entrainment of the ventricular tachycardia could not be distinguished from over-drive suppression. In all seven episodes, the tachycardia was later interrupted by pacing at more rapid rates. The successful pacing rate ranged from 111-141% (mean 125%) of the spontaneous ventricular tachycardia rate. It is concluded that when utilizing rapid ventricular pacing to interrupt ventricular tachycardia, a critical pacing rate may be required before interruption is achieved. Pacing at rates slower than the critical rate but faster than the spontaneous ventricular tachycardia rate may only transiently entrain the ventricular tachycardia to the pacing rate without interrupting it. During the period of transient entrainment, fusion QRS complexes are likely to be present.     

Shift of Atrial Reentrant Tachycardia with Transient Entrainment to an Uncommon and a Common Type of Atrial Flutter

Atrial reentrant tachycardia (ART) which demonstrated transient entrainment shifted to an uncommon type of atrial flutter (AF) with premature atrial stimulation, and then returned to ART spontaneously, Subsequently, this ART shifted to a common type of AF by rapid atrial pacing, which was further transformed into an uncommon type of AF and finally terminated by rapid atrial pacing. The mechanism of AF in clinical cases is still controversial, but in this case, AF, both uncommon and common types, is considered due to macro-reentry within the atria. To explain (he shift of ART to AF and mutual transformation between common and uncommon type of AF, we made a schematic figure of reentry loop within (he atria of ART and AF.     

Use of Transient Entrainment During Ventricular Tachycardia to Localize a Critical Area in the Reentry Circuit for Ablation

We have previously shown that demonstration of any of the criteria for transient entrainment is possible only when pacing is performed orthodromically proximal to the area of slow conduction in a reentrant circuit with an excitable gap. Pacing orthodromically distal to the area of slow conduction will not permit demonstration of the transient entrainment criteria (concealed entrainment). Additionally, the demonstration of one form of concealed entrainment, namely pacing during a ventricular tachycardia from a site which increases the tachycardia to the pacing rate but does not change the morphology of the QRS complexes, we suggest also identifies the area of slow conduction is a keystone for maintenance of the reentrant circuit, ablation of this area should be expected to provide effective therapy of the tachycardia. Thus, we propose that using the principles of transient entrainment, one should be able to localize a critical area of slow conduction in the reentrant circuit of Q ventricular tachycardia, ablate it effectively, and thereby successfully treat the ventricular tachycardia.     

Coincident Idiopathic Left Ventricular Tachycardia and Atrioventricular Nodal Reentrant Tachycardia: Control by Radiofrequency Catheter Ablation of the Slow Atrioventricular Nodal Pathway

A healthy 37-year-old male presented with a history of frequent palpitations and sustained wide QRS complex tachycardia with a right bundle branch block and left axis morphology. Serial electrophysiological studies revealed two inducible tachycardias, which were shown to represent atrioventricular nodal reentrant tachycardia and idiopathic left ventricular tachycardia. Transformation from one tachycardia to the other occurred spontaneously as well as following atrial or ventricular pacing. Radiofrequency catheter ablation of the slow atrioventricular nodal pathway resulted in cure of atrioventricular nodal reentrant tachycardia and the prevention of spontaneous recurrence of ventricular tachycardia, suggesting a role of atrioventricular nodal reentrant tachycardia in triggering the clinical episodes of ventricular tachycardia. The patient has remained asymptomatic without antiarrhythmic therapy for 8 months.     

Electrophysiological Characteristics During Slow Pathway Ablation of Posterior Atrio ventricular Junctional Reentrant Tachycardia

The purpose of this study was to compare the electrophysiological characteristics of posterior and anterior atrioventricular junctional reentrant tachycardia (AVJRT) during radiofrequency (RF) catheter ablation of a slow pathway. Twenty-four patients with common A VJRT, including 4 posterior (P) and 20 anterior AVJRT (A) were studied. We analyzed the retrograde atrial activation sequence of junctional rhythm and the presence of transient HA block during slow pathway ablation. When HA block developed, the AH interval before ablation and immediately after the end of energy delivery was measured. Successful ablation sites were divided into three groups; high (H), middle (M), and low (L) from the His bundle to the floor of the coronary sinus orifice. The results were: (1) the number of successful ablation sites were H 0, M 1, L 3 in P and H 1, M 8, L 11 in A; (2) the HA interval during AVJRT in P was longer than that in A (109 ± 48 ms vs 43 ± 6 ms, P < 0.01); (3) the retrograde atrial activation sequence during Junctional rhythm was strictly concordant with that during AVJRT in both groups, but HA block developed during slow pathway ablation more often in P than in A (100% vs 30%, P < 0.01); and (4) The AH interval did not lengthen after HA block developed in P. These data suggest that another pathway does exist from the A V node to the atrium in addition to anterograde fast pathway and slow pathway, and that this pathway is used as the retrograde limb of P.