Conductive Properties of the Reentrant Pathway of Ventricular Tachycardia During Entrainment From Outside and Within the Zone of Slow Conduction

Ventricular tachycardia (VT) was entrained with rapid ventricular pacing outside and within the zone of slow conduction (SCZ), and the conductive properties of the reentrant pathway were compared between the two pacing sites. Underlying heart diseases were old myocardial infarction (n = 2), postoperative tetralogy of Fallot (n = 1) or double outlet of the right ventricle (n = 1), dilated cardiomyopathy (n = 1), and pulmonary regurgitation of unknown cause (n = 1). Rapid pacing was continued for 5–10 seconds, and the time interval from paced stimulus to the entrained electrogram at the exit from SCZ (St-Ex) or to the QRS complex (St-QRS) was measured. Rapid pacing was performed at three or more cycle lengths after a decrement in steps of 10 msec. During rapid pacing outside of SCZ and entrainment of VT, constant fusion and progressive fusion were observed, and St-Ex and St-QRS showed the same response pattern: either a frequency dependent prolongation in 4 of 7 VTs or a constant time interval in the others VTs. When rapid pacing was attempted within SCZ, the response of the time intervals from paced site to the QRS (St-QRS) was the same as those observed during pacing outside SCZ except for one VT. In VT with repaired tetralogy of Fallot, the frequency dependent prolongation was observed during pacing from outside of SCZ but not within SCZ. Diseased myocardium extending widely into the outflow tract of the right ventricle may be responsible for the frequency dependent prolongation of St-Ex. In conclusion, the conductive property of the reentrant pathway might be assessed by observing the response patterns of St-Ex or St-QRS interval during transient entrainment of VT outside of SCZ, but exceptions may exist.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

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.     

Entrainment of Ventricular Tachycardia by Sinus Rhythm

Entrainment of ventricular tachycardia (VT) may be manifest as fixed and progressive QRS fusion with ventricular and, rarely, atrial pacing. Only a single example of spontaneous VT entrainment by another rhythm, rapid atrioventricular nodal tachycardia, has been reported. This article describes an example of fixed and progressive QRS fusion between conducted sinus rhythm and VT consistent with entrainment. In contrast to entrainment with pacing, entrainment of VT by sinus rhythm occurred with drug-mediated arrhythmia slowing and demonstrated progressive QRS fusion at a constant cycle length. However, it did not demonstrate unfused but entrained QRS complexes. The resulting short PR interval and wide QRS mimicked a preexcited rhythm.     

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.     

Ventricular Tachycardia in Healing Canine Myocardial Infarction: Evidence for Multiple Reentrant Mechanisms

Prior studies have demonstrated that unimorphic VT, sometimes due to epicardial reentry, can be induced in healing canine MI; however, the characterization of the types of reentry involved has differed among prior studies. The purpose of this study was to further characterize the spectrum of epicardial reentrant circuits during induced VT in experimental canine MI. Experimental MI was created by total occlusion of the LAD in dogs. Five days later, programmed stimulation was used to induce VT, which was mapped on the epicardium using a combination of vector and isochronol techniques. Pathological analysis was used to determine regions of transmural MI. Epicardial reentrant circuits were identified in eight dogs. The mean cycle length of induced VT was 212 ± 32 ms. In 3 of 8 experiments, a region of transmural MI was present, which formed at least a portion of a central zone of block around which reentrant impulses circulated. In five experiments, reentry was functional in nature, although the characteristics of the region of functional conduction block were variable. Long lines of functional block, short lines of block with slow conduction transverse to fiber orientation, and leading circle reentry were each observed in different experiments. Although a zone of slow conduction was identified in seven of the experiments, slow conduction transverse to fiber orientation appeared crucial in maintaining reentry in only three experiments. Multiple reentrant mechanisms of VT may be present in this single canine infarction model. Although a zone of slow conduction is usually present, the characteristics of the region of block are highly variable. However, epicardial reentry accounted for only a minority of induced arrhythmia episodes.     

Longitudinal Dissociation within the Reentry Pathway of Ventricular Tachycardia

SATULLO, G., ET AL.: Longitudinal Dissociation within the Reentry Pathway of Ventricular Tachycardia. Two cases of nonsustained, repetitive ventricular tachycardia are analyzed. In both, the episodes of tachycardia do not contain random numbers of beats, but the complexes in each phase of tachycardia are either always in even numbers (case 1) or always in odd numbers (case 2). This indicates longitudinal dissociation within the reentry circuit: i.e., there are two functionally separate pathways in some part of the reentry circuit, and the reciprocating impulse runs alternatively through the two pathways. Tachycardia ends due to block of the impulse always in the same pathway, thus, the number of beats in each episode of tachycardia is always either in odd or even numbers. (PACE, Vol. 13, December, Part 1 1990)     

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).     

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.     

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.     

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.     

Demonstration of Purkinje Potential During Idiopathic Left Ventricular Tachycardia: A Marker for Ablation Site by Transient Entrainment

A Marker for Ablation Site by Transient Entrainment. During VT of QRS morphology with right bundle branch block and left axis deviation in a patient without obvious structural heart disease, entrainment by pacing from the right ventricular outflow tract and high right atrium was demonstrated. During entrainment of VT, a Purkinje potential preceding the QRS and recorded at the left ventricular midseptum was activated by orthodromic impulses in the reentry circuit. The interval between the Purkinje potential and the earliest left ventricular activation was decrementally prolonged with shortening of pacing cycle length. Radiofrequency energy was applied to this site, resulting in successful elimination of VT. Therefore, the Purkinje potential represented activation by an orthodromic wavefront in the reentry circuit, while the orthodromically distal site to this potential showed an area of slow conduction with decremental property.     

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.