Observations on Induction and Termination of Paroxysmal Supraventricular Tachycardia by External Pacing

Paroxysmal Supraventricular tachycardia (PSVT) can be reproducibly induced and terminated by critically timed atrial or ventricular depolarizations. In this study, noninvasive trans-cutaneous (external) cardiac pacing (NTCPJ was compared to endocardial ventricular pacing for the termination and induction of PSVT. In 24 patients, either atrioventricular (AV) nodal reentrant tachycardia or AV reciprocating tachycardia was reproducibly terminated with either critically timed ventricular depolarizations or overdrive ventricular pacing from an endocardial right ventricular site. There were 32 trials of NTCP attempts to interrupt PSVT in the 24 patients. External pacing was successful at terminating PSVT in 23 patients and in 30 of 32 (94%) trials. In 20 patients, there were 26 trials of external pacing attempts to induce PSVT. External pacing initiated PSVT in 21 of 26 trials (81%). The pacing sequences used to induce and terminate PSVT with external pacing were copied from the endocardial sequences. The external pacing threshold averaged 77 ± 22 mA but the current needed to terminate PSVT was about 1.5 greater than threshold at 117 ± 27 mA. Serial external pacing studies were performed in seven patients. The thresholds for external pacing were similar from trial to trial as were the mode of termination and induction between the endocardial and external methods. External pacing can terminate most AV reciprocating tachycardias and many AV nodal reentrant tachycardias. It appears promising as a means of inducing PSVT. However, the high stimulation amplitudes needed will prohibit wide acceptance of external pacing for induction and termination of PSVT.     

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.     

Treatment of Ventricular and Supraventricular Tachyarrhythmias by Transcutaneous Cardiac Pacing

The efficacy of noninvasive transcutaneous cardiac pacing (TCP) in the treatment of tachyarrhythmic events was tested in 24 patient: 14 with ventricular tachycardia, seven with supraventricular tachycardia and three with atrial flutter. Six (42.9%) ventricular tachycardias were interrupted: in two of the ten patients on whom underdrive pacing was attempted and in all four cases in which overdrive stimulation was possible. Five of the six supraventricular tachycardias utilizing an atrioventricular bypass tract were interrupted, while the TCP was unsuccessful on the only patient with atrioventricular nodal reentrant tachycardia. TCP failed to interrupt the arrhythmia in the three cases of atrial flutter. No clinically significant untoward effects (in particular tachycardia acceleration or ventricular fibrillation) were observed, except for a tolerable thumping sensation on the chest during pacing. In four patients, TCP effects on cardiac activation was evaluated by endocavitary recording: while the mean ventricular threshold was 70 mA, atrial capture was possible on only two patients at a current intensity of 140 and 150 mA. We consider our preliminary experience with TCP in the treatment of tachycardias encouraging. The technique was easily and rapidly usable and it was immediately successful in the majority of atrioventricular reentrant tachycardias and in a relevant percentage of ventricular tachycardias. In this latter setting TCP was mostly effective in the slower tachycardias where overdrive pacing was possible. A further experience with devices provided by higher pacing rates is warranted.     

Simultaneous AV Nodal Reentrant and Ventricular Tachycardias

Simultaneous AV nodal reentrant and ventricular tachycardias were observed during the course of an electrophysiological study in a 51-year-old patient who suffered from recurrent attacks of sustained ventricular tachycardia. Occurrence of simultaneous tachycardias was facilitated by the fact that both tachycardias had a similar cycle length. Ventricular tachycardia was most probably initiated by AV nodal tachycardia previously induced by atrial extrastimulation following the administration of atropine.     

Paroxysmal tachycardia in children and teenagers with normal sinus rhythm and without heart disease

The purpose of this study was to evaluate the value of esophageal programmed stimulation in children and teenagers with normal sinus rhythm ECG and normal noninvasive studies, having palpitations and syncope, and no documented tachycardias. Paroxysmal tachycardias are frequent in children and are often related to accessory connection. These tachycardias are sometimes difficult to prove. Transesophageal atrial pacing was performed at rest and during infusion of isoproterenol in 31 children or adolescents aged 9-19 years (16 +/- 3 years) with normal sinus rhythm ECG and suspected or documented episodes of paroxysmal tachycardia. Sustained tachycardia was induced in 27 patients, at rest in 13 patients, and after isoproterenol in 14 remaining patients. Atrioventricular nodal reentrant tachycardia was found as the main cause of paroxysmal tachycardia (22 cases). Six patients were followed by a vagal reaction and dizziness. These patients had spontaneous tachycardia with syncope. In three other patients, atrial fibrillation was also induced. Concealed accessory pathway reentrant tachycardia was identified in three patients. In two patients, a regular wide tachycardia with right bundle branch block morphology was induced; the diagnosis of verapamil-sensitive ventricular tachycardia was made in a second study by intracardiac study. In conclusion, atrioventricular nodal reentrant tachycardia was found as the main cause of symptoms in children with normal sinus rhythm ECG. Syncope is frequently associated and provoked by a vagal reaction. This diagnosis could be underestimated in adolescents frequently considered as hysterical because noninvasive studies are negative.     

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.     

The Clinical Use of External Noninvasive Pacing in the Termination of Sustained Ventricular Tachycardia

In order to evaluate the potential use of external cardiac pacing (EXP) in the clinical termination of sustained ventricular tachycardia (VT), we attempted VT terminations in seven patients. All had recurrent sustained monomorphic ventricular tachycardia (mean rate 145 beats/min), which had previously required cardioversion. During subsequent VT episodes, all seven underwent overdrive pacing with EXP at a pulse amplitude of 120 mA, and rates of 200 pulses/min. A total of 18 of 18 episodes of VT were successfully terminated by EXP alone. In one patient, the first attempt at EXP termination of one episode of VT resulted in an acceleration of the tachycardia, which was then terminated by EXP. All patients tolerated EXP well with minimal sedation. We conclude that EXP may be an effective clinical modality for the termination of sustained monomorphic ventricular tachycardia.     

Long-Term Antitachycardia Pacing Experience for Supraventricular Tachycardia

A pacemaker was used to control drug-resistant reentrant supraventricular tachycardia (SVT) in 40 patients. An antitachycardia pacemaker was implanted in 37 for SVT; in one for ventricular tachycardia that could also be used to terminate SVT; in one SVT could be terminated with an activity rate variable pacemaker; and in one a DDD pacemaker was used for prevention and termination of SVT. Twenty patients had AV nodal reentrant tachycardias, eight had tachycardias due to a concealed accessory pathway, eight had a Wolff-Parkinson-White syndrome, three had reentrant atrial tachycardias, and one had atrial flutter. Twenty-two patients were paced from the right atrium, five from the coronary sinus, ten from the right ventricle, and three had a DDD pacemaker. During a total follow-up period of 1,503 (mean 38) months an estimated 16,240 episodes of tachycardia were terminated promptly at home, 58 required several attempts, 57 episodes lasted longer than 30 minutes but did not require medical attention, and 11 required hospital admission. Hospital admission for SVT decreased from one per patient-month (in the 3 months before implantation) to 1 per 137 patient-months after implantation. Additional reentrant tachycardias occurred in 13 patients. Antiarrhythmic drug therapy in combination with a conservative antitachycardia pacing mode was required in four patients paced from the atrium to avoid pacing induced atrial fibrillation. Antiarrhythmic drug therapy was used in 42% of patients to help control SVT. Conclusions: (1) Drug-resistant SVTs can be safely and effectively managed on the long-term with antitachycardia pacemakers. (2) Rapid termination of SVT improved the quality-of-life significantly by avoiding prolonged episodes of tachycardia and repetitive hospital admissions.     

Electrical Termination of Tachyarrhythmias by Discrete Pulses

Reentrant tachycardias can often be terminated by discrete pacing stimuli that penetrate the reentrant circuit. The ability of discrete stimuli to terminate an arrhythmia depends on the timing of the stimulus, the distance from the site of reentry where the stimulus is applied, the electrophysiologic properties of the myocardium between the site of stimulation and the site of reentry, and the size of the reentrant circuit.
Modes of pacing used to terminate tachycardia have included single or multiple timed extrastimuli, overdrive pacing, burst pacing and competitive asynchronous (underdrive) pacing. Patient-triggered devices that deliver asynchronous pacing stimuli are routinely available. Newer devices have been developed that automatically sense the onset of tachycardia and respond with pacing stimuli. These devices have been highly effective in selected patients with supraventricular tachycardia. The seriousness of occasional pacing-induced acceleration of ventricular tachycardia or conversion to ventricular fibrillation has limited the application of these devices in patients with ventricular arrhythmias. Pre-implantations electrophysiologic studies are necessary to document arrhythmia mechanisms and to determine the feasibility of various pacing modalities in treating the tachycardia. The potential for complicating arrhythmias (atrial fibrillation/flutter or ventricular fibrillation) must also be tested.
Future devices designed for terminating tachycardias with discrete pulses should be capable of being programmed to respond with one or more of the various modalities available. These devices should automatically and reliably sense both tachycardia onset and termination, and should adjust their responses appropriately if initial stimulation sequences fail to terminate the arrhythmia.     

Rapid Ventricular Tachycardia Due to His-Purkinje Reentry

Two patients developed rapid His-Purkinje reentrant tachycardia during programmed ventricular stimulation for evaluation of recurrent ventricular tachycardia. In Patient 1, His-Purkinje reentry induced a morphologically distinct ventricular tachycardia which may have been a reentrant circuit operating independently for several cardiac cycles. His-Purkinje reentry was not inducible in Patient 2 until lidocaine was given. Following lidocaine administration, sustained His-Purkinje reentrant tachycardia was initiated by 2 premature ventricular stimuli. The tachycardia was rapid (240 beats per minute) and required cardioversion.     

Two Different Reentrant Circuits of Ventricular Tachycardia in a Patient with an Extensive Anterior Infarction: Evaluation Using Electrical Catheter Ablation Techniques

Two morphologically distinct sustained ventricular tachycardias were initiated by programmed stimulation during attempted catheter ablation in a patient with an old anterior myocardial infarction. Right bundle branch block configuration of ventricular tachycardia, which was identical to the spontaneously occurring tachycardia, was initiated and displayed fragmented mid-diastolic potential at the apicolateral left ventricular site. Evidence of a critical slow conduction area was observed during delivery of electrical stimuli to this area. Following a 150-joule electrical shock delivered to this area, right bundle branch block pattern of ventricular tachycardia was no longer inducible but a new sustained monomorphic ventricular tachycardia with left bundle branch block pattern was initiated. The mid-diastolic fragmented activity at the ablation site became electrical activation of bystander area that was not participating in the left bundle branch block type of the ventricular tachycardia circuit. The critical slow conduction area was identified at the apicoseptal left ventricular site that was separated more than 5 cm from the ablation site. We speculate that two morphologically distinct sustained monomorphic ventricular tachycardias may be due to two different reentrant circuits and not the different expression of the same circuit.     

Clinical Experience with a New Software-Based Antitachycardia Pacemaker for Recurrent Supraventricular and Ventricular Tachycardias

The Intermedics Intertach 262-12 tachycardia reversion pulse generator was implanted in 14 patients (six male, eight female, mean age at implantation 45 +/- 16 years) with recurrent symptomatic tachycardias. Six patients had atrioventricular (AV) nodal reentrant tachycardia, three patients had orthodromic tachycardia with Wolff-Parkinson-White syndrome, two had circus movement tachycardia via a concealed bypass tract, two had ventricular tachycardia, one patient had atrial flutter. Mean duration of symptoms before implantation was 8 +/- 4 years and mean number of antiarrhythmic drug trials was 3.5 +/- 1. The primary tachycardia response made consisted of autodecremental pacing in one patient, burst pacing in two patients, and adaptive scanning of the initial delay or burst cycle length in eleven patients. The secondary tachycardia response mode consisted of autodecremental pacing in four patients, burst pacing in three patients and burst scanning in four patients. Tachycardia response was automatic in all but one patient with ventricular tachycardia. During a follow-up period of 30.5 +/- 10.6 months, one patient with ventricular tachycardia died from a nonarrhythmic cause. Reinterventions were necessary due to electrode fracture in one patient and due to pacemaker software defect in another one. Two patients underwent surgical cure of their arrhythmia: one patient with atrial flutter and one patient with AV nodal reentry tachycardia, 24 months and 11 months postpacemaker implantation, respectively. Four patients required digitalis to prevent pacing induced atrial fibrillation. Other proarrhythmic effects were not encountered. The pacemaker proved to be a versatile system with reliable tachycardia detection and termination functions. It provided a valuable adjunctive therapy in these selected patients.     

A Case Report Demonstrating Spontaneous Change in Tachycardia Terminating Window

A patient who received a patient-activated pacemaker system for termination of paroxysmal, drug-resistant, ventricular tachycardia is described. During the pre-implant invasive electrophysiological (EP) study and the three post-implant non-invasive EP studies, tachycardias were easily and reproducibly terminated by two stimuli using the interval scanning mode. On the fourth day post-implant, this pacing mode no longer terminated tachycardia at rest. A new pacing mode using more stimuli was then found to terminate the tachycardia reproducibly under various physiological conditions. This case report demonstrated a spontaneous change in the tachycardia terminating window and the usefulness of versatility in antitachycardia pacemaker systems.     

Mechanisms for the Success and Failure of Pacing for Termination of Ventricular Tachycardia: Clinical and Hypothetical Considerations

The effectiveness of pacing techniques for termination of ventricular tachycardia is well established, and of great value in the elec-trophysiologic laboratory, and, to a more limited degree, for chronic therapy using implanted anti-tachycardia devices. Although it appears that most clinical ventricular tachycardias are due to reentrant mechanisms, responses to antitachycardia pacing have often been difficult to understand. In this paper, clinical observations are correlated with hypothetical constructs and considerations, in an attempt to derive some general principles related to the success and failure of pacing for ventricular tachycardia. In these analyses, it appears that properties of conductivity and refractoriness in the myocardium are as important as the properties of the tachycardia circuit. Programmed extrastimuli or rapid pacing result in shortening of the effective refractory period of the myocardium, together with depressed conduction velocity of the stimulated wavefront. However, the changes in wavefront conductivity do not occur in step with changes in the effective refractory period; as a result, the stimulated wavefront arrives at the tachycardia circuit in a pattern which differs from the stimulation pattern. In general, it appears that termination of the tachycardia is favored when the stimulated wavefront arrives at the tachycardia circuit at a point when it cannot enter the circuit in an antegrade direction. These conditions are favored by a refractory period in the circuit which is moderately long compared to that of the myocardium. Constructions explaining the observation of a tachycardia termination zone are presented, together with explanations for failure to achieve termination, and for various patterns of acceleration.     

Development of an Interactive Computer-Guided Method for Radiofrequency Catheter Ablation of Ventricular Tachycardia

The purpose of this study was to develop a simple computer-guided approach to localizing ventricular tachycardias during ventricular mapping. Six patients with sustained monomorphic ventricular tachycardia were connected to a 32-lead computer body surface mapping system. Isoarea maps of induced ventricular tachycardia were recorded. Then a pacing probe was placed in either the right or left ventricle, and maps were generated from a variety of sites. Differences between ventricular tachycardia and pace map maxima X,Y coordinates were utilized to guide catheter manipulation and localization. In 6 of 6 patients (100%) this method appeared to provide a systematic approach to ventricular tachycardia localization. Computer-generated correlations as well as the X,Y coordinates of the QRS isoarea maxima were used to determine proximity to the ventricular tachycardia foci and direct catheter manipulation. In the next three patients this method was applied prospectively to help guide catheter manipulation during ventricular tachycardia (two right ventricular outflow tract tachycardias, and one left ventricular tachycardia). After a mean of 4.0 ± 1.7 radiofrequency applications, ventricular tachycardia was no longer inducible, and at 7 ± 0 months follow-up there have been no arrhythmia recurrences. We conclude that online computerized body surface mapping can assist in localizing ventricular tachycardia. Differences in maxima during pace maps and in-situ ventricular tachycardias can help with catheter manipulation as well as with more precise identification of focal tachycardias. This technique appears to hold the promise of a simple computer-guided method that may facilitate radiofrequency catheter ablation.     

Cross-ventricular endless loop tachycardia during biventricular pacing

This report describes the development of an unusual pacemaker tachycardia in a patient with a conventional dual chamber pacemaker used for biventricular pacing in the VVIR mode. The atrial channel was connected to the left ventricle and the ventricular channel to the right ventricle. The tachycardia was sustained by sensing of the T wave by the "atrial channel" which triggered pacing by the "ventricular channel. " This "cross-ventricular" endless loop tachycardia is a reentrant pacemaker tachycardia like classic endless loop tachycardia and can be prevented by appropriate programming of the pacemaker.     

The Importance of Antitachycardia Pacing for Patients Presenting with Ventricular Tachycardia

The initial experience from electrophysiological studies showed that pacing induced termination of ventricular tachycardias is usually possible but requires a critical pacing sequence. Studies on the resetting phenomenon showed, in most instances of failure of termination, that the "limiting factor" to produce ventricular tachycardia termination is usually failure to produce block within the circuit rather than failure to access or interact with the ventricular tachycardia origin. The resetting response is related to tachycardia termination in a number of ways. Of note is that a steeply increasing resetting pattern usually predicts tachycardia termination. Between 50% and 90% of induced ventricular tachycardias will be terminated by trains of rapid ventricular pacing. The analysis of the pacing rate necessary for termination shows that it varies widely. Paced cycle lengths of < 80% of tachycardia cycle length are necessary in at least 20% of tachycardias. In contrast, the incidence of acceleration is closely related to the paced cycle length: it is negligible with paced cycle lengths over 80% of tachycardia cycle length and increases to 36% with paced cycle lengths below 76% of tachycardia cycle length. Present information about efficacy of antitachycardia pacing in spontaneous tachycardias suggests that it is extremely effective, with over 90% success. However, it is likely that these data correspond to a selected group of tachycardias.     

His Bundle Recordings in Double Tachycardias Not Due to Digitalis Intoxication

Electrophysiological studies were performed in a patient with chronic chagasic cardiomyopathy, recurrent sustained ventricular tachycardia, and a history (without electrocardiographic documentation) of paroxysmal atrial flutter. Ventriculoauricular conduction occurred during short bursts of ventricular pacing. Moreover, the retrograde P of ectopic ventricular beats which appeared after pacing was stopped precipitated an atrial tachyarrhythmia with an irregular atrial rate. In addition, burst ventricular pacing, performed while this atrial tachyarrhythmia was present, initiated and subsequently terminated a ventricular tachycardia with similar characteristics to the one occurring spontaneously. The double (atrial and ventricular) tachycardias described in this communication were different from those previously reported in that the arrhythmias were not due to digitalis toxicity, but resulted from the modality of ventricular stimulation performed in a patient who had the specific type of cardiomyopathy seen in the chronic stage of Chagas' disease.     

Diagnostic Value of Synchronized Transesophageal Atrial Pacing

Synchronized transesophageal atrial pacing (single and double extrastimuli) was used in 137 patients with various tachycardias inducible by atrial pacing during transesophageal electrophysiological study (EPS). This pacing mode in five patients initiated atrioventricular tachycardias with ipsilateral bundle branch block not seen when using other pacing modes. During the tachycardia, single or double extrastimuli caused ipsilateral bundle branch block disappearance in two patients with atrioventricular tachycardia, and changed AV activation ratio in one patient with atrioventricular junctional reentrant tachycardia. This pacing mode causes very little discomfort, what is important in children, and enhances diagnostic abilities of transesophageal EPS. So, this pacing mode should be used routinely as one of the steps of transesophageal EPS.     

Why Is Catheter Ablation Less Successful than Surgery for Treating Ventricular Tachycardia that Results from Coronary Artery Disease?

Nearly 80% of patients with coronary artery disease who have map-directed surgery for control of ventricular tachycardias require no drug therapy to prevent recurrences, while fewer than 50% of patients undergoing catheter ablation have similar outcomes. Catheter ablation will fail if arrbythmogenic sites are incompletely ablated by lesions that are too small or too far away from the reentrant pathway or if all arrbythmogenic sites are not identified. The underlying assumptions used to guide site selection are that: (a) ventricular tachycardias arise from reentrant mechanisms; (b) monomorphic ventricular tachycardias with similar QRS morphologies arise from the same pathway; (c) the ventricular tachycardia initiated during the procedure represents the patient's spontaneous arrhythmia; (d) the endocardial site that should be ablated can be identified from cardiac activation maps produced during induced ventricular tachycardia or from ancillary techniques; and (e) the patient has only one or two reentrant pathways. Relying on incorrect assumptions may account for the difference in success rates. Patients may have similar appearing ventricular tachycardias that arise from different pathways, and the entire thin layer of viable tissue between the infarct and the endocardium may contain many reentrant pathways. Some ventricular tachycardias may arise from the myocardium away from the endocardium, while others may arise from the epicardium. Small lesions may not be large enough to eliminate all possible reentrant pathways. Catheter ablation may be less successful because the lesions are inadequate, the assumptions guiding the selection of arrhythmogenic tissue are incorrect, or all arrhythmogenic sites are not identified. The primary reason catheter ablation is less successful than surgery in the treatment of ventricular tachycardias is that catheter ablation does not ablate as much tissue as is removed by surgery. The success rate of catheter ablation probably can be improved if the amount of tissue ablated is increased.