Device Interaction—Antitachycardia Pacemakers and Defibrillators for Sustained Ventricular Tachycardia

We evaluated the combined use of permanent automatic antitachycardia pacemakers and implanted defibrillators in fen patients with recurrent monomorphic sustained ventricular tachycardia (VT). Pacemaker programming was VVI-T automatic burst in eight patients, VVI-T magnet mode in one patient, and VVI in one patient. Device interactions occurred in four patients, requiring changes in pacemaker programming. These included defibrillator multiple counting during pacing, in-appropriate pacemaker bursts initiating VT, inappropriate reset of the pacemaker antitachycardia mode by defibrillation, defibrillator discharge after pacemaker VT termination, and defibrillator VT reinitiation. Two patients required pacemaker programming out of the antitachycardia mode, and two required a change in antitachycardia pacing parameters. Seven patients remain in automatic VVI-T and three in VVI modes. Mean follow-up is 13 months and all patients are alive. Thus, although pacemaker/ defibrillafor combinations function well for patients with more than one VT rate, device interactions occur frequently and may require pacemaker reprogramming or elimination of the overdrive mode. Combined use of these devices should be cautiously considered when single device therapy is unsatisfactory. Devices that combine both pacing and defibrillation features may reduce adverse interaction.     

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.     

Long-Term Therapy of Antitachycardia Pacing for Supraventricular Tachycardia

Long-term antitachycardia pacing therapy with the InterTach 262-12 and 262-16 was evaluated in 32 consecutive patients (mean age 50 +/- 13 years) with recurrent, drug refractory supraventricular tachycardia. AV nodal reentrant tachycardia was present in 20 patients, Wolff-Parkinson-White syndrome in ten patients, and a reentrant tachycardia due to Mahaim fibers in one patient. During follow-up of 39 +/- 17 months, 250 persistent tachycardia episodes occurred in 22 patients. By adjusting detection and termination mode, recurrent supraventricular tachycardia could be controlled in 19 of 32 patients (60%) by antitachycardia pacing alone. Concomitant antiarrhythmic drug therapy was required in ten of 32 patients (30%). During follow-up antitachycardia pacing became ineffective in three patients (10%). Thus, chronic antitachycardia pacing proved to be safe and effective in selected patients with drug refractory supraventricular tachycardia and could significantly improve quality of life by rapid termination of recurrent supraventricular tachycardia episodes.     

The Relationship between Pacing Site and Induction or Termination of Sustained Monomorphic Ventricular Tachycardia by Antitachycardia Pacing

Background: With the development of left ventricular pacing for cardiac resynchronization, there is an interest in the possibility of improving ventricular antitachycardia pacing (ATP) efficacy by pacing from the LV electrode(s).
Objective: This study assessed the efficacy of pacing delivered from the left coronary vein (LCV) compared to that delivered from the right ventricular apex (RVA) upon ventricular tachycardia (VT) induction and termination.
Methods: Sixty patients undergoing provocative ventricular electrophysiology (EP) studies in three centers were enrolled. Multipolar EP catheters were placed in the atrium, the RVA, and LCV. VT induction was attempted from the RVA and LCV in random order. Upon detection of monomorphic VT, burst ATP for up to 10 pulses at 88% VT cycle length was delivered from the RVA or LCV, in a random order, and crossed over when possible. Identical VT morphologies were reinduced to allow paired comparison of RVA versus LCV ATP.
Results: Data from 55 patients were analyzed. Thirty-four morphologically distinct monomorphic VT types were induced in 22 patients. ATP succeeded in 18 (55%) and VTs in 13 patients. RVA ATP terminated 15 of 23 (65%) VTs, and LCV ATP terminated 10 of 23 (43%) VTs (P = 0.14). ATP delivered ipsilateral to the earliest activation site required 5.0 ± 2.6 pulses to terminate compared to 4.8 ± 1.7 pulses when delivered from the contralateral site (P = 0.90). Paired comparison was possible for 13 VT morphologies in 11 patients. Paired RVA and LCV ATP efficacy was identical (54 % vs 54%, P = 1.0).
Conclusion: ATP delivered from a LCV lead offers no efficacy advantage over pacing from the RVA. (PACE 2010; 27–32)     

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.     

Permanent Antitachycardia Pacemaker Therapy for Ventricular Tachycardia

This article describes our experience with an antitachycardia pacemaker alone (N = 3) or in combination with an automatic implontoble cardioverter defibrillator (AICD, N = 8) in the treatment of ventricular tochycardia. EJeven patients (mean ejection fraction 31%, mean oge 67 years) received an antitachycardia pacemaker. Nine had their units programmed for automatic antitachycardia pacing, one unit was programmed to automatic antitachycardia pacing by magnet activation only, and one to tachycardia detection and bradycardia support. Of the nine patients with automatic antitachycardia pacing, seven received appropriate and successful pace termination of spontaneous ventricular tachycardia at up to 120 times per month. Eight of these nine have had AICD implantations as well. There were no operative complications. Over a mean (± SD) follow-up of 12.1 ± 9.3 months (range 3–29 months), there have been two deaths, both due to heart failure. There have been four AICD discharges in three patients. Two units discharged in a clinically appropriate setting. The other two units, both with rate cutoffs <200 beats/min, were inadvertently triggered by the antitachycardia pacemaker and/or the underlying rate. In addition to the careful selection of the defibrillator rate cutoff, adverse device-device interactions were avoided by careful intraoperative lead positioning, and the disabling of bradycardia pacing when not needed or contraindicated. Antitachycardia pacing, with the safety provided by the AICD, is an effective treatment for patients with medically refractory ventricular tachycardia.     

Termination Of Sustained Tachycardia By External Noninvasive Pacing

Invasive cardiac pacing has proved useful in the induction and termination of reentrant sustained tachycardias. In one of our two cases, programmed ventricular extra-stimulation was used to induce sustained ventricular tachycardia from the endocardial surface of the right ventricle. Induced ventricular tachycardia was terminated by burst ventricular pacing with an external cardiac pacemaker. In our second patient, external pacing was effective at inducing and terminating sustained supraventricular tachycardia. These patients illustrate that the principles of terminating sustained reentrant tachycardia with invasive pacing may also apply to noninvasive external pacing. The usefulness of this approach in treating reentrant tachycardias needs further evaluation.     

Ventricular Pacing Induced Ventricular Tachycardia in Patients with Implantable Cardioverter Defibrillators

Appropriately timed noncompetitive ventricular pacing potentially may initiate ventricular tachycardia in patients prone to these arrhythmias. The combination of bradycardia pacing and stored electrograms in a currently available cardioverter defibrillator provides an opportunity to evaluate the occurrence of such pacing induced ventricular tachycardia. During a surveillance period of 18.7 ± 11.4 months, stored electrograms documented 302 episodes of ventricular tachycardia in 77 patients. Five patients (6.5%) demonstrated 25 episodes (1–16 per patient) of ventricular tachycardia that were immediately preceded by an appropriately paced ventricular beat (8.3% of all episodes of ventricular tachycardia). All five patients had prior myocardial infarctions and a history of monomorphic ventricular tachycardia occurring both spontaneously and in response to programmed electrical stimulation. Antitachycardia pacing terminated pacing induced ventricular tachycardia in 22 episodes; in one episode antitachycardia pacing accelerated ventricular tachycardia. In two cases shock therapy was aborted for nonsustained ventricular tachycardia. We conclude that, in selected postinfarction patients with recurrent sustained monomorphic ventricular tachycardia treated with implantable cardioverter defibrillators, appropriately timed ventricular pacing may induce ventricular tachycardia.     

Long-Term Management of Ventricular Tachycardia by Implantable Automatic Burst Tachycardia-Terminating Pacemakers

This report describes the Jong-term follow-up of two patients who received implantable automatic burst tachycardia-terminating ventricular pacemakers for the treatment of drug-refractory sustained ventricular tachycardia. After implantation, both pulse generators continued to terminate ventricular tachycardia without any major complications. In one patient, after three years, many episodes of ventricular tachycardia were slower than the tachycardia-detection criterion rate of 137 per minute; ventricular tachycardia was then terminated by chest wall stimulation that activated the burst function of the pacemaker. In this particular patient, the pulse generator was removed after four and one-half years and replaced with a DDD system because of the pacemaker syndrome and attacks of ventricular tachycardia, often at a rate of about 100/minute. In the second patient, the pacemaker continued to terminate ventricular tachycardia for over five and one-half years as determined by the repeated activation of the flag (memory) function of the pacemaker indicating detection of tachycardia by the pulse generator and resultant delivery of burst pacing.     

Recurrent Ventricular Tachycardia Induced by an Atrial Synchronous Ventricular-Inhibited Pacemaker

Atrial synchronous pacemakers have been known to cause a variety of cardiac arrhythmias. Of particular concern are those arrhythmias invoiv ing a pacemaker stimuius occurring on a T wave, because these may lead to ventricuiar tachycardia. The Medtronic 2409 ASVIP pacemaker is an atrial synchronous pacemaker with several features de signed to decrease the likelihood of such arrhythmias. We report a patient in whom a normally func tioning Medtronic 2409 ASVIP pacemaker, despite these features, induced recurrent ventricular tachycardia. Conditions which predisposed this patient to pacemaker-induced re-entrant arrhythmias are discussed. [PACE, Vol. 5, July-August, 1982]     

Pacing for Ventricular Tachycardia

Plusieurs problèmes restent à résoudre avant que les stimulateurs puissent jouer un rôle majeur dans le traitement de la tachycardie ventriculaire. Nous citons des exemples pour illustrer quelques difficultés à résoudre. les mécanismes qui contribuent au succès ou à l'échec de la stimulation antitachycardie sont discutés. L'avenir de cette stimulation sera plus assuré dès que ces appareils serent équipés d'un cardioverteur-défibrillateur de secours.     

Recurrent Ventricular Tachycardia Responsive to Verapamil

We describe five young patients with recurrent ventricular tachycardia in the absence of organic heart disease. In all patients tachycardia could be terminated or prevented with verapamil. Tachycardia in four patients was very similar, with a QRS pattern of right bundle branch block and left axis deviation. Electrophysiology studies in two patients showed that VT was inducible in one patient (rapid atrial or ventricular pacing, ventricular extrastimuli) but not in the other. The clinical and electrocardiographic similarities in these patients suggest that their ventricular tachycardias may share a common pathophysiology and may be dependent on slow channel activity.     

Bedside Termination of Sustained Ventricular Tachycardia by Transesophageal Atrial Pacing

Transesophageal atrial pacing was used to terminate hemodynamically stable sustained monomorphic ventricular tachycardia in two patients. The procedure was performed at the bedside, no anesthesia was required, there were no complications, and one of the patients went home after the procedure was performed. This method should be considered prior to using direct current cardioversion in patients with hemodynamically stable sustained monomorphic ventricular tachycardia.     

''Long-Term Results of Antitachycardia Pacing in Patients with Supraventricular Tachycardia

Between 1979 and 1984 the Cybertach-60, (Intermedics, Inc. Model 262-01), a programmable, automatic antitachycardia pacemaker was implanted in 11 patients who had drug-refractory supraventricular tachycardia (SVT). The patients have been followed for a total of 64-108 (mean 84 months). All patients were symptomatic and had failed two or more drugs and six patients had required prior DC cardioversion. The mechanism of supraventricular tachycardia was atrioventricular (AV) nodal reentry in six patients, AV reentry in four patients, and atrial tachycardia in one patient. Preoperatively all patients had reliable termination of the tachycardia without induction of atrial fibrillation by pacing methods available to Cybertach-60. Postimplant, Cybertach-60 reliably terminated all episodes of tachycardia without ancillary drug therapy. Nevertheless, at long-term follow-up antitachycardia pacing was effective and safe in the minority (36%), with only four patients out of eleven still using a pacemaker for supraventricular tachycardia. One of these four patients required additional drug therapy. In one of the patients, the Cybertach-60 was replaced after 78 months by a more advanced device, (Intertach, Intermedics, Inc.) because of a depleted Cybertach-60 battery. In seven patients who no longer use antitachycardia pacing for termination of tachycardia, one patient developed atrial fibrillation during tachycardia termination (at 58 months postimplant). Three patients experienced induction of tachycardia or atrial fibrillation by the pacemaker due to undersensing of sinus P waves (at 36, 48, and 51 months).(ABSTRACT TRUNCATED AT 250 WORDS)     

Resetting of Tachycardia Cycle by Single and Double Ventricular Extrastimuli in Recurrent Sustained Ventricular Tachycardia

In two cases with recurrent sustained ventricular tachycardia (VT) due to re-entry, the response pattern to extrastimuli during the tachycardia was studied. In each case, right ventricular extrastimuli with longer coupling intervals during VT were followed by fully compensatory pauses and with shorter coupling intervals reset the tachycardia cycle. In one case, a plateau was produced by a single extrastimulus, resembling that seen in the response curve of sinus node automaticity as well as ectopic atrial tachycardia. Two successive stimuli produced three definite zones, i.e., fully compensatory, reset producing a plateau, and progressive prolongation zones with shortening of the coupling intervals between the two stimuli, and terminated the tachycardia with further shortening of the coupling intervals. In conclusion, resetting phenomenon was confirmed on two cases with re-entrant VT. This phenomenon cannot be used as a criterion to determine the mechanism responsible for VT.     

Comparative Effectiveness of Pacing Techniques for Termination of Well-Tolerated Sustained Ventricular Tachycardia

Ventricular tachycardias can be terminated by a variety of pacemaker techniques, including rapid and slow stimulation. Fast tachycardias are typically poorly tolerated, and require prompt intervention, usually with rapid pacing. Termination of ventricular tachycardia by slow or single capture pacemaker stimulation techniques is attractive, because of its presumed safety and the possibility of using simple implantable pacers. To identify factors favoring termination, single capture stimulation was used in 390 episodes of ventricular tachycardia in 21 patients, 16 with coronary artery disease, able to tolerate ventricular tachycardia forseveral minutes. Single capture stimulation terminated 223 episodes (57%) in 18 patients, and two were accelerated. Of 157 episodes exposed to 2–3 programmed extrastimuli or rapid pacing 149 (94%) were terminated and 7 were accelerated. Direct current cardioversion was needed in 12 episodes. Without medications, only two patients tolerated VT. Only one patient had reliable termination with single capture stimulation over several days. Systolic blood pressure was similar in episodes terminated and not terminated by single capture stimulation, but the ventricular rate was significantly lower in episodes terminated, 116 ± 19 vs. 133 ±24 (p<0.001). Termination of ventricular tachycardia was not affected by QRS morphology. Single capture termination of ventricular tachycardia is largely unpredictable, with limited reproducibility over a period of time. Although comparatively safe, single capture techniques are not likely toprove useful in the long-term treatment of many patients with recurrent ventricular tachycardia.     

Idiopathic Recurrent Parasystolic Ventricular Tachycardia in a Child

An asymptomatic 3¹/₂-year-old boy demonstrated parasystolic ventricular tachycardia with AV dis-sociation, early sinus capture beats, marked variability in coupling intervals between conducted and ectopic beats, fusion beats, and interectopic intervals which were multiples of the ectopic cycle length. The arrhythmia initially responded to quinidine, reappeared over an 11-month observation period, and finally was suppressed at a high quinidine dose. An invasive and noninvasive work-up failed to demonstrate organic heart disease.     

Maximal Rate of Tachycardia Development: Sinus Tachycardia with Sudden Exercise vs. Spontaneous Ventricular Tachycardia

In addition to providing basic physiologic information, knowledge of the maximal rate of sinus tachycardia development may be helpful in developing algorithms permitting new generations of antitachycardia pacemakers to distinguish accurately between sinus and ventricular tachycardia. To determine the maximal rate of sinus tachycardia development, 50 normal subjects rushed up 100 stairs as rapidly as possible, with continuous electrocardiographic monitoring. During the first second of exercise, the mean cardiac cycle length shortened from 709 to 570 ms, equivalent to an increase in heart rate from 85 to 105 beats per minute, or 20 beats per minute per second. Thereafter, a more gradual decrease in cycle length occurred. Differences between men and women, smokers and non-smokers, and sedentary compared to active subjects were all insignificant. Analysis of 50 spontaneous episodes of ventricular tachycardia also revealed a sequential but more abrupt decrease in the cycle length during the first second from 757 to 360 ms, equivalent to a rate increase from 79 to 167 beats per minute, or 88 beats per minute per second. After approximately 1 ¹/₄ seconds, the ventricular tachycardia cycle length remained virtually constant. Baseline cycle lengths were similar in the sinus and ventricular tachycardia groups, but differed in all subsequent beats, although overlap for individual subjects did occur.     

The Role of Combination Therapy with Mexiletine and Procainamide in Patients with Inducible Sustained Ventricular Tachycardia Refractory to Intravenous Procainamide

This study evaluated the role of serial electropharmacological testing on combination therapy with mexiletine and procainamide in 20 patients with inducible sustained ventricular tachycardia (VT) refractory to intravenous procainamide. The clinical arrhythmias were cardiac arrest in five patients, sustained VT in 11 patients, and recurrent syncope of presumably arrhythmic origin in four patients. The mean left ventricular ejection fraction (LVEF) was 0.40 +/- 0.12 (mean +/- SD). All patients had inducible sustained VT at baseline and after administration of intravenous procainamide. All 20 patients underwent electropharmacological testing on combination therapy with mexiletine and procainamide. The mean cycle length of inducible sustained VT was 251 +/- 48 ms at baseline, 324 +/- 81 ms on intravenous procainamide (P less than 0.014 vs baseline), and 365 +/- 82 ms on combination therapy (P less than 0.0001 vs baseline, P = NS vs intravenous procainamide). Combination therapy did not suppress VT inducibility, nor did it make VT more difficult to induce in 19 of 20 patients. The remaining one patient had a partial response (runs of nonsustained VT, longest 10 seconds). Furthermore, combination therapy did not significantly prolong the VT cycle length over and above that observed during testing with intravenous procainamide. Therefore, in patients with inducible sustained VT refractory to procainamide during initial electropharmacological testing, mexiletine in combination with procainamide appears to be of little or no value and serial electropharmacological testing on these drugs is of limited usefulness. Early initiation of alternative therapy may be the preferred clinical option.     

Dual Chamber Rate Responsive Pacing to Allow Sotalol Therapy for Ventricular Tachycardia

In order to allow the use of sotalol to control ventricular tachycardia (VT), dual chambe rate responsive (DDDR) pacemakers were implanted in ten patients aged 6 to 73 years (mean 50 years) Nine presented with monomorphic VT (seven inducible at baseline electrophysiological study (EPS)) ant one with syncope (monomorphic VT at EPS). On sotalol, VT was initiated in only one. This patien received sotalol in the absence of an effective alternative agent. The mean dose was 468 ± 269 mg/day Indications for pacing were symptomatic sotalol induced bradycardia (7), sinus node dysfunction (1) postoperative complete heart block (1), and infra-His block at baseline EPS (1). At least five of these patients would have been candidates for an implantable cardioverter defibrillator had sotalol required discontinuation. Initially, nine patients were paced in DDDR mode and one, with normal AV conduciioi on sotalol, in AAIR. One patient was unable to tolerate sotalol despite pacing. One patient died suddenly after 35 months of symptom-free follow-up. There was a significant improvement in symptomatic statu, (P = 0.03) after pacing among the other eight patients with no recurrence of VT. The implantation of DDDR pacemaker may be indicated in selected patients with serious cardiac arrhythmias. With such < device programmed to an appropriate mode, sotalol can be used successfully where otherwise contraindi cated by bradycardia or preexisting conduction disease. For some patients this may obviate the expense inconvenience, and attendant risks of implantable cardioverter defibrillator implantation.