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.     

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.     

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.     

Termination and Acceleration of Ventricular Tachycardia with Autodecremental Pacing, Burst Pacing, and Cardioversion in Patients with an Implantable Cardioverter Defibrillator

This multicenter study reports the outcome of ventricular tachycardia (VT) therapy (conversion or acceleration) and the relationship to initial tachycardia cycle length and other clinical variables using an implantable device with the capability of autodecremental or burst pacing, Cardioversion, and defibrillation. The device was implanted in 444 patients (mean age 58 ± 15 years) with 1,240 episodes of VT induced with noninvasive programming and reported in a multicenter database. Only the first sequence attempted for conversion by pacing or Cardioversion was assessed, and Cardioversion energies were 0.2–5 J. Autodecremental pacing was used to treat 700 induced episodes of VT during titration of pacing therapies (57% converted and 12% accelerated), burst pacing to treat 357 episodes (49% converted and 11% accelerated), and Cardioversion to treat 183 episodes (82% converted and 4% accelerated). Cardioversion was the most effective treatment and had the lowest acceleration rate. Shorter VT cycle lengths were more likely to accelerate with burst pacing and longer VT cycle lengths to convert with both burst and autodecremental pacing. Patients with higher ejection fractions were more likely to convert with autodecremental and burst pacing. Use of Cardioversion, higher ejection fraction, absence of unrepaired aneurysm, longer VT cycle lengths, coronary artery disease, and use of autodecremental pacing predicted conversion. Lower ejection fraction and VT cycle lengths ± 300 msec predicted tachycardia acceleration.     

Intravenous Disopyramide Phosphate and Ventricular Overdrive Pacing in the Termination of Paroxysmal Ventricular Tachycardia

Both antiarrhythmic drugs and bursts of rapid ventricular pacing provide alternatives to DC cardioversion for the treatment of paroxysmal ventricular tachycardia. This report considers the individual and combined success of burst ventricular pacing and intravenous disopyramide phosphate in the tretment of 11 examples of paroxysmal ventricular tachycardia. Rapid ventricular pacing, at a rate of up to 50 beats/min faster than the tachycardia rate terminated 7 of the tachycardias. Intravenous disopyramide resulted in increased tachycardiac cycle length (342 +/- 34 ms-385 +/- 56 ms), increased QRS complex width (147 +/- 42 ms-180 +/- 41 ms) and termination of 8 the tachycardias. The remaining 3 tachycardias could be terminated by bursts of ventricular pacing following the infusion of disopyramide. Of these, 2 could not be terminated prior to disopyramide. The use of both techniques allowed the extinction of all 11 tachycardias and prevented the need to proceed to DC conversion.     

Randomized Cross-Over Evaluation of Two Adaptive Pacing Algorithms for the Termination of Ventricular Tachycardia

Objective: In a randomized, cross-over study we evaluated the efficacy of rate adaptive constant cycle length (BURST)and autodecremental (RAMP)pacing for termination of sustained monomorphic ventricular tachycardia. Methods: An external device capable of delivering the same types ofantitachycardia pacing as the newer generation implantable cardioverter defibrillators wos used. Thirty-one patients with ischemic and nonischemic cardiomyopathy and documented clinical ventricular tachycardia or ventricularfibrillation were examined during routine invasive electrophysiological studies. RAMP and BURST pacing were each attempted in 54 matched pairs of induced ventricular tachycardia. After a therapy was applied, the tachycardia was reinitiated and the other therapy applied during the second episode so that a total of 108 ventricular tachycardia episodes were studied. Results: Overoll efficacy of ventricular tachycardia pace termination was 69% and the time required to stop ventricular tachycardia was 14.1 ± 11.3 seconds. The ability to terminate ventricular tachycardia by RAMP (72%)or BURST (65%)pacing was not significantly different. However, time to terminate ventricular tachycardia by HAMP (It.8 ± 8.5 sec)was significantly shorter than by BURST (16.4 ± 13.5), P < 0.001. Acceleration of ventricular tachycardia was uncommon with both pacing modes, 7/108 (7%). The ability to pace terminate ventricular tachycardia was cycle length dependant. The highest success was with ventricular tachycardia cycle length between 300 and 350 msec. The success rate decreased with faster and also slower ventricular tachycardia. Conclusions: 1. Rate adaptive pacing methods for ventricular tachycardia termination are effective and safe. 2. Autodecremental fiAMP pacing afford quicker ventricular tachycardia termination than constant cycle length BURST pacing. 3. The ability to terminate ventricalar tachycardia is cycle length dependent with cycle length range of 300–350 msec being most responsive to pace termination     

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.     

Safety and Efficacy of Pacing for Ventricular Tachycardia

This study was undertaken to determine the safety and efficacy of three different pacing modalities on the termination of ventricular tachyarrhythmias. Thirty-two patients were studied in the electrophysiology laboratory. Three randomized pacing modalities were selected for attempted conversion: auto increment, auto burst, and random burst. In all three groups, arrhythmias with cycle lengths shorter than 230 ms required DC shock, with one exception. Those longer than 230 ms were terminated by pacing in 85% of cases. There was a 15% rate of acceleration. Thus, antitachycardia pacing for ventricular tachyarrhythmias should be considered only with defibrillating back-up.     

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.     

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.     

Successful Treatment of Ventricular Tachycardia by Physiological Pacing

The case is presented of a young patient with atrioventricular (AV) block but no evidence of other disease; in this patient exercise or stress-related syncope continued after implantation of a ventricular inhibited (VVI) pacemaker. Investigation revealed exercise-induced limited rapid multiform ventricular tachycardia (VT) which was associated with faintness or syncope. Temporary atrial triggered ventricular inhibited ventricular (VDD) pacing resulted in enhanced exercise tolerance with no significant arrhythmia. A permanent full function dual chamber [DDD] pacemaker was implanted and prevented the VT. There have been no further exercise-related symptoms during two years 0f follow up.     

Long-term Management of Recurrent Paroxysmal Tachycardia by Cardiac Burst Pacing

Sixteen patients with either recurrent symptomatic supraventricular tachycardia (SVT) (ten) or ventricular tachycardia (VT) (six) unresponsive to drug treatment underwent insertion of chronic overdrive cardiac pacing devices for arrhythmia control. All patients with SVT followed for longer than 2.5 years required concomitant drug therapy for rhythm control. In addition, one of the ten patients required amiodarone and three required nonpharmacologic therapy (catheter ablation of the atrioventricular junction (one), surgical ablation of the Kent bundle and/or bundle of His (two). In the six patients with VT, only one patient used the device successfully. In the other five patients, either the arrhythmia failed to respond to burst overdrive pacing (three) or overdrive acceleration resulted (two). One death in the latter group was related to induction of rapid VT followed by ventricular fibrillation. Long-term follow-up of patients with paroxysmal SVT shows that virtually all require concomitant drug therapy and may require aggressive medical or surgical procedures for arrhythmia control. Use of ventricular overdrive pacing for those with VT appeared singularly disappointing in that pacing proved either ineffective (three) or resulted in overdrive acceleration (two) in 5/6 patients.     

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.     

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.     

Amiodarone or Procainamide for the Termination of Sustained Stable Ventricular Tachycardia: An Historical Multicenter Comparison

Objectives: The objective was to compare the effectiveness of intravenous (IV) procainamide and amiodarone for the termination of spontaneous stable sustained ventricular tachycardia (VT). Methods: A historical cohort study of consecutive adult patients with stable sustained VT treated with IV amiodarone or procainamide was performed at four urban hospitals. Patients were identified for enrollment by admissions for VT and treatment with the study agents in the emergency department (ED) from 1993 to 2008. The primary measured outcome was VT termination within 20 minutes of onset of study medicine infusion. A secondary effectiveness outcome was the ultimate need for electrical therapy to terminate the VT episode. Major adverse effects were tabulated, and blood pressure responses to medication infusions were compared. Results: There were 97 infusions of amiodarone or procainamide in 90 patients with VT, but the primary outcome was unknown after 14 infusions due to administration of another antidysrhythmic during the 20‐minute observation period. The rates of VT termination were 25% (13/53) and 30% (9/30) for amiodarone and procainamide, respectively. The adjusted odds of termination with procainamide compared to amiodarone was 1.2 (95% confidence interval [CI] = 0.4 to 3.9). Ultimately, 35/66 amiodarone patients (53%, 95% CI = 40 to 65%) and 13/31 procainamide patients (42%, 95% CI = 25 to 61%) required electrical therapy for VT termination. Hypotension led to cessation of medicine infusion or immediate direct current cardioversion (DCCV) in 4/66 (6%, 95% CI = 2 to 15%) and 6/31 (19%, 95% CI = 7 to 37%) patients who received amiodarone and procainamide, respectively. Conclusions: Procainamide was not more effective than amiodarone for the termination of sustained VT, but the ability to detect a significant difference was limited by the study design and potential confounding. As used in practice, both agents were relatively ineffective and associated with clinically important proportions of patients with decreased blood pressure. ACADEMIC EMERGENCY MEDICINE 2010; 17:297–306 © 2010 by the Society for Academic Emergency Medicine