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Initiation of ventricular tachycardia by interruption of pacemaker-mediated tachycardia in a patient with a dual-chamber implantable cardioverter defibrillator

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Initiation of ventricular tachycardia by interruption of

pacemaker-mediated tachycardia in a patient with a

dual-chamber implantable cardioverter defibrillator

Citation for published version (APA):

Van Gelder, B. M., Meijer, A., Dekker, L. R., & Bracke, F. A. (2009). Initiation of ventricular tachycardia by interruption of pacemaker-mediated tachycardia in a patient with a dual-chamber implantable cardioverter defibrillator. Pacing and Clinical Electrophysiology : PACE, 32(9), 1227-1230. https://doi.org/10.1111/j.1540-8159.2009.02469.x

DOI:

10.1111/j.1540-8159.2009.02469.x Document status and date:

Published: 01/09/2009

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Pacemaker-Mediated Tachycardia in a Patient with a

Dual-Chamber Implantable Cardioverter Defibrillator

BERRY M. VAN GELDER, P

H

.D., ALBERT MEIJER, M.D., P

H

.D., LUKAS R. DEKKER, M.D.,

P

H

.D., and FRANK A. BRACKE, M.D., P

H

.D.

From the Department of Cardiology, Catharina Hospital, Eindhoven, the Netherlands

A 74-year-old man with a dual-chamber implantable cardioverter defibrillator implanted 3 years before experienced multiple ventricular tachycardias (VTs). All episodes were initiated by pacemaker-mediated tachycardia (PMT) that was either stopped by atrial undersensing or the tachycardia termination algorithm of the device. After the termination of PMT, two rapid ventricular paced beats, the first initiated by artificial triggering and the second due to retrograde conduction of the first one, initiated VT that was successfully terminated by antitachycardia pacing or a direct current shock of the device. All episodes revealed this pattern of initiation with a short-long-short ventricular sequence inducing VT. (PACE 2009; 32: 1227–1230)

pacemaker-mediated tachycardia, ventricular tachycardia, tachycardia termination algorithm, short-long-short sequence, implantable cardioverter defibrillator

Introduction

Pacemaker-mediated tachycardia (PMT) can be encountered in patients with dual-chamber pacemakers or dual-chamber implantable car-dioverter defibrillators (ICD) in the presence of retrograde ventriculo-atrial (V-A) conduction.1,2 PMT can be stopped successfully by a tachycardia termination algorithm that prolongs the post ven-tricular atrial refractory period (PVARP) for one beat.3We report on a patient with a dual-chamber ICD that after the termination of PMT had one paced beat with retrograde conduction that trig-gered a second ventricular stimulated beat. The sequence of short (by PMT), long (by the tachycar-dia termination algorithm), and short sequence (by the ventricular triggered beat) induced through ret-rograde conduction repeatedly initiated sustained ventricular tachycardia (VT) in this patient.

Case Report

A 74-year-old patient with a previous myocar-dial infarction, who received a Guidant Vitality DR 1871 ICD (Boston Scientific, St. Paul, MN, USA) because of spontaneous monomorphic VT was hospitalized because of arrhythmic storm.

The atrial lead impedance had increased to a value>3,000 and the atrial electrogram showed spurious signals causing oversensing in the atrial channel evoking rapid ventricular stimulation (Fig. 1).

Address for reprints: Berry M. van Gelder, Ph.D., Department of Cardiology, Catharina Hospital, Michelangelolaan 2, 5623 EJ Eindhoven, The Netherlands. Fax:+31.40.2447885; e-mail: carlgr@cze.nl

Received August 29, 2008; revised October 6, 2008; accepted October 24, 2008.

Recordings of the onset of the VT have an identical pattern for all the episodes (Fig. 2). It started with ventricular pacing at the maximum tracking rate due to PMT. The PMT is interrupted by the tachycardia termination algorithm of the device that prolongs the PVARP for one cycle af-ter 16 beats at the maximum tracking rate (Fig. 2., episodes 1 and 4) or in less than 16 beats at max-imum tracking by undersensing of a retrograde P-wave (Fig. 2., episodes 2 and 3).

After the termination of PMT, the pacemaker starts atrioventricular sequential stimulation at the sensor-indicated rate because atrial noncapture ventricular pacing is followed by retrograde con-duction, which evokes one ventricular paced beat at the maximum tracking rate (Fig. 2, episode 1). A similar pattern after the termination of PMT can be seen by artificial triggering in the atrial channel (Fig. 2., episodes 2–4). These two ven-tricular paced beats with a short coupling inter-val (463 ms) were preceded by a relative long ventricular interval (1,085 ms) and a short ven-tricular paced interval due to PMT-initiated VT. This pattern of initiation with a short-long-short sequence was seen in all VT episodes. In all recordings, far-field ventricular activity is sensed in the atrial channel, which, however, played no role in the mechanism of tachycardia initiation or termination.

To avoid recurrence of the problem, the sys-tem was programmed to the single-chamber mode at a low ventricular stand-by rate, which prevented further arrhythmias related to the previous de-scribed mechanism. Implantation of a new atrial lead will be performed at the elective replacement time of the device, which is anticipated within 1.5 years.

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VAN GELDER, ET AL.

Figure 1. Programmer strip recording showing the atrial electrogram, ventricular electrogram,

shock lead electrogram, and annotations. The atrial electrogram shows spurious signals that trigger ventricular stimulation. The atrial lead impedance had increased above 3,000. Anno-tations: AP-Sr, VP-Sr= Atrial/ventricular pacing at the sensor driven rate; AS = atrial sensing; (AS)= atrial sensing in atrial refractory period; [AS] = atrial sensing in atrial blanking period;

VP-MT= ventricular pacing at maximum tracking rate.

Figure 2. Four episodes showing the onset of ventricular tachycardia with an almost identical pattern. The PMT is

terminated by the tachycardia termination algorithm in episodes 1 and 4, and by atrial undersensing in episodes 2 and 3. After the termination of PMT, the first ventricular paced beat gives retrograde conduction due to atrial noncapture (episode 1) or artificial atrial triggering (episodes 2–4).

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Discussion

Pacemaker-related tachycardia has already been reported in the early days of cardiac pac-ing.4,5PMT awareness started shortly after the in-troduction of devices with the capability of sens-ing and pacsens-ing in the atrium and pacsens-ing the ven-tricle synchronous with these atrial events. Due to the properties of the device, retrograde V-A con-duction could be sensed by the atrial amplifier, giving rise to ventricular pacing again with V-A conduction, thus initiating pacemaker-mediated or “endless-loop” tachycardia.1,2

After application of a programmable PVARP, the initiation of PMT could be controlled by pro-gramming a PVARP long enough to ignore the retrograde P-wave. As an additional protection against sustained PMT, a tachycardia termination algorithm was incorporated in these devices.3The termination algorithm detects pacing at the max-imum tracking rate following atrial sense events, and after 16 consecutive ventricular paced beats, PVARP is extended for one beat, which ignores retrograde atrial activation thus breaking PMT.

There might be several causes for the ini-tiation of PMT (e.g., atrial noncapture, artifi-cial atrial triggering), but they all have in com-mon that ventricular pacing is not preceded by atrial depolarization or the interval between atrial

Figure 3. Surface electrocardiogram leads aVR, II, and atrial lead signal. The onset of PMT

(left panel) and monomorphic VT (right panel). This illustrates that the first two beats of the PMT (arrows) and the first two beats initiating VT (arrows) are identical, with the same coupling interval of 463 ms (encircled) between both beats. For further explanation see text.

depolarization and ventricular pacing is long enough to regain atrial excitability by ventricular stimulation.

In our patient, it was clear that all episodes of PMT were initiated by artificial atrial trigger-ing due to spurious signals caused by a conductor break in the atrial lead (Fig. 1). Figure 2 demon-strates the termination of the PMT by the tachycar-dia termination algorithm that prolongs PVARP at the 16th beat of the PMT. This is shown by the an-notations at the last beat of the PMT in which the retrograde P wave is within the prolonged refrac-tory period indicated by the annotation (AS), in spite of the identical coupling interval of 463 ms.

The “short-long-short” ventricular sequence is a well-known phenomenon responsible for the initiation of polymorphic ventricular arrhythmias in long QT syndromes.6–8Ventricular arrhythmias evoked by a short-long-sort sequence are triggered either by early after depolarization or dispersion of repolarization.6In our patient, RR-intervals during VT were stable and, we presume a monomorphic VT is most likely.9,10

The intervals and morphology of the QRS complexes initiating VT (Fig. 3, right panel) are identical to the first two QRS complexes of the PMT (Fig. 3, left panel). In both situations, the first ventricular stimulus is initiated by artificial

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VAN GELDER, ET AL.

atrial triggering through spurious signals, leading to retrograde atrial activation. This atrial activa-tion again triggers a ventricular stimulus, in both circumstances with an identical coupling interval of 463 ms, determined by the upper tracking rate of the device. In the right panel (Fig. 3), it is fol-lowed by a ventricular premature beat initiating monomorphic VT, whereas in the left panel (Fig. 3) PMT is continued. The difference between both recordings is the “long” interval preceding VT and PMT with, respectively, 950 ms and 675 ms and the rhythm preceding this “long” interval, which is a regular fast rhythm (PMT) in the right panel (Fig. 3) and irregular in the left panel.

Long-short-long sequences are a well-known trigger for monomorphic VTs in ICD patients.11,12 In the PREVENT study, this long-short-long mech-anism as the cause of monomorphic VTs and the beneficial effect on reduction of VTs by

appli-cation of a rate smoothing algorithm has been demonstrated.11

The initiation of PMT could be further pre-vented by programming the device to a VVI pac-ing mode at a low stand-by rate. As this was clin-ically well tolerated by the patient, it was de-cided to avoid premature generator replacement or closely timed surgical procedures and to post-pone replacement of the malfunctioning atrial lead to the time of generator replacement.

Conclusions

This case report demonstrates that PMT and the algorithm to terminate this device arrhythmia create a short-long-short ventricular interval se-quence, which repeatedly initiated VT. The ini-tiation could be prevented by programming the pacing system to a single-chamber pacing mode, which was a feasible option in our patient.

References

1. Den Dulk K, Lindemans FW, Bar FW, Wellens HJJ. Pacemaker re-lated tachycardias. Pacing Clin Electrophysiol 1982; 5:476–485. 2. Furman S, Fisher JD. Endless loop tachycardia in an AV universal

(DDD) pacemaker. Pacing Clin Electrophysiol 1982; 5:486–489. 3. Van Gelder LM, El Gamal MIH, Baker R, Sanders RS.

Tachycar-dia termination algorithm: A valuable feature for interruption of pacemaker mediated tachycardia. Pacing Clin Electrophysiol 1984; 7:283–287.

4. Castellanos A, Lemberg L, Rodriguez-Tocker L, Berkovitz BV. Atrial synchronized pacemaker arrhythmias: Revisited. Am Heart J 1968; 76:199–207.

5. Castellanos A, Lemberg L. Pacemaker arrhythmias and electrocar-diographic recognition of pacemakers. Circulation 1973; 47:1382– 1391.

6. Surawicz B. Torsades de pointes: Unanswered questions. J Nippon Med Sch 2002; 69:218–223.

7. Locati EH, Maison-Blanche P, Dejode P, Cauchemez B, Coumel P. Spontaneous sequences of onset of torsade de pointes in patients with acquired prolonged repolarization: Quantitative analysis of Holter recordings. J Am Coll Cardiol 1995; 25:1564–1575.

8. Viskin S, Alla SR, Barron HV, Heller K, Saxon L, Kitzis I, van Hare GF, et al. Mode of onset of torsade de pointes in congenital long QT syndrome. J Am Coll Cardiol 1996; 28:1262–1268.

9. Jackman WM, Friday KJ, Anderson JL, Aliot EM, Clark M, Lazzara R. The long QT syndromes: A critical review, new clinical observa-tions and a unifying hypothesis. Prog Cardiovasc Dis 1988; 31:115– 172.

10. Roden DM, Woosley RL, Primm RK. Incidence and clinical features of the quinidine-associated long QT syndrome: Implications for pa-tient care. Am Heart J 1986; 111:1088–1093.

11. Wietholt D, Kuehlkamp V, Meisel E, Hoffmann E, Stellbrink C, Neuzner J, Seidl K, et al. on behalf of the PREVENT Study Investigators. Prevention of sustained ventricular tachyarrhyth-mias in patients with implantable cardioverter-defibrillators—The PREVENT study. J Intervent Card Electrophysiol 2003; 9:383– 389.

12. Marchlinsky FE, Callans DJ, Gottlieb CD, Schwartzman D, Preminger M. Benefits and lessons learned from stored electrogram information in implantable defibrillators. J Cardiovasc Electrphys-iol 1995; 6:832–851.

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