Europace Advance Access originally published online on July 9, 2008
Europace 2008 10(10):1238-1242; doi:10.1093/europace/eun176
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CASE REPORTS
Short–long–short sequence caused by ventricular safety pacing inducing ventricular tachycardia in a patient with a dual-chamber implantable cardioverter defibrillator
Cardiology Department, Lariboisière Hospital, Paris 7 University, 2 Rue Ambroise Paré, 75475 Paris Cedex 10, France
Manuscript submitted 25 March 2008. Accepted after revision 11 June 2008.
* Corresponding author. Tel: +33 1 49 95 82 23; fax: +33 1 49 95 82 06. E-mail address: antoine.leenhardt{at}lrb.aphp.fr
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Abstract |
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Ventricular safety pacing (VSP) is an algorithm used to prevent crosstalk inhibition and ventricular capture during the vulnerable period. We report a 78-year-old man with implantable dual-chamber defibrillator, in whom clusters of ventricular tachycardias (VTs) were provoked by the VSP. During rapid DDDR pacing, the delivery of the VSP after every other atrial-paced beat resulted in short–long–short ventricular sequences and induced VTs. An atrial-based lower rate timing, long atrioventricular pacing interval, and automatic gain control also accounted for this arrhythmogenic ventricular sequence. The VSP and the subsequent VT were eliminated by decreasing the pacing rate.
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Introduction |
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Ventricular safety pacing (VSP) is an algorithm used to prevent crosstalk inhibition and ventricular capture during the vulnerable period. It delivers short-coupled ventricular stimuli after atrial pacing when sensing any activation in the ventricular lead after the end of the ventricular blanking period. Although it is a protective feature embedded in many of the pacemakers and implantable cardioverter defibrillators (ICDs) currently used, we experienced a patient with a dual-chamber ICD, in whom clusters of ventricular tachycardias (VTs) were induced by the VSP. Such proarrhythmic effects of the VSP have, to the best of our knowledge, not been described.
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Case report |
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A 78-year-old man presented for his regular consultation. He had a history of coronary artery disease with an inferior wall myocardial infarction in 1973. He had experienced spontaneous VT episodes with a cycle length ranging from 480 to 300 ms since 1984 even under the administration of β-adrenergic blocker and amiodarone and received an ICD implantation in 1997. The system at the latest consultation consisted of a Belos DR-T (Biotronik, Berlin, Germany), Kainox RV 75 (Biotronik), tripolar ventricular lead positioned in the right ventricular apex, and Fineline II EZ (Guidant Inc., St Paul, MN, USA), atrial lead positioned in the right atrial appendage.
The programmed parameters during consultation included the following: pacing mode, DDD; pacing rate, 60 b.p.m.; paced atrioventricular (AV) delay, 330 ms; atrial pacing output, 1.0 V at 0.5 ms; ventricular pacing output, 1.8 V at 0.5 ms; ventricular sensitivity, 1.0 mV; post-atrial pacing ventricular blanking period, 52 ms; and VT detection interval, 520 ms, which was determined from the slowest spontaneous VT cycle length of 480 ms plus a 40 ms safety margin. With these settings and taking 80 mg of nadolol and 200 mg of amiodarone daily, the patient did not experience any sustained ventricular tachyarrhythmias during the previous 6 years. Although the patient showed first-degree AV block, the native ventricular conduction was preserved by prolonging the paced AV interval to 330 ms (Figure 1). Bradycardia pacing was delivered for 97% of the atrial beats and 31% of the ventricular beats. The measured P- and R-waves were 3.6 and 14.9 mV, respectively, and the pacing threshold of the atrial and ventricular leads was 0.5 and 1.0 V at 0.5 ms, respectively. During atrial pacing, a small far-field atrial potential was exhibited in the ventricular electrogram but was never sensed owing to the ventricular blanking period (Figure 1). The chest X-ray showed that both the ventricular and atrial leads were properly positioned (Figure 2).
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The patient had a decreased left ventricular function with an ejection fraction of 40% and moderate degree of mitral valve regurgitation. Because he complained of dyspnoea on exertion, his ICD was newly programmed to DDDR pacing at 60–100 b.p.m. Two hours after the consultation, he came back to the hospital because he had received an ICD discharge while hurrying to catch a taxicab. The device was interrogated and the stored electrograms were retrieved (Figure 3). Seven VTs with a mean cycle length of 450 ms were recorded: six treated with antitachycardia pacing and one with cardioversion. Prior to the occurrences of those VTs, his heart rate increased to 100 b.p.m. with AV sequential pacing. An AV interval during this rate–response rapid pacing was 330 ms, and spontaneous ventricular conduction preserved during DDD pacing at 60 b.p.m. was not observed. The VSP with an AV interval of 100 ms was frequently observed due to the far-field detection of an atrial activation by the ventricular lead. Every VT episode was preceded by a premature ventricular contraction (PVC) following a short–long–short ventricular sequence resulting from the delivery of the VSP after every other atrial-paced beat during DDDR pacing. No PVCs in the absence of this short–long–short sequence were observed. After reprogramming the ICD back to DDD pacing at 60 b.p.m., the far-field sensing of the atrial activation in the ventricular lead disappeared, and neither any VSP nor VT was observed.
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Discussion |
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Crosstalk is one of the serious complications occurring with dual-chamber pacemakers and ICDs,1
,2 and it is defined as the inappropriate detection of a spontaneous or pacemaker-generated event in one channel by the other channel, which can cause the inhibition of the second channel’s output. There are two functions designed to prevent the crosstalk inhibition. One is the ventricular blanking period that coincides with the atrial stimulus. This prevents the detection of the atrial spike or activation that could cause the inhibition of the ventricular channel output and was set to 52 ms in the present case. An additional backup system is the VSP, which prevents asystole if crosstalk occurs due to atrial far-field activity sensed after the blanking period of the ventricular electrode. In the present case, ICD was programmed to deliver a ventricular stimulus 100 ms after the atrial pacing when ventricular electrode sensed any activity 52–100 ms after the atrial pacing. Even if the event sensed by the ventricular electrode is a QRS complex, the ventricular safety stimulus falls within the ventricular refractory period and does not induce ventricular fibrillation.
In the present case, we observed that every VT developed after a PVC, which was provoked by a short–long–short ventricular sequence resulting from the delivery of the VSP after every other atrial-paced beat (Figure 3). As the PVCs were observed only after these short–long–short sequences, the VTs could also be considered to have been induced by these peculiar ventricular sequences. Recent paper describes that ventricular proarrhythmia induced by the pacing facilitated short–long–short sequence is common in patients with ICDs,3 but such arrhythmogenic sequence provoked by VSP has, to the best of our knowledge, not yet been demonstrated. This arrhythmogenic short–long–short ventricular sequence was also attributed to the shorter atrial pacing cycle length (600 ms), contributing to the ‘short’ part of the sequence, and longer AV interval (330 ms), contributing to both the ‘short’ and ‘long’ parts of the sequence, during the newly programmed rate–response mode than those during the DDD pacing at 60 b.p.m. An atrial-based lower rate timing during the DDD pacing also accounted for the ‘long’ part of the short–long–short sequence. Thus, decreasing the upper limit of the pacing rate or shortening the paced AV interval would be beneficial in treating those pacing-induced VTs. The prolongation of the ventricular blanking period to prevent the detection of far-field activation and the following VSP would be the another way to treat patients, but it also increases the risk of ventricular pacing in the vulnerable period of a PVC occurring during the blanking period when pacing in DDDR with a long AV interval.4 We reprogrammed the ICD back to DDD pacing at 60 b.p.m., which resulted in the disappearance of both the VSP and the VT.
Crosstalk is more common with unipolar systems or integrated bipolar leads because of the wide separation of the electrodes.5,6 Far-field sensing of the atrial activity by the true bipolar electrodes located in the right ventricular apex is rare, but has been reported.7,8 In the present case, there was no far-field atrial detection during DDD pacing at 60 b.p.m.; however, a small potential after atrial pacing, which was within the ventricular blanking period, was visible in the ventricular electrograms (Figure 1). As the crosstalk developed only during the rate–response rapid pacing, we considered that the source of the crosstalk in this case was the atrial depolarization rather than the atrial stimulus. The time delay between the atrial pacing stimulus and the atrial electrogram in Figure 3 strongly suggested that atrial capture latency9 exacerbated by rapid pacing made far-field atrial electrograms detectable more than 52 ms after the atrial stimulus, i.e. beyond the ventricular blanking period, in the ventricular lead and led to the VSP. Further, an automatic sensing system of the ICD used in this patient could affect the far-field sensing of the atrial activation. The Biotronik and Guidant ICD systems use automatic gain control, in which the maximum sensitivity is attained sooner and maintained longer than auto-adjusting sensitivity,10 which was used in the Medtronic and St Jude ICD systems. An ICD with automatic gain control behaviour was used more frequently in patients with spontaneous ventricular oversensing than in those without.10 Especially during ventricular pacing, the slope of the sensitivity curve in the automatic gain control becomes steeper as the pacing heart rate gets more increased. Studies11,12 reported that the frequency of the crosstalk increased more as the paced heart rate became faster, and it was suggested that, at higher rates, decreasing ventriculo-atrial intervals led to an increased frequency of crosstalk.12 It is thus presumable in the present case that the longer ventriculo-atrial interval after the VSP may have prevented successive crosstalk, which then resulted in the short–long–short arrhythmogenic sequence.
In summary, we report a novel form of pacing-induced tachycardia, which was provoked by the VSP. The delivery of the VSP after every other atrial-paced beat during DDDR pacing is around 100 b.p.m., which resulted in short–long–short ventricular sequences and induced clusters of VTs. After decreasing the pacing rate, the far-field sensing of the atrial activation causing VSP disappeared and VT did not recur.
Conflict of interest: none declared.
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References |
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[1] Helguera ME, Pinski SL. Cross-talk inhibition and asystole resulting from postshock high-output pacing: a new form of implantable cardioverter-defibrillator proarrhythmia. Heart Rhythm (2005) 2:310–2.[CrossRef][Web of Science][Medline]
[2] Curwin JH, Roelke M, Ruskin JN. Inhibition of bradycardia pacing caused by far-field atrial sensing in a third-generation cardioverter defibrillator with an automatic gain feature. Pacing Clin Electrophysiol (1996) 19:124–6.[CrossRef][Medline]
[3] Sweeney MO, Ruetz LL, Belk P, Mullen TJ, Johnson JW, Sheldon T. Bradycardia pacing-induced short-long-short sequences at the onset of ventricular tachyarrhythmias: a possible mechanism of proarrhythmia? J Am Coll Cardiol (2007) 50:614–22.
[4] Pieterse MG, den Dulk K, van Gelder BM, van Mechelen R, Wellens HJ. Programming a long paced atrioventricular interval may be risky in DDDR pacing. Pacing Clin Electrophysiol (1994) 17:252–7.[CrossRef][Medline]
[5] Peters W, Kowallik P, Wittenberg G, Scholl C, Meesmann M. Inappropriate discharge of an implantable cardioverter defibrillator during atrial flutter and intermittent ventricular antibradycardia pacing. J Cardiovasc Electrophysiol (1997) 8:1167–74.[CrossRef][Web of Science][Medline]
[6] Schecter SO, Greenberg SM, Hoch DH, Cesa M, Levine JH. Inappropriate discharges of an implantable cardioverter defibrillator secondary to automatic adjustable gain of atrial tachycardia. Pacing Clin Electrophysiol (1997) 20:1721–2.[CrossRef][Medline]
[7] Barold SS, Garrigue S, Clementy J. Far-field P-wave sensing by the right ventricular lead of conventional dual chamber pacemakers. J Interv Card Electrophysiol (2002) 6:77–80.[CrossRef][Web of Science][Medline]
[8] Ben Zur UM, Gross JN, Goldberger MH, Tilkemeier PL, Weyman AK, Furman S. Oversensing of pacemakers in the bipolar pacing configuration: paradoxic resolution with programming to unipolar sensing. Am Heart J (1994) 128:617–9.[CrossRef][Web of Science][Medline]
[9] Nguyen NX, Yang PT, Huycke EC, Keung EC, Deedwania P, Sung RJ. Effects of beta-adrenergic stimulation on atrial latency and atrial vulnerability in patients with paroxysmal supraventricular tachycardia. Am J Cardiol (1988) 61:1031–6.[CrossRef][Web of Science][Medline]
[10] Sweeney MO, Ellison KE, Shea JB, Newell JB. Provoked and spontaneous high-frequency, low-amplitude, respirophasic noise transients in patients with implantable cardioverter defibrillators. J Cardiovasc Electrophysiol (2001) 12:402–10.[CrossRef][Web of Science][Medline]
[11] Byrd CL, Schwartz SJ, Gonzales M, Ciraldo RJ, Yahr WZ, Sivina M, et al. Rate responsive pacemakers and cross talk. (Abstract). Pacing Clin Electrophysiol (1988) 11:798.
[12] Combs WJ, Reynolds DW, Sharma AD, Bennett TD. Cross-talk in bipolar pacemakers. Pacing Clin Electrophysiol (1989) 12:1613–21.[CrossRef][Medline]
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