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ARRHYTHMIA OF THE MONTH Section Editor: Fred Morady, M.D. 2:1 Tracking of Sinus Rhythm in a Patient with a Dual-Chamber Implantable Cardioverter De brillator: What is the Mechanism? SERGIO L. PINSKI, M.D. From the Section of Cardiology, Rush Medical College and Rush-Presbyterian-St. Luke’s Medical Center, Chicago, Illinois Case Presentation A 49-year-old woman with hypertrophic obstructive car- diomyopathy received a dual-chamber pacemaker in 1995. It resulted in signi cant reduction in the intraventricular pressure gradient and signi cant improvement in symp- toms. She developed ventricular tachycardia, and the pace- maker was replaced with a dual-chamber implantable car- dioverter de brillator (ICD). The ventricular pacing lead was extracted, and the preexistent atrial lead (P wave: 3 mV) and a new active- xation, “integrated” bipolar de - brillation lead (Sprint SVC 6945; Medtronic Inc., Minne- apolis, MN, USA) were connected to a GEM DR 7271 (Medtronic) generator. Programming was as follows: pac- ing mode DDD, lower rate 60 beats/min, upper rate 120 beats/min, sensed AV delay 100 msec, ventricular output 4 V at 0.4 msec, maximum atrial sensing 0.3 mV, maximum ventricular sensitivity 0.3 mV, postventricular atrial refrac- tory period (PVARP) 310 msec, postpace ventricular blank- ing 240 msec, premature ventricular complex (PVC) re- sponse ON. Immediately after lead connection, an unusual pattern of pacemaker alternans was seen (Fig. 1). Only every other sinus beat was tracked as expected. The other beats presented intrinsic conduction with a PR interval longer than the programmed AV delay. What is the mech- anism for the alternans? Commentary Pacemaker alternans has been de ned as a beat-to-beat change (with a 2:1 pattern) in the amplitude, polarity, or con guration of the pacemaker stimulus or resultant paced waveform, complex, or segment. 1 Here, we extend the def- inition to include a case of 2:1 failure to track the sinus P wave, resulting in alternation of paced and intrinsically conducted QRS complexes. Failure to track the P wave results from atrial undersens- ing, which can be true or functional (i.e., a P wave suf - ciently large to be sensed but falling in the refractory period). Analysis of telemetered electrograms and event markers allows expeditious and de nitive diagnosis of the mechanism of undersensing (Fig. 2). In this case, lack of tracking was due to functional atrial undersensing. The P waves had consistent amplitude ; 4 mV. There was over- sensing of the paced T wave occurring 400 msec after the ventricular pulse (coinciding with the maximum 1 dV/dt of the T wave de ection in the electrogram). This oversensing triggered a new PVARP. The T wave (a ventricular sensed event that follows a ventricular event without an intervening atrial event) was interpreted by the device as a PVC. Be- cause the PVC response was enabled, the PVARP was extended to 400 msec. This ensured that the next sinus P wave (falling ; 310 msec afterward) was sensed in the refractory period (AR) and therefore was not tracked. The T wave from the resulting conducting beat was of much lower amplitude and slew rate, and it was not oversensed. Track- ing of the subsequent P wave reinitiated the sequence. Functional P wave undersensing due to PVARP reinitia- tion by inapparent ventricular signals has been described, and the role of automatic PVARP extension in its perpetu- ation highlighted. 2 Paraskevaidis et al. 3 reported a patient with a DDD pacemaker and complete heart block in whom oversensing of the paced T waves resulted in 2:1 atrial tracking and pacing below the lower rate limit. However, the incidence of this phenomenon in patients with pacemak- ers appears extremely uncommon. The sensing algorithms in ICDs tend to promote paced T wave oversensing. 4 To ensure ventricular brillation detection, pacing onset trig- gers a rapid increase in sensitivity. For example, in the GEM device at nominal settings, sensitivity is set at 1.35 mV at the end of the 240-msec postpace blanking, and thereafter decays toward 0.3 mV with a 450-msec constant. Thus, the estimated sensitivity at time of T wave detection was ; 0.9 mV. Reprogramming of the ventricular maximum sensitivity to 0.6 mV abolished T wave oversensing, and 1:1 tracking of sinus rhythm was achieved (Fig. 3). At this setting, the sensitivity was automatically set at 1.8 mV at the end of the postpace blanking and was still . 1.5 mV by the time the T wave was oversensed at the prior setting of 0.3-mV maxi- mum sensitivity. Ventricular brillation was promptly and J Cardiovasc Electrophysiol, Vol. 12, pp. 503-504, April 2001. Address for correspondence: Sergio L. Pinski, M.D., Rush-Presbyterian-St. Luke’s Medical Center, 1750 W. Harrison Street, JS-1091, Chicago, IL 60612. Fax: 312-942-5862; E-mail: [email protected] Figure 1. Surface lead II showing 2:1 tracking of sinus rhythm. 503 Reprinted with permission from JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Volume 12, No. 4, April 2001 Copyright ©2001 by Futura Publishing Company, Inc., Armonk, NY 10504-0418

2:1 Tracking of Sinus Rhythm in a Patient with a Dual-Chamber Implantable Cardioverter Defibrillator: What is the Mechanism?

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Page 1: 2:1 Tracking of Sinus Rhythm in a Patient with a Dual-Chamber Implantable Cardioverter Defibrillator: What is the Mechanism?

ARRHYTHMIA OF THE MONTHSection Editor: Fred Morady, M.D.

2:1 Tracking of Sinus Rhythm in a Patient with aDual-Chamber Implantable Cardioverter De� brillator:

What is the Mechanism?SERGIO L. PINSKI, M.D.

From the Section of Cardiology, Rush Medical College and Rush-Presbyterian-St. Luke’ s Medical Center, Chicago, Illinois

Case Presentation

A 49-year-old woman with hypertrophic obstructive car-diomyopathy received a dual-chamber pacemaker in 1995.It resulted in signi� cant reduction in the intraventricularpressure gradient and signi� cant improvement in symp-toms. She developed ventricular tachycardia, and the pace-maker was replaced with a dual-chamber implantable car-dioverter de� brillator (ICD). The ventricular pacing leadwas extracted, and the preexistent atrial lead (P wave: 3mV) and a new active-� xation, “integrated” bipolar de� -brillation lead (Sprint SVC 6945; Medtronic Inc., Minne-apolis, MN, USA) were connected to a GEM DR 7271(Medtronic) generator. Programming was as follows: pac-ing mode DDD, lower rate 60 beats/min, upper rate 120beats/min, sensed AV delay 100 msec, ventricular output 4V at 0.4 msec, maximum atrial sensing 0.3 mV, maximumventricular sensitivity 0.3 mV, postventricular atrial refrac-tory period (PVARP) 310 msec, postpace ventricular blank-ing 240 msec, premature ventricular complex (PVC) re-sponse ON. Immediately after lead connection, an unusualpattern of pacemaker alternans was seen (Fig. 1). Onlyevery other sinus beat was tracked as expected. The otherbeats presented intrinsic conduction with a PR intervallonger than the programmed AV delay. What is the mech-anism for the alternans?

Commentary

Pacemaker alternans has been de� ned as a beat-to-beatchange (with a 2:1 pattern) in the amplitude, polarity, orcon� guration of the pacemaker stimulus or resultant pacedwaveform, complex, or segment.1 Here, we extend the def-inition to include a case of 2:1 failure to track the sinus Pwave, resulting in alternation of paced and intrinsicallyconducted QRS complexes.

Failure to track the P wave results from atrial undersens-ing, which can be true or functional (i.e., a P wave suf� -ciently large to be sensed but falling in the refractoryperiod). Analysis of telemetered electrograms and eventmarkers allows expeditious and de� nitive diagnosis of themechanism of undersensing (Fig. 2). In this case, lack of

tracking was due to functional atrial undersensing. The Pwaves had consistent amplitude ; 4 mV. There was over-sensing of the paced T wave occurring 400 msec after theventricular pulse (coinciding with the maximum 1 dV/dt ofthe T wave de� ection in the electrogram). This oversensingtriggered a new PVARP. The T wave (a ventricular sensedevent that follows a ventricular event without an interveningatrial event) was interpreted by the device as a PVC. Be-cause the PVC response was enabled, the PVARP wasextended to 400 msec. This ensured that the next sinus Pwave (falling ; 310 msec afterward) was sensed in therefractory period (AR) and therefore was not tracked. The Twave from the resulting conducting beat was of much loweramplitude and slew rate, and it was not oversensed. Track-ing of the subsequent P wave reinitiated the sequence.

Functional P wave undersensing due to PVARP reinitia-tion by inapparent ventricular signals has been described,and the role of automatic PVARP extension in its perpetu-ation highlighted.2 Paraskevaidis et al.3 reported a patientwith a DDD pacemaker and complete heart block in whomoversensing of the paced T waves resulted in 2:1 atrialtracking and pacing below the lower rate limit. However,the incidence of this phenomenon in patients with pacemak-ers appears extremely uncommon. The sensing algorithmsin ICDs tend to promote paced T wave oversensing.4 Toensure ventricular � brillation detection, pacing onset trig-gers a rapid increase in sensitivity. For example, in theGEM device at nominal settings, sensitivity is set at 1.35mV at the end of the 240-msec postpace blanking, andthereafter decays toward 0.3 mV with a 450-msec constant.Thus, the estimated sensitivity at time of T wave detectionwas ; 0.9 mV.

Reprogramming of the ventricular maximum sensitivityto 0.6 mV abolished T wave oversensing, and 1:1 trackingof sinus rhythm was achieved (Fig. 3). At this setting, thesensitivity was automatically set at 1.8 mV at the end of thepostpace blanking and was still . 1.5 mV by the time the Twave was oversensed at the prior setting of 0.3-mV maxi-mum sensitivity. Ventricular � brillation was promptly and

J Cardiovasc Electrophysiol, Vol. 12, pp. 503-504, April 2001.

Address for correspondence: Sergio L. Pinski, M.D., Rush-Presbyterian-St.Luke’ s Medical Center, 1750 W. Harrison Street, JS-1091, Chicago, IL60612. Fax: 312-942-5862; E-mail: [email protected]

Figure 1. Surface lead II showing 2:1 tracking of sinus rhythm.

503Reprinted with permission fromJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Volume 12, No. 4, April 2001Copyright ©2001 by Futura Publishing Company, Inc., Armonk, NY 10504-0418

Page 2: 2:1 Tracking of Sinus Rhythm in a Patient with a Dual-Chamber Implantable Cardioverter Defibrillator: What is the Mechanism?

reproducibly detected with a worst-case scenario maximumsensitivity of 1.2 mV, ensuring an adequate “sensing safetymargin.” The device was left at 0.6 mV maximum sensitiv-ity and 100% ventricular pacing con� rmed by eventcounters and ECG ambulatory monitoring. Alternatively, Twave oversensing could have been eliminated by extendingthe postpace ventricular blanking close to the maximumallowable of 440 msec.5 However, this would have severelyrestricted the maximum programmable pacing rate. Tomaintain a wide window for ventricular tachyarrhythmiadetection, the GEM DR device allows the ventricular blank-ing to occupy only up to 50% of the ventricular pacinginterval (minus 50 msec if ventricular safety pacing inenabled). This limitation is partially circumvented in ICDsthat incorporate a programmable dynamic ventricular pacedblanking period that shortens automatically at faster rates.6 ,7

Shortening of the PVARP and disabling of the PVC re-sponse would not have solved the primary problem andwould have left the patient prone to endless loop tachycar-dia.

In single-chamber ICDs, T wave oversensing generallyresults in inhibition of the next pacing stimulus, conse-quently lengthening the effective pacing escape interval.Most instances are of little clinical consequence, but theresulting bradycardia may become symptomatic. In patientswith long QT syndrome, the slower paced rate furtherprolongs the QT interval, may perpetuate oversensing,8 andlead to development of torsades de pointes. Oversensing ofpaced T waves also can invoke “rate stabilization” algo-rithms and perpetuate pacing in patients without bradycar-dia.9 As demonstrated in this case, the manifestations of Twave oversensing in patients with dual-chamber ICDs canbe more complex.

References

1. Kleinfeld M, Barold SS, Rozanski JJ: Pacemaker alternans: A review.PACE 1987;10:924-933.

2. Barold SS: Timing cycles and operative characteristics of pacemakers.In Ellenbogen KA, Kay NG, Wilkoff BL, eds: Clinical CardiacPacing. WB Saunders, Philadelphia, 1995, p. 633.

3. Paraskevaidis S, Mochlas S, Hadjimiltiadis S, Louridas G: IntermittentP wave sensing in a patient with DDD pacemaker. PACE 1999;22:689-690.

4. Reiter MJ, Mann DE: Sensing and tachyarrhythmia detection problemsin implantable cardioverter de� brillators. J Cardiovasc Electrophysiol1996;7:542-558.

5. Mann DE, Damle RS, Kelly PA, Landers M, Otto L, Reiter MJ:Comparison of oversensing during bradycardia pacing in two types ofimplantable cardioverter-de� brillator systems. Am Heart J 1998;136:658-663.

6. Pinski SL, Haw J, Trohman RG: Usefulness of a dynamic post-paceventricular blanking period in dual-chamber, rate-responsive implant-able de� brillators. (Abstract) PACE 1999; 22:897.

7. Ellenbogen KA, Edel T, Moore S, Higgins S, Paci� co A, Wilber D,Wood MA, Rogers R, Dahn A, Zhu A, and the Ventak AV II DR StudyInvestigators: A prospective randomized-controlled trial of ventricular� brillation detection time in a DDDR ventricular de� brillator. PACE2000;23:1268-1272.

8. Perry GY, Kosar EM: Problems in managing patients with long QTsyndrome and implantable cardioverter-de� brillators: A report of twocases. PACE 1996;19:863-867.

9. Pinski SL: Inappropriate pacing due to autoperpetuation of the ven-tricular rate stabilization algorithm: A manifestation of T-wave over-sensing by ICDs. PACE 2000;23:1446-1447.

Figure 2. Surface lead II, telemetered event markers (M), and telemetered atrial (A, left panel), or ventricular (V, right panel) electrogram during 2:1tracking. AR 5 atrial sensed event in refractory period; AS 5 atrial sensed event; VP 5 ventricular paced event; VS 5 ventricular sensed event.Calibration for electrograms is 1 mV per small square.

Figure 3. Consistent 1:1 tracking after reprogramming of ventricularmaximum sensitivity to 0.6 mV. Abbreviations as in Figure 2.

504 Journal of Cardiovascular Electrophysiology Vol. 12, No. 4, April 2001