managed ventricular pacing facilitating atrioventricular nodal reentrant tachycardia

DEVICE ROUNDS

Managed Ventricular Pacing FacilitatingAtrioventricular Nodal Reentrant TachycardiaDANIEL R. FRISCH, M.D.,* ANAND S. KENIA, M.D.,* PAUL WALINSKY, M.D.,*and JOSHUA BALOG, M.D.†From the *Thomas Jefferson University Hospital, Jefferson Heart Institute, Philadelphia, Pennsylvania; and †RobertWood Johnson University Hospital, New Brunswick, New Jersey

managed ventricular pacing, atrioventricular nodal reentrant tachycardia, pacing

Case SummaryAn 81-year-old woman with a history of

coronary artery disease (left ventricular ejectionfraction of 50%) and severe pulmonary hyper-tension underwent placement of a dual-chamberpacemaker (EnRhythm, P1501DR, Medtronic, Inc.,Minneapolis, MN, USA) to treat episodes ofsyncope caused by a junctional rhythm at a rateof 30 beats/min following episodes of narrowcomplex tachycardia. To preserve native ventric-ular activation, the device was programmed toa rate responsive mode, AAIR/DDDR (managedventricular pacing, MVP) with a lower rate limitof 60 pulses/min (ppm) and an upper rate limit of120 ppm.

The patient subsequently had recurrentepisodes of paroxysmal, short-RP tachycardia onECG (Fig. 1). Intracardiac recordings from thedevice showing initiation and ventricular pacingduring supraventricular tachycardia (SVT) areshown in Figures 2(A) and (B). Reprogrammingthe device to the DDDR mode with a pacedatrioventricular (AV) interval of 180 ms and asensed AV interval of 150 ms prevented furtherepisodes of tachycardia. What is the explanation?

CommentaryMVP was developed to minimize ventricular

pacing in patients at risk for ventricular pacing-induced atrial fibrillation, heart failure, or death.1With MVP enabled, the device paces in AAI

Conflict of Interest: None.

Address for reprints: Daniel R. Frisch, M.D., Thomas JeffersonUniversity Hospital, Jefferson Heart Institute, Mezzanine, 935Chestnut Street, Philadelphia, PA 19107. Fax: 215-503-3976;e-mail: Daniel.Frisch@Jefferson.edu

Received July 17, 2013; revised September 18, 2013; acceptedSeptember 23, 2013.

doi: 10.1111/pace.12318

mode unless there is no ventricular-sensed eventbefore the next atrial-paced or -sensed event. Ifthere is no ventricular-sensed event, it deliversventricular backup pacing with an 80-ms AVinterval after the second atrial-paced or -sensedbeat and then reverts to AAI pacing for thesubsequent beat. If there is no ventricular-sensedevent between the third and fourth atrial-sensed or-paced beats, the device switches to DDD pacing,periodically testing for resumption of native AVconduction.2

The tracing in Figure 2(A) shows the initiationof the tachycardia with a premature atrial beatand a prolonged AV interval. The prematureatrial beat (demarcated with an arrow) fails toconduct in the antegrade direction in the fast AVnodal pathway, but does conduct over the slowpathway. Because the device was programmedto MVP mode it allowed for the 420-ms AVinterval, which allowed antegrade slow pathwayconduction, retrograde fast pathway conduction,and initiation of the tachycardia. Because the atrialelectrogram occurs nearly simultaneously with theventricular depolarization, the atrial electrogramoccurs within the postventricular atrial blankingperiod and is censored from the marker channels.Simultaneous atrial and ventricular activation isconsistent with a diagnosis of atrioventricularnodal reentrant tachycardia (AVNRT) or atrialtachycardia (AT) with an AV interval equal tothe tachycardia cycle length (TCL).3 Figure 2(B)illustrates ventricular entrainment of the SVT,with a V-A-V response, thus demonstrating areentrant mechanism and excluding AT.4 Thereis a large differential between postpacing interval(PPI) and TCL (PPI-TCL = 120 ms) and a significantincrease in the entrained ventriculoatrial (VA)interval compared to the fixed VA interval duringtachycardia. This further supports a diagnosisof AVNRT.5,6 Using an implantable device fornoninvasive electrophysiology testing has beenwell described.7

©2013 Wiley Periodicals, Inc.

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MVP FACILITATING AVNRT

Figure 1. Twelve-lead ECG of the short RP tachycardia.

Pacing in the DDD mode likely preventedfurther episodes of AVNRT by preventing long AVintervals, unlike the MVP mode, which permitslong AV intervals as long as a ventricular eventoccurs before the subsequent atrial-paced or-sensed event. It is important to note that thisphenomenon is not unique to the MVP modeand that AVNRT has also been described duringDDD pacing as well.8 AVNRT may occur in othercircumstances where dual AV nodal physiologyexists and a long AV delay has been programmed.An analogous pacemaker reentrant tachycardiacan be seen with long AV delays allowing forretrograde pathway recovery where the retro-grade P wave falls outside the postventricularatrial refractory period (PVARP), resulting intachycardia.9,10 Pacing with a shorter AV intervallikely prevented initiation of AVNRT becauseventricular pacing interrupts slow pathway con-duction through the AV node or caused retrogradeconcealed conduction into the fast pathway thatcaused the circulating wave front to collide withthe still refractory slow pathway of the AVnode.

Although changing modes from MVP to DDDdoes account for most of the ability for AVNRTto occur, the PVARP needs to be evaluated aswell. An atrial premature depolarization thatoccurs during PVARP will not be followed by a

ventricular-paced output and could also lead toinitiation of AVNRT. Shortening of the PVARPallows fewer opportunities for APDs to conductover the slow pathway. Only very short-coupledAPDs will not be interrupted by ventricularpacing. A limitation to shortening the PVARP isthat if the upper tracking rate is set to a lowrate, then a premature atrial contraction occurringoutside the shortened PVARP could still resultin native ventricular conduction consequentlycausing AVNRT.

Although this patient’s AVNRT was incessantprior to the reprogramming, this patient had noepisodes of AVNRT in the subsequent 48 hours.Unfortunately, because of intolerance of forcedright ventricular pacing due to development ofheart failure, possibly secondary to dyssynchronyin the setting of abnormal left ventricular functionand pulmonary hypertension, the patient wasreferred for an electrophysiology study. The studyconfirmed AVNRT and a slow pathway ablationwas performed successfully. With subsequentreprogramming to MVP, there was no furtherAVNRT and the patient’s symptoms improved.

This case illustrates a potential problemwith MVP pacing in patients with long AVconduction intervals and dual AV nodal pathwayphysiology, which can be alleviated by DDDprogramming.

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Figure 2. Intracardiac recordings through the pacemaker. (A) Notice how the AV interval prolongs significantlyafter the premature atrial beat (demarcated with an arrow), initiating the short RP tachycardia. (B) Entrainment ofthe tachycardia demonstrating a V-A-V response, prolongation of the VA interval during entrainment compared totachycardia, a long PPI-TCL, and a fixed VA interval after entrainment. AV = atrioventricular; PPI = postpacinginterval; TCL = tachycardia cycle length; VA = ventriculoatrial.

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6. Michaud GF, Tada H, Chough S, Baker R, Wasmer K,Sticherling C, Oral H, et al. Differentiation of atypical atri-oventricularr node re-entrant from orthodromic reciprocatingtachycardia using a septal accessory pathway by the response

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7. Flectcher RD., Wish M., Cohen A. The use of the implanted pace-maker as an in vivo electrophysiology laboratory. J Electrophysiol1987; 1:425–433.

8. Jenkins NP, Bennet DH. Intermittent complete atrioventricularblock associated with typical atrioventricular nodal reentranttachycardia. Heart 1998; 80:418–419.

9. Dennis MJ, Sparks PB. Pacemaker mediated tachycardia as acomplication of the autointrinsic conduction search function.Pacing Clin Electrophysiol 2004; 27:824–826.

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