Medtronic CRM Product Performance Report

Interactions between Cardiac Pacing and Ventricular Arrhythmia Initiation

Purpose of this Information

This article is intended to provide information for consideration when programming pacemaker operation in ICDs and pacemakers.

Background

Right ventricular pacing has been associated with increased risk of appropriate therapy for ventricular tachycardia (VT) and ventricular fibrillation (VF) in ICD patients.1 Abrupt changes in ventricular cycle lengths (short-long-short, S-L-S) may precede initiation of VT/VF in some instances. S-L-S sequences may be permitted in all forms of cardiac pacing. The pause lengths depend upon pacing mode and lower rate programming.2-4 Because pauses may be associated with VT/VF initiation, pause suppression algorithms have been developed in ICDs. Although pause suppression may have utility in specific patients with repolarization abnormalities and pause dependent VT, it has not been shown to reduce arrhythmia incidence in the general ICD population.5 Conversely, S-L-S sequences may occur with ventricular pacing in a variety of ways, including atrial tracking of premature atrial contractions (PACs) or by terminating pauses with ventricular paced beats.6 In some patients, the ectopic depolarization pattern of a ventricular paced beat may be pro-arrhythmic, independent of pause timing. These observations have further enforced the desire to reduce unnecessary ventricular pacing.

Clinical Trial Observations

Medtronic-sponsored clinical trials were retrospectively analyzed to further understand pause-mediated (i.e., S-L-S) scenarios prior to VT/VF. S-L-S onset scenarios were observed in a minority of patients in all pacing modes. Pacemaker interactions prior to VT/VF are dependent on patient conditions, as well as the technical aspects of pacing operation (i.e., pacing mode, lower rate and AV interval). Because a very low frequency of ventricular pacing is observed during Managed Ventricular Pacing (MVP)7-9 or VVI 40 pacing modes,10 the long interval tended to terminate with a ventricular sense. In DDD mode, the long interval tended to be terminated by a ventricular pace. Long intervals of > 1000 ms prior to VT/VF were rare in MVP mode. In these analyses, only an association between cardiac pacing and VT/VF initiation can be observed, causality cannot be established. The ongoing MVP (Managed Ventricular Pacing vs. VVI 40 Pacing) Trial, a 2-year, 1000-patient prospective, randomized trial in ICD patients may offer more insight into the frequency of VT/VF across pacing modes.11

Pacemaker Patients

In pacemaker patients, ventricular pacing has been associated with higher incidence of AT/AF and heart failure hospitalization.12,13 MVP provides atrial rate support while dramatically reducing ventricular pacing in patients with sinus node dysfunction and transient AV block.9 However, as stated in Medtronic reference manuals, depending upon the patient’s intrinsic rhythm and conduction, MVP may allow ventricular cycle variation and occasional pauses of up to twice the lower rate.

DDD pacing with long AV intervals may reduce ventricular pacing and may decrease the potential length of pauses compared to MVP. However, DDD with long AV interval programming does not appear to be as effective as AAI-based pacing modes at reducing ventricular pacing,13,14 may lead to endless loop tachycardia,14,15 and does not completely eliminate pauses. Also, in DDD mode, a higher programmed lower rate or activation of rate response can lead to an increase in AV conduction times and a higher percentage of ventricular pacing. The potential benefits of reducing ventricular pacing must be weighed against the potential for longer ventricular pauses. Therefore, careful consideration should be given to pacemaker mode and lower rate programming, particularly in the setting of frequent AV block and repolarization abnormalities due to congenital Long QT, electrolyte imbalances, and some medications which prolong QT.

Conclusion

Pacemaker operation may interact with VT/VF initiation in a variety of ways. The patient’s heart failure status, arrhythmia substrate, medications, and the relative importance of maintaining ventricular synchrony vs. ensuring ventricular rate support must be weighed when choosing optimal hardware (ICD vs. pacemaker) and pacemaker programming (pacing mode, lower rate, etc.).

References

  1. Steinberg JS, Fischer A, Wang P, et al. The clinical implications of cumulative right
    ventricular pacing in the Multicenter Automatic Defibrillator Trial II. J Cardiovasc
    Electrophysiol.     April 2005;16(4):359-365.
  2. Pinski SL, Eguia LE, Trohman RG. What is the minimal pacing rate that prevents Torsades
    de Pointes? Insights from patients with permanent pacemakers. PACE. November 2002;
    25(11):1612–1615.
  3. Goldman DS, Levine PA. Pacemaker-mediated polymorphic ventricular tachycardia. PACE.
    October 1998; 21(10):1993–1995.
  4. Gray CJ, Basta M, Sapp JL, Parkash R, Gardner MJ. Inappropriate application of managed
    ventricular pacing in a patient with Brugada syndrome leading to polymorphic ventricular
    tachycardia, ventricular fibrillation and implantable cardioverter debrillator shocks. Heart
    Rhythm    . 2006, Abstract P1-89.
  5. Friedman PA, Jalal S, Kaufman S, et al. Effects of a rate smoothing algorithm for prevention
    of ventricular arrhythmias: results of the Ventricular Arrhythmia Suppression Trial
    (VAST). Heart Rhythm. May 2006;3(5):573-580.
  6. Himmrich E, Przibille O, Zellerhoff C, et al. Proarrhythmic effect of pacemaker
    stimulation in patients with implanted cardioverter-defibrillators. Circulation.
    July 15, 2003;108(2):192-197.
  7. Sweeney MO, Ellenbogen KA, Casavant D, et al. Multicenter, prospective, randomized trial
    of a new atrial-based Managed Ventricular Pacing Mode (MVP) in dual chamber ICDs. J
    Cardiovasc Electrophysiol    . 2005:16:1-7.
  8. Sweeney MO, Shea JB, Fox V, et al. Randomized pilot study of a new atrial-based minimal
    ventricular pacing mode in dual-chamber implantable cardioverter-defibrillators. Heart
    Rhythm    . July 2004;1(2):160-167.
  9. Gillis AM, Purerfellner H, Israel CW, et al. Reducing unnecessary right ventricular pacing
    with the managed ventricular pacing mode in patients with sinus node disease and AV
    block. PACE. July 2006; 29(7):697–705.
  10. The DAVID Trial Investigators. Dual-chamber pacing or ventricular backup pacing
    in patients with an implantable defibrillator: the Dual Chamber and VVI Implantable
    Defibrillator (DAVID) Trial. JAMA. December 25, 2002;288(24):3115-3123.
  11. Sweeney MO, Ellenbogen KA, Whellan D, et al. The Managed Ventricular Pacing vs.
    VVI 40 Pacing (MVP) Trial: Clinical Background, Rationale, Design and Implementation.
    J Cardiovasc Electrophysiol. 2006 (In Press).
  12. Sweeney MO, Hellkamp AS, Ellenbogen KA, et al. Adverse effect of ventricular pacing on
    heart failure and atrial fibrillation among patients with normal baseline QRS duration
    in a clinical trial of pacemaker therapy for sinus node dysfunction. Circulation. June 17,
    2003;107(23):2932-2937.
  13. Nielsen JC, Kristensen L, Andersen HR, et al. A randomized comparison of atrial and
    dual-chamber pacing in 177 consecutive patients with sick sinus syndrome:
    echocardiographic and clinical outcome. J Am Coll Cardiol. August 20, 2003;42(4):614-623.
  14. Nielsen JC, Pedersen AK, Mortensen PT, Andersen HR. Programming a fixed long
    atrioventricular delay is not effective in preventing ventricular pacing in patients with
    sick sinus syndrome. Europace. April 1999; 1(2):113–120.
  15. Dennis MJ, Sparks PB. Pacemaker mediated tachycardia as a complication of the
    autointrinsic conduction search function. PACE. June 2004;27(6 Pt 1):824-826.