RV Pacing - How Low is Low Enough

It is widely accepted that long term RV apical pacing has detrimental effects on the myocardial function and, as a result, the clinical outlook for patients. RV apical pacing facilitates an unnatural and unfamiliar depolarisation pathway giving an electrophysiological left bundle branch block appearance on the surface ECG. It is this unusual pathway that allows for remodelling of the LV. Le Clercq et al 1 reported this remodelling as thinning of the areas of myocardium which were activated earlier than normal and a characteristic thickening of the areas which were activated later than normal. The clinical picture of such patients is one of reduced systolic function, increased hospital admissions, worsening of CHF and increased incidence of AF. It is widely accepted that haemodynamically significant intrinsic activation is the gold standard where possible in patients requiring permanent pacing.

The DAVID trial 2 was a landmark study that randomised ICD patients (no brady indication) to DDDR with a low rate limit of 70bpm or VVI pacing at 40bpm. It was predicted that the DDDR group would have improved haemodynamics due to the nature of dual chamber pacing and the AV synchrony; however, it was the DDDR group who had increased all cause mortality at the one year follow up. It was demonstrated that the poor performance of the DDDR group was related to the high percentage of RV pacing. Olshamsky et al 3 challenged these findings when he presented his findings of the INTRINSIC RV trial at the HRS meeting in 2006 when he claimed that the high rate of RV pacing was to blame and not the device itself. He hypothesised that by utilising algorithms to minimise RV pacing, dual chamber pacing would equal or better single chamber pacing. INTRINSIC RV looked at 1530 patients implanted with a dual chamber ICD, patients with very high pacing rates were excluded and a remaining 988 patients were then randomised to DDDR with an AV search hysteresis algorithm programmed on and the other group were programmed VVI 40bpm back up pacing. There was a definite trend in favouring the DDDR group and a trend towards superiority of this group, although the study design was not powered to detect superiority. From these results, we could surmise that DDDR pacing with an AV hysteresis algorithm to minimize RV pacing is an acceptable method of pacing 4 5

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The MOST study 6 in 2002 was a 6 year trial which compared VVIR with DDDR with an end point of non fatal stroke or death from any cause, the outcome was a significant reduction in hospitalizations in the DDDR group. Sweeny et al 7 used a study population extracted from this study to look at the effects of DDDR and VVIR pacing on heart failure hospitalization and AF. The results showed an obvious linear relationship between the percentage of V pace and the increased risk of AF and heart failure hospitalization. He revealed that the extent of increased risk of AF was 1% for each 1% increase in V pace. He also demonstrated that the risk of heart failure hospitalization increased 2.5 fold when ventricular pacing reached 80% or more. However, heart failure hospitalizations can be reduced to 2% by reducing pacing to less than 10%.

An interesting question then arises, should pacing therefore be as low as possible? Ad hoc analysis of the available data would suggest that too little pacing could also be detrimental and the lowest rates of death and hospitalisation appear in the 10 – 19% RV pacing group 4. It is vital to consider the patient when making assumptions regarding the necessity of pacing. For example, some patients with a definite pacing indication will require some degree of pacing, this is an inevitable situation in patients with symptomatic bradycardia. It would be unacceptable to assume that these patients would require the same degree of pacing minimization strategies as those with a pure ICD indication. It is also unlikely that in order to reduce the possible risk of heart failure and AF you would sacrifice the primary function of the pacemaker – to pace during episodes of symptomatic bradycardia, especially since this is the likely primary indication for the device. It would seem acceptable that in these patients that it is the haemodynamic significance of the electro-mechanical event that should dictate whether or not intrinsic or paced events are preferred.

The main aim would appear to be to programme an optimal AV delay to encourage appropriate and haemodynamically significant intrinsic ventricular depolarization rather than artificial paced depolarization.

The normal AV interval is 120 – 210 ms 8 with AVI (sensed) 30 – 50 ms shorter than AVI (paced). Von Knorre et al 9 examined this concept of programmable AV delays in DDD pacemakers with 200 patients using left atrial electrography, in an attempt to define a programmability standard. He found that in atrial sensed stimulation the optimal AV delay was between 40 – 205 ms and in atrial paced stimulation the optimal AV delay was between 85 – 245 ms

It could be proposed that programming a long AV delay will inevitably uncover some form of underlying intrinsic rhythm. This was investigated by Neilson et al10 who examined sick sinus syndrome patients with normal AV conduction who were randomized to AAIR and DDDR with a fixed long AV delay. Although these fixed AV delays were effective in 2/3 of patients, 1/3 of patients suffered sub optimal pacemaker function and were more at risk of pacemaker arrhythmias. Long AV delays can impede appropriate DDDR function such as delayed AF detection, impaired mode switching and susceptibility to Endless Loop Tachycardia. From a physiological standpoint AV delays that are too long can shorten filling time and therefore negatively impact on cardiac output. Conversely AV delays that are programmed too short will not allow for intrinsic rhythm and will inevitably give way to more pacing.

Optimization of the AV delay is a means of uncovering intrinsic rhythm which restores the hearts natural and effective depolarization pathways. Considering that a properly timed AV delay can contribute to between 13% and 40% of the cardiac output, it would seem that this is a worthwhile aspect of programming11. All devices should offer some kind of algorithm or programming option which allows for as much programmability of these parameters as possible in order to maximize the cardiac output and reduce the complications associated with RV pacing. It is also clear that there is no single answer to the difficulties that RV pacing imposes. Perhaps there is no magic number which pacing needs to fall below to ensure patients have a positive response to the device. Search hysteresis algorithms have the potential to adjust and respond to individual dynamic patients rhythms and continually self optimize in order to quickly react to any changes the patient may experience. With intelligent device programming it should be possible to limit the dreaded negative outcomes associated with RV apical pacing.

 

References

1. LeClercq C, Gras D, Le Helloco A, Nocil L , Haemodynamics importance of preserving the normal sequence of ventricular activation in permanent cardiac pacing, Am Heart J 1995 129 1133 - 1141

2. Sharma AD, Rizo-Patron C, Hallstrom AP, et al; DAVID Investigators. Percent right ventricular pacing predicts outcomes in the DAVID trial. Heart Rhythm. 2005;2:830-834

3. Olshansky B, Day JD, Moore S, et al. Is dual chamber programming inferior to single chamber programming in an implantable cardioverter defibrillator? Results of the INTRINSIC RV study. Program and abstracts from the Heart Rhythm Society 2006 Annual Scientific Sessions; May 17-20, 2006; Boston, Massachusetts

4. Olshansky B, Day J, McGuire M, Hahn S, Brown S, Lerew DR. Reduction of right ventricular pacing in patients with dual-chamber ICDs. Pacing Clin Electrophysiol. 2006;29:237-243

5. Gardiwal A, Hong Yu, OswaldH, Luesebrink U, Ludwig A, Pichlmaier AM, Drexler H, Klien G, Right ventricular pacing is an independent predictor for ventricular tachycardia / ventricular fibrillation occurrence and heart failure events in patients with an implantable cardioverter defibrillator, Europace 2008 10 (3) 358 -363

6. Link MS, Hellkamp AS, Estes III NAM, et al., for the MOST Study Investigators. High incidence of pacemaker syndrome in patients with sinus node dysfunction treated with ventricular-based pacing in the Mode Selection Trial (MOST). J Am Coll Cardiol 2004;43:2066–71.

7. 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. 2003;107:2932–2937

8. S. S. Barold Adverse effects of ventricular desynchronization induced by long-term right ventricular pacing J. Am. Coll. Cardiol., August 20, 2003; 42(4): 624 - 626.

9. Von Knorre GH, Ismer B, Voss W,Petzson M, Pulya K , What range of programmable AV delay is necessary in anti bradycardia DDD stimulation? Pacing Clin Electophysiol 1998 21 264 – 267

10. Neilson JC, Pederson AK, Morternson PT, Anderson HR, Programming a fixed AV delay is not effective in preventing ventricular pacing in patients with sick sinus syndrome, Europace 1999 1 113- 120

11. Ovsyscher I, Zimlichman R, Katz A, Bondy C, Furman S, Measurements of cardiac output by impendence cardiography in pacemaker patients at rest : effects of various atrioventricular delays, J Am Cardiol 1993 March1 21 (3) 761 – 767