Europace Advance Access originally published online on August 1, 2007
Europace 2007 9(9):798-804; doi:10.1093/europace/eum149
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PACING FOR ATRIAL FIBRILLATION
No evidence of automatic atrial overdrive pacing efficacy on reduction of paroxysmal atrial fibrillation
1 Department of Cardiology, St. Lucas Andreas Hospital, J.Toorpstraat 164, 1061AEAmsterdam, the Netherlands; 2 University of Utrecht, Utrecht, the Netherlands; 3 ZOL Campus St. Jan, Genk, Belgium; 4 Clinique du Sud Luxembourg, Arlon, Belgium; 5 St. Franciscus Gasthuis, Rotterdam, the Netherlands; 6 Turku University Central Hospital, Turku, Finland; 7 Amphia Hospital, Breda, the Netherlands; 8 Tartu University Hospital, Tartu, Finland; 9 North-Estonian Central Hospital, Tallinn, Estonia; 10 Tampere University Hospital, Tampere, Finland; 11 Middelheim Hospital, Antwerp, Belgium; 12 Centre Hospitalier Hutois, Huy, Belgium; 13 Queen Mary Hospital, Hong Kong, China
Manuscript submitted 12 June 2006. Accepted after revision 29 June 2007.
* Corresponding author. Tel: +31 20 510 8911.E-mail address: w.g.devoogt{at}planet.nl
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Abstract |
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Aims Paroxysmal atrial fibrillation (PAF) is frequently encountered in pacemaker patients, most commonly in sick sinus syndrome. The combination of site-specific pacing in conjunction with an overdrive algorithm combined with antiarrhythmic drugs on the incidence of PAF in patients with a conventional indication for pacing is unknown.
Methods and results Patients with pacemaker indication and PAF received a DDDR-pacemaker, which included an automatic atrial overdrive (AO) algorithm. The atrial lead was implanted in either the right atrial appendage (RAA) (n = 83) or the right low-atrial septum (LAS) (n = 94). The algorithm was switched on or off in a 3 month, single blind crossover design and antiarrhythmic drugs were kept stable. A control group of 96 patients (LAS, n = 14; RAA, n = 84) without PAF served as controls to assess any proarrhythmic effect of overdrive pacing. Atrial fibrillation (AF) burden defined as cumulative time in mode switch was not reduced during automatic AO from either the RAA or from the LAS. The reduction was not effective both for AF of short (<24 h) and long (
24 h) duration. There was no atrial proarrhythmia induced by the overdrive algorithm in the control group.
Conclusions We could not demonstrate a reduction of AF burden defined as cumulative time in AF by the AO algorithm, in patients who are paced for standard indications and PAF, neither from the RAA nor from the LAS.
Key Words: Paroxysmal atrial fibrillation, Atrial fibrillation, Pacing, Alternative site pacing, Atrial overdrive algorithm
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Introduction |
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Paroxysmal atrial fibrillation (PAF) is a common arrhythmia in patients undergoing permanent pacing, most common in sick sinus syndrome.1
–3 This unfavourable development can be impacted in a more favourable manner with chronic atrial pacing than with ventricular pacing.4–9 The proposed beneficial mechanisms include a reduction in the dispersion of atrial refractoriness that is a consequence of short-long atrial intervals, and secondly inhibition of atrial premature beats that are commonly initiating events for PAF and resulting also in shortening of post-extra systolic pauses. These measures can prevent and reduce the incidence of bradycardia-dependent atrial tachy-arrhythmias.10 Site-specific pacing has also been reported to have antiarrhythmic properties in comparison to pacing from the right atrial appendage (RAA). Implantation of the atrial lead in the low-right atrial septum (LAS) shortens the inter-atrial conduction time compared with pacing from the RAA,11,12 but data of this pacing method are conflicting.13 The increased homogeneity of atrial activation as well as repolarization is thought to be mechanisms by which atrial septal stimulation modifies the arrhythmogenic substrate resulting in prevention of PAF.14 In electrophysiological studies, atrial fibrillation (AF) was reproducibly induced with atrial extra stimuli delivered during RAA pacing, but not with LAS pacing applying identical critical coupling intervals.15
An automatic atrial overdrive (AO) pacing algorithm has recently been designed to reduce AF burden.16 A prospective study was performed to assess the usefulness of this algorithm to prevent and suppress AF episodes combined with antiarrhythmic drugs in patients requiring first implant of a pacemaker. Furthermore, the additional effect of RAA vs. LAS pacing was also investigated in this multicentre study.
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Methods |
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Study design
This was a multicentre, single-blinded crossover outcome study. Patients were recruited who had a conventional pacemaker indication and a history of PAF in the 6 months prior to implantation. All patients received a DDD(R) pacing system that incorporated an automatic AO algorithm (AF SuppressionTM, St. Jude Medical, Sylmar, CA, USA). The atrial lead was implanted in either the RAA or the LAS. Patients were randomized to a group where the AO algorithm was switched on for 3 months after randomization, followed by a period of 3 months with AO algorithm off. A reversed sequence was carried out in another randomized group. A group of patients who required pacing for standard indications, but who did not have documented episodes or a history of PAF served as control group to evaluate the potential proarrhythmic effect of the automatic AO algorithm.
Study endpoints
Primary: The effect of the AO algorithm switched on and off on (1) the cumulative mode switch duration (AF burden) and (2) the number of mode switches.
Secondary: (1) The effect on cumulative mode switch duration (AF burden) and mode switches in relation to RAA or LAS pacing with AO and (2) proarrhythmic effects when AO is enabled.
Inclusion criteria
Patients undergoing their first pacemaker implant for a conventional pacemaker indication and a history of PAF in the 6 months prior to the implant. Control group: patients with first pacemaker implant and conventional pacemaker indication without history of AF in the last 6 months before implantation.
Exclusion criteria
Patients who needed pacing, but had either persistent or permanent AF or a reversible cause of AF, and patients expected to not tolerate high pacing rates due to significant angina pectoris or NYHA class 3 or 4 heart failure.
Recruitment
The study was conducted according to the Declaration of Helsinki. Written informed consent was obtained before pacemaker implant as approved by local medical ethical committees at each participating hospital.
Randomization
Randomization to the AO algorithm occurred 6–10 weeks after implant to allow lead maturation and demonstration of stability while excluding implantation-related arrhythmias. During the initial 6–10-week period, the antiarrhythmic regimen was optimized. While this could be unique for each patient, once the formal randomization process was initiated, the pharmacologic regimen was kept stable. At randomization, the AO was either enabled or disabled in a randomized manner for a period of 3 months each utilizing a crossover design. Randomization was single-blinded. The site of atrial lead insertion was not randomized, but left to the discretion and skill of the implanting physician. Thus, the study was prospective but not randomized concerning the atrial implant site.
Pacing leads
Low-right atrial septum and RAA lead locations were confirmed using both fluoroscopy and a standard 12 lead ECG.17 A Tendril 1388T or 1488T bipolar active fixation lead (St. Jude Medical) was preferred on behalf of a short tip ring spacing. Tip ring spacing is 10 mm (1388T) or 13.8 mm (1488T). The right ventricular lead was inserted in the apex in all patients.
Pacemaker and programming
Either an Integrity AFx DRTM (model 5346) 96.9% or Identity DRTM (model 5376) 2.6% or a Trilogy DAO 0.5% pacemaker (St. Jude Medical) was implanted. Integrity, Identity and Trilogy pacemakers have an identical AO algorithm and identical automatic mode switch (AMS) features. Programmable parameters were standardized for the purpose of this study. The paced and sensed AV delays were 170 and 150 ms, respectively; the bipolar atrial sensitivity was set 0.5 mV. The post-ventricular atrial blanking (PVAB) was programmed to 125 ms or was adapted on an individual basis after specific assessment for the presence of a far-field R-wave if the interval from the ventricular stimulus to the far-field signal exceeded the minimum programmed PVAB interval. The AMS detection rate was set at 225 bpm. All other programmable parameters were maintained at the standard shipped settings.18
The AO algorithm pacing operates by incrementally increasing the atrial pacing rate upon detection of two intrinsic atrial events within any 16 consecutive cardiac cycles, increasing until no further atrial sensed events occur or until the maximum sensor rate is achieved. This pacing rate is maintained for a programmable duration following which it decreases beat-by-beat until the intrinsic atrial rate recurs, and is detected or the lower pacing rate or sensor rate is reached (Figure 1).
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Medication
Drug treatment was required to be stable during the study.
Atrial fibrillation burden
This parameter was calculated by mode switch (MS) duration as the time between visits minus the total sampled time (obtained from the printouts). The reason for this approach is that the total sampled time mentioned on the printouts is the time not in MS. AF burden is expressed as percentage of time in MS (Figure 2).
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Data analysis
For within-group comparisons the 2-sided paired t-test was used, for between group comparisons the 2-sided unpaired t-test was used for statistical analyses. In case data was not normally distributed, loge-transformations were performed and in case these did not hold, non-parametric techniques were used (i.e. Wilcoxon–Mann–Whitney test and Wilcoxon-signed-rank test). Summary data are expressed as mean ± SD or numbers and percentages of patients.
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Results |
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Study population
From February 2000 to December 2002, 280 patients were enrolled. Forty-seven patients did not have their three visits. However, there were more patients excluded from the per-protocol (PP) analysis (Figure 3).
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The dropouts are presented in Figure 3 with respect to the different groups of patients and the time when the dropout occurred. Out of the 280 patients enrolled in the study, 209 were fit for the PP population. Taking out the replacements, a total of 194 patients are left in the PP population. From the 194 patients, the AF burden calculation was possible for 184 patients (due to missing printouts or missing sections in the pacemaker printouts in 10 patients).
Demographic and clinical baseline characteristics of these 184 patients are depicted in Table 1. The number of patients with exclusive sinus node disease and the number of patients with a history of paroxysmal AF and a brady tachycardia syndrome was clearly larger than that of the control group (P = 0.01).
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Atrial pacing leads
A Tendril 1388T lead was used in 23.7%, a Tendril 1488T lead in 54.1% and a Membrane EX 1474T in 11.9%, a Membrane EX 1470 in 5,7% and other leads in <5%.
Medication
The use of amiodarone, coumadine and sotalol was significantly higher in the patient group with a history of AF compared with the control group. Amiodarone, P = 0.0201 (month 3) and P = 0.0056 (month 6); coumadine, P = 0.0201 (month 3) and P = 0.0193 (month 6); Sotalol, P < 0.0001 (months 3 and 6). No significant changes of antiarrhythmic drugs were observed during the study (Table 2).
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Atrial fibrillation outcome
Mode switch
In the RAA group, AO did not diminish the number of AMS episodes. When AO was enabled, the mean ( ± SD) number of MS occurrences was 230 ( ± 790). When AO was disabled, the mean ( ± SD) number of MS occurrences was 1383 ( ± 9666) (P = 0.4132). Due to the fact that the variation of the data was enormous and no statistical difference was found. In the LAS pacing group, the enabled AO algorithm was associated with 1567 ± 6074 episodes and 1721 ( ± 5899) episodes when AO was disabled (ns). In the control group, the incidence of AMS episodes was 602 ( ± 2090) with the AO algorithm enabled while there were 1218 ( ± 7413) episodes with AO disabled (ns).
Atrial fibrillation burden
AF burden was not reduced with the AO algorithm enabled neither in the RAA or LAS group with a history of AF, nor in the control group (Figure 4).
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We further classified the AF burden according to the duration of AMS longer and shorter than 24 h (short AF episodes). The results show no reduction of AF burden for both long and short episodes with AO in both lead positions. Furthermore, the trend towards increased AF burden in time did not reach a significant value (P = 0.1168). This was recorded in all groups. No relative reduction in AF progression was seen in any group attributable to the AO algorithm.
The AF burden in the control group was small and was not changed by the AO algorithm, 1.6 ( ± 2.2%) (median=1.3%) without and 4.2 ( ± 15.4%) (median=1.2%) with AO (P = ns), effectively excluding a proarrhythmic effect.
Pacing incidence with atrial overdrive
When the AO algorithm was enabled, the prevalence of atrial pacing in all groups exceeded 90% pacing. Enabling of the algorithm was also accompanied by an increase in ventricular pacing (Table 3).
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Discussion |
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Key results
In patients who required pacing for standard indications and had documented paroxysmal AF prior to device implantation, the AO algorithm did not reduce the AF burden regardless of the site of atrial stimulation. There was no benefit with AF burden reduction with LAS pacing compared with RAA pacing. This negative result was achieved in conjunction with stable antiarrhythmic drug therapy in these patients. Although the AO algorithm resulted in a higher cumulative percentage of atrial (49 ± 33 to 93 ± 7%) and ventricular stimulation (56 ± 39 to 64 ± 37%), this does not appear to be proarrhythmic as demonstrated by the findings of the control group. No significant change of mode switch episodes with AO pacing was observed.
A previous study16 using the AO algorithm has shown the efficacy of AF burden reduction with RAA stimulation. However, only symptomatic AF was measured using event recording, and asymptomatic episodes of AF were not registered. Asymptomatic AF occurs even more commonly than episodes of symptomatic AF19 and the use of the antiarrhythmic medications might affect the symptomatology without changing the actual AF burden.
In our study, we could neither demonstrate a reduction of asymptomatic AF burden after switching on the AO algorithm in a group of patient with symptomatic AF before the implantation, nor the difference of reduction of AF burden between long (>24 h) and short (<24 h) periods of AF.
Atrial overdrive algorithm
This pacing algorithm was designed to increase the atrial pacing rate in response to intrinsic atrial activity (sinus rhythm and atrial premature beats). This can result in suppression and/or prevention of atrial ectopy and modify favourably the arrhythmogenic substrate. Previous studies explored the efficacy of the concept of automatic AO by showing a reduction of atrial arrhythmias.13,16 We could not confirm these results.
The site of atrial stimulation
Previous studies have suggested that an increase in the AF free interval by multi-site AO pacing in patients on medication.20–22 This however demands a more complicated implantation technique and adaptation to the pacemaker system than single-site atrial pacing. These studies did not restrict the use of antiarrhythmic medication, which continued to be adjusted during follow up. Single-site high-atrial septum pacing was described as an alternative site to reduce depolarization and repolarization dispersion to prevent AF.12 In this study, however AF burden was not measured and medication not optimized. Other studies performed pacing in the superior part of the atrial septum as an alternative site in the atrial septum for successful shortening of total atrial activation time.12 The ability to induce PAF when pacing from the RAA has been ascribed to the non-uniform anisotropic characteristics of the posterior triangle of Koch.23 Pacing in the right LAS at the triangle of Koch has been proposed to be an attractive single-site method to prevent and suppress AF.11,24 In our study, AO was ineffective in association with pacing from either the RAA or the LAS and there appeared to be no incremental benefit when combining the algorithm with LAS pacing. The results were achieved in patients on antiarrhythmic medications. Using a different overdrive algorithm, another recent study did not find any change in overall AF burden.13 However during subgroup analysis, only patients paced in the septal region (various positions) were associated with a trend to AF burden suppression. The difference observed on the overall efficacy may be related to the patient population, cumulative percentage of atrial pacing, concomitant antiarrhythmic agents and the AO algorithm used.
Atrial fibrillation burden and automatic mode switch
For a prospective study evaluating a preventive algorithm, the ideal end-point would be the actual number of AF episodes rather than the cumulative duration of these episodes. The actual number of AMS episodes was large with a large standard deviation. As we have shown on a subsequent study involving 57 patients who were subjected to 7 days of continuous Holter monitoring, the cumulative duration of AMS correlated with the cumulative duration of AF documented on the Holter monitor recordings. However, the number of episodes reported by the AMS histogram did not correlate with the number of AMS episodes documented on the Holter study being far larger. This discrepancy was attributed to signal drop-out causing the pulse generator to exit AMS and then re-engage AMS on multiple occasions within a single AF episode.25
In this study, the activation of AO was not associated with significant change in AF burden when burden was defined as cumulative duration. In addition, there was no trend in the reduction in the number of mode switch episodes although on further analysis, this was shown to be an unreliable marker. Thus, although AF burden may be a better indicator for reduction of AF than the number of onset of AMS because AF burden is less susceptible to the short periods of AF under-sensing by the pacemaker during continuous AF, it is not an appropriate marker for the evaluation of a preventive algorithm. The relative insensitive atrial sensitivity setting of 0.5 mV (see Methods) is believed to be responsible for a higher number of AMS due to under sensing during continuous AF. Further improvements in atrial sensing with either new lead configurations or with higher sensitivity settings are anticipated to mitigate the observed unreliability of AMS for the amount of AF episodes.26
Control group
The percentage of mode switch in the control group was minimal although the actual reported numbers of AMS was high, which further raising questions about the utility of the number of AMS episodes with these devices as programmed for this study and suggesting that in addition to intermittent undersensing of true arrhythmias, there may be false mode switch episodes as well even though none lasted for a protracted period of time. No significant increase occurred when the AO algorithm was enabled. The increase in atrial pacing from 40 ± 33% to 92 ± 7% did not have any atrial proarrhythmic effects in the control group.
Study limitations
The follow-up period was relatively short and future studies may be needed to clarify the long-term effects of this hybrid treatment. The trend to an increase in AF burden in a short period of time might have influenced the results. In common with previous studies,13,27 there was a obvious drop-out, which clarified why at the end of the study the follow-up data were available in only 66% of the randomized patients. Although the AO algorithm was effective in maintaining 
93% stimulation in the atrium, the amount of time paced in the right ventricle during AO increased as well which may have caused deleterious effects on AF incidence and heart failure, as are reported after the execution of the study.6,28 It may thus be appropriate to programme a longer AV interval and/or AV hysteresis to reduce the frequency of ventricular pacing.29 At the time the study was designed (1999), sample size was calculated on the base of a 45% reduction in mode switches. Mode switches however did not prove to be a reliable endpoint as observed in later studies and published in 2006.25 Reduction of electrocardiographic total duration of the AF burden turned out to be a more reliable parameter to quantify AF burden instead of the number of onsets of mode switch. The sample size calculation as presented by Padeletti et al.30 and Warman et al.31 was not known at the time of study design. The estimation of the sample size of our study therefore has limitations.
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Conclusion |
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We could not demonstrate a reduction in AF burden defined as cumulative time in AF by the AO algorithm, in patients who are paced for standard indications and PAF, neither from the RAA nor from the LAS.
This may reflect the study sample size under powerment and limitation of the diagnostic endpoints, which were all derived from the implanted devices and/or the current programming of the implanted devices and this study should be repeated taking these factors into account.
On the basis of the control group, there was no evidence for a proarrhythmic effect of the algorithm in a group of patients who may not have been susceptible to PAF.
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Appendix |
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Investigators participated in this study
Michael Anelli-Monti, LKH—University of Klinikum, Graz, Austria; Philip De Vusser, ZOL Campus St. Jan, Genk, Belgiuml; Dia El Allaf, Centre Hospitalier Hutois, Huy, Belgium; Peter Geelen, O.L. Vrouw Ziekenhuis, Aalst, Belgium; Georges H. Mairesse, Clinique du Sud Luxembourg, Arlon, Belgium; Dirk Stockman, Middelheim Ziekenhuis, Antwerp, Belgium; Roland Van Acker, St Augustinus Kliniek, Wilrijk, Belgium; Chu-Pak Lau, Queen Mary Hospital, Hong Kong, China; Hung-Fat Tse, Queen Mary Hospital Hong Kong, China; Indrek Roose, Tartu University Hospital, Tartu, Estonia; Hasso Uuetoa, North-Estonian Central Hospital, Tallinn, Estonia; Jüri Voitk, North-Estonian Central Hospital, Tallinn, Estonia; Liisa Hämäläinen, North-Karelia Central Hospital, Joensuu, Finland; Juhani Koistinen, Turku University Hospital, Turku, Finland; Pekka Raatikainen, Oulu University Hospital, Oulu, Finland; Sinikka Yli-Mäyry, Tampere University Hospital, Tampere, Finland; Nico Breuls, Merwedeziekenhuis (A. Schweizer) Dordrecht, the Netherlands; Willem de Voogt, St Lucas Andreas Ziekenhuis, Amsterdam, the Netherlands; Hans Hartog, Diakonessenhuis, Utrecht, the Netherlands; Mike Scheffer, Sint Clara Ziekenhuis, Rotterdam, the Netherlands; Juta Schroeder-Tanka, St Lucas Andreas Ziekenhuis, Amsterdam, the Netherlands;Pieter Stolwijk, Ziekenhuis Rijnstate, Arnhem, the Netherlands; Alfons Timmermans, Medisch Spectrum Twente, Enschede, the Netherlands; Paul van den Bergh, Streekziekenhuis, Zevenaar, the etherlands; Arjan van den Bos, Amphia Ziekenhuis, Breda, the Netherlands; Rob van Mechelen, St Franciscus Gasthuis, Rotterdam, the Netherlands; Frank van Rey, Sint Maartens Gasthuis, Venlo, the Netherlands; Eric Viergever, Groene Hart Ziekenhuis, Gouda, the Netherlands; Pär-Lennart Ågren, Falu Lasarett Hospital, Falun, Sweden.
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Acknowledgements |
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The study was supported by an unrestricted grant from St. Jude medical.
Conflict of interest: W.D.V. has received speaker fees from Vitatron, Guidant and St Jude Medical and consultancy fees from St Jude Medical during the study period. G.H.M. has received speaker fees from St Jude Medical during the study period.
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References |
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