Europace Advance Access originally published online on June 11, 2007
Europace 2007 9(9):790-797; doi:10.1093/europace/eum111
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
PACING FOR ATRIAL FIBRILLATION
The use of atrial overdrive and ventricular rate stabilization pacing algorithms for the prevention and treatment of paroxysmal atrial fibrillation: the Pacemaker Atrial Fibrillation Suppression (PAFS) study
1 Cardiology Department, Eastbourne District General Hospital, East Sussex NHS Trust, Kings Drive, Eastbourne BN21 2UD, UK; 2 Department of Clinical Epidemiology and Biostatistics, University of Birmingham, Birmingham, UK; 3 Cardiology Department, William Harvey Hospital, Ashford, UK; 4 Cardiology Department, Royal Sussex County Hospital, Brighton, UK; 5 Cardiology Department, Ashford and St Peters Hospital, Chertsey, UK
Manuscript submitted 5 January 2007. Accepted after revision 29 April 2007.
* Corresponding author. Tel: +44 1323 435869; fax: +44 1323 435821. E-mail address: neil.sulke{at}esht.nhs.uk
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionLimitationsConclusionAcknowledgementsReferences |
|---|
Aims The PAFS study is a randomized, multicentre investigation of the effects of third generation anti-atrial fibrillation pacemaker algorithms in patients with paroxysmal atrial fibrillation (PAF).
Methods and results 182 patients (72 ± 9 years, 55% male) with at least three symptomatic episodes of PAF within prior 3 months resistant to two anti-arrhythmics were enrolled. A pacemaker-derived atrial fibrillation (AF) burden of 1–50% was required in the initial induction phase. Seventy-nine patients fulfilled these criteria and were randomized to four, month-long phases in a crossover design. Algorithm phases were ‘rate soothing’ on, ‘ventricular rate stabilization’ on, and ‘All on’, which included these two algorithms plus post-AF response. The algorithm phases were compared to ‘All off’ dual chamber universal mode (DDD 60) for the analysis. Forty-two percent of patients enrolled in the monitoring phase had no AF. The percentage of AF induced by premature atrial contractions (PACs) was significantly reduced by rate soothing from 25 to 17% (P < 0.05). There was no significant change in AF burden, AF episode number, quality of life, or symptoms with any algorithm (P = ns).
Conclusion The rate-soothing algorithm by atrial overdrive pacing reduced PAC-initiated PAF. However, there was no overall change in AF burden, PAF episodes, patient symptoms, or quality of life. Forty-two percent of PAF patients did not show any AF after enrolment, suggesting that bradycardia pacing alone eliminates AF.
Key Words: Paroxysmal atrial fibrillation, Atrial fibrillation, Premature atrial contraction, Detailed onset report, Far-field R-wave
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionAcknowledgementsReferences |
|---|
Atrial-based pacing has been shown to reduce the incidence of atrial fibrillation (AF) when compared with ventricular-based pacing in patients with sick sinus syndrome and AV block.1
–5 This could be due to ventricular pacing inducing or perpetuating AF whilst atrial pacing reduces AF.6–8 These observations led to the development of physiologic pacemakers with specific algorithms designed to deliver increased atrial and reduced ventricular pacing.
Atrial pacing may be beneficial by reducing temporal dispersion of atrial refractoriness associated with bradycardia9 and overdrive suppression of premature atrial contractions (PACs).10–12 Atrial overdrive-pacing algorithms can broadly be grouped as either continuous or triggered, the latter being initiated by an event such as a PAC or termination of an AF episode.13 Some studies assessing the therapeutic benefit of anti-AF algorithms have provided neutral results (Camm et al., personal communication).14–16 However, ADOPT-A, PAF-PACE, and a study using closed loop stimulation all showed significant benefit.17–19
Ventricular pacing during AF has been shown to regularize the ventricular rhythm.20 The RASTAF II study demonstrated that ventricular rate stabilization reduced ventricular rate irregularity, improved patient preference, and hall-walk distance.21 Although initial investigation of this therapy showed promise, the AF SYMPTOMS study did not detect any symptomatic or functional benefit.22
The present study was designed to evaluate continuous atrial overdrive, post-AF response, and ventricular rate regularization pacing algorithms both separately and in combination, with monitoring of these effects by sophisticated Holter functions incorporated into the pacemaker. Patients with and without a conventional bradycardia indication for pacing were assessed. The ventricular rate stabilization algorithm was designed for symptom control, whereas atrial overdrive and post-AF response were designed to prevent AF occurrence.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionAcknowledgementsReferences |
|---|
Patient selection and study protocol
The study was approved by the Local Research Ethics Committee of participating centres. The trial was conducted at four centres in the United Kingdom in compliance with the Declaration of Helsinki. Patients were enrolled after obtaining written informed consent between November 2002 and December 2004. Enrolment could be performed before or after pacemaker implantation according to the criteria below.
Patients were implanted with Vitatron Selection 9000 and later Vitatron T70 dual chamber universal mode with rate response (DDDRP) pacemakers if they had at least three episodes of symptomatic AF in the prior 3 months, had surface ECG documentation of at least one episode of atrial fibrillation within the past year, and were refractory to at least two anti-arrhythmic drugs. Exclusion criteria were permanent AF, unstable angina, recent myocardial infarction or thoracic surgery, AF due to a reversible cause, AV nodal ablation, congestive heart failure New York Heart Association class III and IV, and pregnancy.
Six weeks after implantation patients were enrolled in the induction phase of the study. Patients were programmed to DDD(R) 50 and followed up after 4 weeks. If they had a device Holter-derived AF burden of between 1 and 50%, they fulfilled criteria for study inclusion and were then randomized. If patients did not meet this criterion they underwent a single reinduction period lasting 4 weeks with appropriate changes to their anti-arrhythmic medication (i.e. stopping anti-arrhythmic medication if AF burden <1% or addition of medication if burden >50%). The same criterion was again used for study randomization. Following randomization no change in medication was permitted. The study flow chart is shown in Fig. 1.
|
Randomized patients were then followed up at 4-week intervals after each of four study phases in a randomly ordered crossover design. Devices were programmed to DDD(R) 60 plus the specified algorithm for each of the four study phases. Program 1 was rate soothing on (RS on), program 2 was ventricular rate stabilization on (VRS on), program 3 was RS, VRS, and post-AF response on (All on), and program 4 was all algorithms off (All off). Patients were required to be in sinus rhythm at the start of each of these four study phases and cardioversion was undertaken as required. Drug therapy was not altered following randomization. At each follow-up visit, pacemaker data was retrieved and saved to diskette. Additionally, at each study follow-up visit, patients were required to complete a symptom diary for the entirety of the study phase, a Short Form-36 questionnaire, a Visual Analogue Scale questionnaire, and a Specific Symptom Frequency Score questionnaire.
Power calculation
It was assumed that at least a 20% change in AF burden was required for it to be clinically meaningful.23 In order to detect this change with a ß two-tailed power of 80%, a sample size of 73 patients was necessary based on findings from the AF therapy study (AFT) (Camm et al., personal communication).
Statistical analyses
Descriptive data were described using standard methods. The primary endpoint was a reduction in AF burden. Programs 1–3 were compared to program 4 (All off) for the statistical analyses. The principal statistical analyses were conducted using repeated measures analysis with patients defined as the subjects, in SAS Proc Mixed (version 9.12, SAS Institute, Cary NC). All measures are defined with 95% confidence intervals. A P-value, if stated, of less than 0.05 was considered significant. Additional statistical models were undertaken to examine the pre-specified potential confounding influence of incorrect sensing on the primary outcome. For binomial outcomes, analogous models were undertaken using non-linear mixed models, with subjects defined as random effects, in SAS NLMIXED.
Secondary endpoints (objective) were AF episodes per day, PACs per day, % atrial pacing, % ventricular pacing, and AF onset mechanism. Secondary endpoints (subjective) included symptom and quality-of-life questionnaire analyses.
Evaluated pacing algorithms
Rate soothing is a dynamic continuous atrial overdrive algorithm designed to pace the atrium at a rate that is just above the intrinsic sinus rate that should be imperceptible to the patient. The maximum atrial overdrive rate is determined by the programmable maximum therapy rate. On detection of an intrinsic atrial depolarization, the pacing rate is increased to 3 beats/min above this rate and is gradually reduced until such time as either the lower rate limit or a further intrinsic atrial signal is detected at the programmable AF deceleration rate.13
Post-AF response is an algorithm designed specifically to suppress early recurrence of atrial fibrillation. After the termination of an AF episode the algorithm is activated and paces the atrium at 80 bpm for up to 600 beats and then slows (by Flywheel) until the lower rate limit or an intrinsic atrial signal is detected at the programmable AF deceleration rate.13
Ventricular rate stabilization aims to reduce the symptoms of conducted AF by reducing ventricular irregularity. The algorithm stabilizes the ventricular rate during AF by initially pacing the ventricle at just below the mean ventricular rate. The pacing rate then increases further after every sensed ventricular event up to a programmable maximum therapy rate. When there are no sensed ventricular events, the pacing rate is lowered until either the lower rate limit or a further intrinsic ventricular signal is detected. After AF termination the pacemaker reduces the dual-chamber pacing rate at the programmable AF deceleration rate from the mean ventricular rate during AF or the maximum therapy rate down to either the lower rate limit or intrinsic atrial rate.
The maximum therapy rate prevents atrial or ventricular pacing above a certain rate for both the RS and VRS algorithms. This was programmed to 100 bpm for all participants. The AF deceleration rate determines the deceleration slope of the pacing rate of all the algorithms used and was set to ‘medium’ for all patients. The time taken for the pacing rate to reduce from 120 to 100 bpm at this setting is 90 s.
Device-derived Holter data
Both the Selection 9000 and T70 pacemakers allow near identical programmable AF detection and termination criteria. The Holters in these devices are extremely comprehensive and have been shown to be up to 100% specific and sensitive for AF burden measurement using 0.5 mV atrial sensitivity programming.24,25 Study classification of an AF episode onset occurred if the atrial rate was above 200 bpm for six ventricular beats or 5 s for the Selection 9000 and T70, respectively. Classification of an AF episode termination occurred if the atrial rate was below 200 bpm for 10 ventricular beats or below 180 bpm for 10 s for the Selection 9000 and T70, respectively.26,27 Device Holters stored the AF burden, total number of AF episodes, and the total number of PACs. AF burden was defined as percentage of total follow-up time with device-derived Holter confirmed AF. In addition, the device stored detailed onset reports (DORs) that allowed analysis of sensing and the AF onset mechanism.28 The DOR provides marker annotation (and electrograms in the T70 device) surrounding the onset of the AF episode. The DOR also provided data on the rate and PAC trend up to 5 min before the AF onset of each episode. Selection 9000 and T70 devices were programmed to store 12 (first 3 and last 9 episodes) and 15 (first 4 and last 11 episodes) per follow up, respectively. The device counters store counts for all atrial and ventricular events allowing for detailed analysis of atrial and ventricular pacing.
Device programming
Devices were programmed to DDD 60 bpm for each of the four study phases. Patients with symptomatic chronotropic incompetence were programmed to a rate responsive setting at the discretion of the local investigator. To maximize atrial sensing the post-ventricular atrial blanking period was set to the minimum value of 50 ms and the sensitivity was set to 0.5 mV. The AV delay was programmed as long as possible in all patients to avoid ventricular pacing. During the induction phases, adjustments to these pre-specified parameters were allowed if required to improve atrial sensing. AF undersensing may be due to either lack of sensitivity or due to blanking of atrial signals. AF oversensing is typically due to far-field R-wave (FFRW) sensing in the atrial channel. Sensing abnormalities were evaluated using the DORs. Once randomized, no basic programming changes were allowed.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionAcknowledgementsReferences |
|---|
A total of 182 patients (86 female) with a mean age of 72.6 ± 9.4 years were enrolled in this study and were entered into the induction phase. Of these, 79 had an AF burden of 1–50% and completed all four study phases and were included in the analysis. Nine patients required a second induction for study entry. Seventy-nine had an AF burden of less than 1% and 18 had an AF burden greater than 50% excluding them from randomization. Eight patients' data were excluded due to protocol violation or death not related to the studied devices following randomization.
The baseline characteristics of patients with an AF burden of <1, 1–50, and >50% are given in Table 1. Objective outcome data is listed in Table 2. The programmed atrial sensitivity was 0.49 ± 0.13 mV, the atrial blanking period was 55.1 ± 20.0 ms, and the AV delay was 232 ± 40 ms.
|
|
Primary endpoint
Mean AF burden was 11.6% in the control phase, 13.1% with ‘All on’, 11.3% with ‘RS on’, and 10.9% with ‘VRS on’. These differences were not significant compared with the control phase ‘All off’. The median AF burden was 3.7% (0.4–15.8) across the trial. Sub-group analysis of patients according to whether they had a conventional bradycardia pacing indication or not did not find any significant beneficial or detrimental effect on AF burden.
Secondary endpoints (objective)
Overall atrial-pacing percentage was 41.1% in the control phase, 82.2% with ‘All on’, 81.7% with ‘RS on’, and 44.7% with ‘VRS on’. The increase in atrial pacing was significantly greater in both the ‘All on’ and ‘RS on’ phases (P < 0.0001).
Overall cumulative ventricular-pacing percentage was 50.0% in the control phase, 62.1% with ‘All on’, 53.2% with ‘RS on’, and 59.1% with ‘VRS on’. The increase in ventricular pacing was significantly greater in both the ‘All on’ and ‘VRS on’ phases (P < 0.0001). Mean cumulative ventricular pacing during sinus rhythm was 56.5% in the control phase, 60.4% with ‘All on’, 59.8% with ‘RS on’, and 47.6% with ‘VRS on’. These differences were not significant, confirming that the VRS algorithm was increasing ventricular pacing significantly (P < 0.0001) during AF episodes only.
Mean number of AF episodes per day was 10.1 in the control phase, 12.2 with ‘All on’, 9.4 with ‘RS on’, and 16.0 with ‘VRS on’. These data were not significantly different. The mean number of PACs per day was 657.8 in the control phase, 613.6 with ‘All on’, 458.9 with ‘RS on’, and 627.5 with ‘VRS on’. There was a non-significant trend towards reduced numbers of PACs per day with the RS algorithm enabled (P = 0.08). The percentage of AF onsets initiated by PACs showed a significant reduction with RS algorithm enabled, during both the ‘RS on’ phase (P < 0.05) and during the ‘All on’ phase (P < 0.01) (Table 3).
|
Secondary endpoints (subjective)
There was no symptom frequency or quality of life (QOL) benefit shown by any algorithm (Fig. 2 A–C). Examination of these data showed that the study was able to detect a 5% relative change within the QOL instruments compared to the control phase. With ‘RS on’ there was a modestly significant reduction (P = 0.03) in the Mental Health subscale of the Short Form-36 questionnaire, however, given the number of comparisons, the neutral primary outcome and the neutral overall difference in Short Form-36 scores this may be considered non-significant.
|
Abberancy
Incorrect sensing was assessed by close examination of the DOR's for each patient and study phase. Mean oversensing of AF episodes due to FFRW was 6% and undersensing due to either inadequate sensitivity or post-ventricular atrial blanking was 19%. The total percentage of AF episodes with incorrect sensing was thus 25% throughout the study period (Fig. 3). When sensing was analysed per study phase, the rate of undersensing did not vary significantly. However, FFRW oversensing was significantly higher in the ‘All on’ (P < 0.001) and ‘VRS on’ (P < 0.01) phases.
|
Using a statistical model that incorporated both the rate of oversensing and undersensing per patient phase did not alter the primary outcome measure (AF burden). Similarly, undertaking the primary analysis including only phases with correctly sensed AF did not affect the neutral primary outcome. Additionally, no evidence for a carry-over effect was found within this trial.
Adverse events
The overall study complication rate due to device implantation was 4% (n = 182). Four patients required lead revision due to dislodgement (three ventricular, one atrial). One patient was upgraded to a T70 because of intractable FFRW oversensing. One patient developed sepsis treated with i.v. antibiotics. One pneumothorax and one subclavian deep vein thrombosis were recorded.
Of the eight patients excluded from the study, six withdrew and two died. Two patients withdrew during the induction phase, one needed atrioventricular node ablation, and one developed anaemia requiring investigation and transfusion. Four patients withdrew following randomization, one required angioplasty, two were protocol violations, and one developed breathlessness with the VRS algorithm and requested to be excluded. Two patients died during the study from non-cardiac causes.
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionAcknowledgementsReferences |
|---|
This is the first randomized, multicentre trial to examine the effects of third generation AF suppression algorithms and VRS in isolation and in combination. The results show that these algorithms along with the post-AF suppression algorithm are safe and well tolerated. However, this study does not show a significant effect on AF burden, AF episode number, or quality of life.
The study design required patients with ‘moderate’ paroxysmal atrial fibrillation (PAF) with induction phase AF burden of 1–50%. These parameters were chosen based on findings of the AFT study (Camm et al., personal communication), where patients with greater than 50% AF burden required recurrent cardioversion episodes which adversely affected data collection and assessment. The minimum burden of 1% allowed reduction in burden to occur that was both detectable and evaluable. Forty-three percent of enrolled patients with proven drug-resistant PAF had an AF burden of less than 1% during the 2-month induction phase suggesting benefit of bradycardia pacing alone. Many studies have shown that up to 80% of AF is asymptomatic so the results of the ADOPT trials which required patient triggering of applied ECG Holters during symptomatic AF episodes must be interpreted with caution.17 Close review of patient symptom diaries in our study in a patient subgroup with correct AF sensing suggests that palpitations can be correlated with device Holters showing concurrent AF occurred during just 10% of AF episodes.27 This may explain why effects on QOL were not detected with the VRS algorithm.
The rate-soothing algorithm designed to suppress PAC's with very gentle overdrive suppression does reduce the proportion of AF episodes initiated by PAC's with a trend towards overall PAC reduction. The effect of PAC reduction was previously seen in the ASPECT trial, however, this is the first study to demonstrate that the proportion of AF preceded by PAC's can be reduced with dynamic atrial overdrive pacing.16 However, in spite of this, AF burden was not reduced. It therefore seems likely that right atrial appendage overdrive pacing does not suppress the most arrhythmogenic PAC's. It is possible that AF episodes, which appear to be of sudden onset, are due to PAC's originating in the left atrium. These may initiate AF within the left atrium and therefore are not detectable or adequately suppressible with a right atrial electrode. Our results contrast with the ADOPT study which showed a 25% relative AF burden reduction with sustained right atrial overdrive pacing.17 It should be noted, however, that this study used transient arrhythmia monitoring as opposed to continuous beat-to-beat device-derived data, relying on patient perception of symptoms to define AF burden. The recently presented SAFARI trial using a similar suite of anti-AF pacing algorithms showed a significant reduction in AF burden.28,29 This difference may be due to the higher rate atrial overdrive pacing or triggered algorithms that were used in this study.
Our finding that the VRS algorithm did not improve symptoms or quality of life in PAF patients is similar to the AF SYMPTOMS trial.22 The maximum therapy rate was restricted to 100 bpm according to manufacturer's instructions to reduce the risk of pacing-induced heart failure.30 It is possible that regularization of ventricular rates above 100 bpm or that further regularization than that achieved is necessary to obtain the significant symptom and quality-of-life improvements that occur with AV node ablation.31,32 It is also possible that quality-of-life questionnaires, although well validated, are not sensitive enough to detect any changes.
It is not yet clear what effect high-percentage ventricular pacing has in this population on PAF burden, frequency, or symptoms. Data from the MOST study suggest that the relative risk of developing an episode of persistent AF is at least doubled in DDDR mode when ventricular pacing is increased from nil to 80%.7 Data from Nielsen et al. show a reduced incidence of AF with atrial inhibited mode with rate response (AAIR) compared to DDDR. It is therefore possible that a beneficial algorithm effect was masked by ventricular pacing.6 Despite programming a long fixed AV delay, the mean rate of ventricular pacing was 50% in the control phase of this study, which contrasts with the AFT study where a fixed AV delay of 150 ms yielded ventricular pacing of 71% (Camm et al., personal communication). We conclude from this that if further reduction in ventricular pacing is proven to be beneficial, specific reduced ventricular pacing modes or algorithms will be necessary to achieve this goal. Further studies are therefore required in this area.
The present study was powered to detect a relative AF burden reduction of 20% that was considered to be the minimum arrhythmia burden reduction to be clinically meaningful. Incorrect AF sensing was approximately 24%. Significant benefit might have been ‘suppressed’ by far-field oversensing with device Holters ‘overcounting’ AF although this is unlikely as only 6% of Holter traces showed this effect. Statistical modelling accounting for incorrect AF sensing was used and this showed no effect on the primary outcome. Excluding all phases that included incorrectly sensed AF also did not affect the primary outcome. It is therefore unlikely that incorrectly sensed AF affected the primary outcome in this study.
Some authors have suggested that long crossover phases are required to evaluate AF therapies but the measured narrow confidence intervals for the primary outcome show that 1-month crossover phases are of sufficient duration to detect clinically relevant changes in AF burden using this study design.23,33,34 Flaws in the AFT study design were addressed so that the large proportion of their study with no AF, which severely limited the statistical power of that study, did not affect the PAFS study (Camm et al., personal communication). By requiring an AF burden cutoff criterion of 1–50% it ensured that our population had more severe PAF than in previous pacemaker studies allowing much shorter crossover phases. Furthermore, we have recently undertaken a drug investigation using 2-week crossover periods with the same AF burden cutoff criteria and were able to demonstrate powerful drug efficacy suggesting that pacemaker Holter assessment of severe PAF is a powerful and sensitive tool to assess therapeutic efficacy.
|
Limitations |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionAcknowledgementsReferences |
|---|
It is feasible that the algorithms assessed in this study may have provided a better outcome if atrial septal pacing was used.
|
Conclusion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionAcknowledgementsReferences |
|---|
The PAFS study demonstrates that third generation pacemaker AF therapy algorithms are safe and well tolerated in patients with symptomatic, drug-resistant PAF. The rate-soothing algorithm reduced the proportion of AF episodes initiated by PACs. However, none of the studied algorithms had an effect on AF burden or quality of life.
|
Acknowledgements |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionAcknowledgementsReferences |
|---|
This study was supported by an unrestricted grant from Vitatron BV, Arnhem, The Netherlands.
Conflict of interest: There are no conflicts of interest to declare.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionAcknowledgementsReferences |
|---|
[1] Andersen HR, Nielsen JC, Thomsen PEB, Thuesen L, Mortensen PT, Vesterlund T, et al. Long term follow-up of patients from a randomized trial of atrial versus ventricular pacing for sick-sinus syndrome. Lancet (1997) 350:1210–16.[CrossRef][Web of Science][Medline]
[2] Kerr CR, Connolly SJ, Abdollah H, Roberts RS, Gent M, Yusuf S, et al, for the Canadian Trial of Physiological Pacing (CTOPP) Investigators. Canadian trial of physiological pacing. Effects of physiological pacing during long-term follow-up. Circulation (2004) 109:357–62.
[3] Lamas GA, Lee KL, Sweeney MO, Silverman R, Leon A, Yee R, et al, for the Mode Selection Trial in Sinus-Node Dysfunction. Ventricular pacing or dual chamber pacing for sinus node dysfunction. N Engl J Med (2002) 346:1854–62.
[4] Lamas GA, Orav EJ, Stambler BS, Ellenbogen KA, Sgarbossa EB, Huang SKS, et al, for the Pacemaker Selection in the Elderly Investigators. Quality of life and clinical outcomes in elderly patients treated with ventricular pacing as compared with dual chamber pacing. N Engl J Med (1998) 338:1097–104.
[5] Toff WD, Camm AJ, Skehan JD. Single-chamber versus dual-chamber pacing for high-grade atrioventricular block. N Engl J Med (2005) 353:145–55.
[6] Nielsen JC, Kristensen L, Anderson HR, Mortensen PT, Pedersen OL, Pedersen AK. A randomised comparison of atrial and dual-chamber pacing in 177 consecutive patients with sick sinus syndrome. J Am Coll Cardiol (2003) 42:614–23.
[7] Sweeney MO, Hellkamp AS, Ellenbogen KA, Greenspon AJ, Freedman RA, Lee KL, et al, for the MOde Selection Trial (MOST) Investigators. 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) 107:2932–37.
[8] Gillis AM. Pacing to prevent atrial fibrillation. Cardiol Clin (2000) 18:25–36.[CrossRef][Medline]
[9] Han J, Millet D, Chizzonitti B, Moe GK. Temporal dispersion of recovery of excitability in atrium and ventricle as a function of heart rate. Am Heart J (1966) 71:481–87.[CrossRef][Web of Science][Medline]
[10] Murgatroyd FD, Nitzsché R, Slade AKB, Limousin M, Rosset N, Camm AJ, et al, for the Chorus Multicentre Study Group. A new pacing algorithm for overdrive suppression of atrial fibrillation. Pacing Clin Electrophysiol (1994) 17:1966–73.[CrossRef][Medline]
[11] Cappucci A, Santarelli A, Boriani G, Magnani B. Atrial premature beats coupling interval determines lone paroxysmal atrial fibrillation onset. Int J Cardiol (1992) 36:87–93.[CrossRef][Web of Science][Medline]
[12] Lam CT, Lau C-P, Leung S-K, Tse H-F, Lee KLF, Tang M-O, et al. Efficacy and tolerability of continuous overdrive atrial pacing in atrial fibrillation. Europace (2000) 2:286–291.
[13] Mitchell ARJ, Sulke N. How do atrial pacing algorithms prevent atrial arrhythmias? Europace (2004) 6:351–62.
[14] Israel CW, H
gl B, Unterberg D, Lawo T, Kennis I, Hettrick D, et al, on behalf of the AT500 Verification Study. Pace-termination and pacing for prevention of atrial tachyarrhythmias: results from a multicenter study with an implantable device for atrial therapy. J Cardiovasc Electrophysiol (2001) 12:1121–8.[CrossRef][Web of Science][Medline]
[15] Lee MA, Weachter R, Pollak S, Kremers MS, Naik AM, Silverman R, et al, for the ATTEST Investigators. The effect of atrial pacing therapies on atrial tachyarrhythmia burden and frequency: results of a randomized trial in patients with bradycardia and atrial tachyarrhythmias. J Am Coll Cardiol (2003) 4(41):1926–32.
[16] Padeletti L, Prerfellner H, Adler SW, Waller TJ, Harvey M, Horvitz L, et al, for the Worldwide ASPECT Investigators. Combined efficacy of atrial septal lead placement and atrial pacing algorithms for prevention of paroxysmal atrial tachyarrhythmia. J Cardiovasc Electrophysiol (2003) 14:1189–95.[CrossRef][Web of Science][Medline]
[17] Carlson MD, Ip J, Messenger J, Beau S, Kalbfleisch S, Gervais P, et al, for the ADOPT Investigators. A new pacemaker algorithm for the treatment of atrial fibrillation. results of the dynamic overdrive pacing trial (ADOPT). J Am Coll Cardiol (2003) 42:627–33.
[18] Wiberg S, Lonnerholm S, Jensen SM, Blomstrom P, Ringqvist I, Blomstrom-Lundqvist C. Effect of right atrial overdrive pacing in the prevention of symptomatic paroxysmal atrial fibrillation: a multicenter randomized study, the PAF-PACE study. PACE (2003) 26:1841–8.[Medline]
[19] Puglisi A, Altamura G, Capestro F, Castaldi B, Critelli G, Favale S, et al. Impact of closed-loop stimulation, overdrive pacing, DDDR pacing mode on atrial tachyarrhythmia burden in brady-tachy syndrome. Eur Heart J (2003) 24:1952–61.
[20] Lee J. Acute testing of the rate-smoothed pacing algorithm for ventricular rate stabilization. PACE (1999) 22(Pt. I):554–61.[Medline]
[21] Yee R. The RASTAF II trial: the effects of ventricular rate stabilization pacing on clinical outcome in atrial fibrillation patients. AHA (2003) 2942. Scientific Sessions abstract.
[22] Tse H-F, Newman D, Ellenbogen KA, Buhr T, Markowitz T, Lau C-P, for the Worldwide AF SYMPTOMS Investigators. Am J Cardiol (2004) 94:939–41.
[23] Padeletti L, Santini M, Boriani G, Botto G, Capucci A, Gulizia M, et al. Temporal variability of atrial tachyarrhythmia burden in bradycardia-tachycardia syndrome patients. Eur Heart J (2005) 26:165–72.
[24] Carlioz O, Perrier E, Thomas O, Fossati F, Jarwe M, Klug D, et al. Accuracy of atrial tachyarrhythmia monitoring in a Selection device: correlation with an external Holter recording. Europace (2000) 7;1(Suppl D):9–10.
[25] Jarwe M, Klug D, Marquie C, et al. Description of an atrial tachyarrhythmia patient population with a dual chamber pacemaker. Europace (2001) 2(Abstract Suppl.):A20.
[26] Hoffmann E, Sulke N, Edvardsson N, Ruiter J, Lewalter T, Capucci A, et al, on behalf of the Atrial Fibrillation Therapy (AFT) Trial Investigators. New insights into the initiation of atrial fibrillation. A detailed intraindividual and interindividual analysis of the spontaneous onset of atrial fibrillation using new diagnostic pacemaker features. Circulation (2006) 113:1933–41.
[27] Veasey R, Silberbauer J, Vrahimides J, Taggu W, Paul V, Sulke N. Do symptoms predict atrial fibrillation episodes in patients with PAF? J Am Coll Cardiol (2006) 42:34A.
[28] Gold M. The impact of atrial prevention pacing on AF burden: primary results of the study for atrial fibrillation reduction (SAFARI) trial. Europace (2006) 8(Suppl. 1):222–3.
[29] Gold MR, Hoffmann E. Rationale and design of a randomized clinical trial to assess the role of overdrive and triggered prevention pacing therapies in reducing atrial fibrillation: the Study of Atrial Fibrillation Reduction (SAFARI). Am Heart J (2006) 152:231–6.[CrossRef][Web of Science][Medline]
[30] Simpson CS, Yee R, Lee JK, Braney M, Klein GJ, Krahn AD, et al. Safety and feasibility of a novel rate-smoothed ventricular pacing algorithm for atrial fibrillation. Am Heart J (2001) 142:294–300.[CrossRef][Web of Science][Medline]
[31] Marshall HJ, Harris ZI, Griffith MJ, Holder RL, Gammage MD. Prospective randomized study of ablation and pacing versus medical therapy for paroxysmal atrial fibrillation: effects of pacing mode and mode-switch algorithm. Circulation (1999) 99:1587–92.
[32] Brignole M, Gianfranchi L, Menozzi C, Alboni P, Musso G, Bongiorni MG, et al. Assessment of atrioventricular junction ablation and DDDR mode-switching pacemaker versus pharmacological treatment in patients with severely symptomatic paroxysmal atrial fibrillation. Circulation (1997) 96:2617–24.
[33] Ricci R, Santini M, Padeletti L, Boriani G, Capucci A, Botto G, et al. Atrial tachyarrhythmia recurrence temporal patterns in bradycardia patients implanted with antitachycardia pacemakers. J Cardiovasc Electrophysiol (2004) 15:44–51.[CrossRef][Web of Science][Medline]
[34] Warman EN, Grammatico A, Padeletti L. Sample size estimates for atrial fibrillation endpoints. Heart Rhythm (2004) 1(2 Suppl.):B52–62. discussion B63.[CrossRef][Web of Science][Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  J. Silberbauer, R. A. Veasey, N. Freemantle, A. Arya, L. Boodhoo, and N. Sulke The relationship between high-frequency right ventricular pacing and paroxysmal atrial fibrillation burden Europace, November 1, 2009; 11(11): 1456 - 1461. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Leclercq, L. Padeletti, R. Cihak, P. Ritter, G. Milasinovic, D. Gras, V. Paul, I.C. Van Gelder, C. Stellbrink, G. Rieger, et al. Incidence of paroxysmal atrial tachycardias in patients treated with cardiac resynchronization therapy and continuously monitored by device diagnostics Europace, October 28, 2009; (2009) eup318v1. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. N. Simantirakis, E. G. Arkolaki, and P. E. Vardas Novel pacing algorithms: do they represent a beneficial proposition for patients, physicians, and the health care system? Europace, October 1, 2009; 11(10): 1272 - 1280. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Purerfellner, L. Urban, G. de Weerd, J. Ruiter, J. Brandt, A. Havlicek, B. Hugl, J. Widdershoven, L. Kornet, and R. Kessels Reduction of atrial fibrillation burden by atrial overdrive pacing: experience with an improved algorithm to reduce early recurrences of atrial fibrillation Europace, January 1, 2009; 11(1): 62 - 69. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||