© 2004 by European Society of Cardiology
Atrial pacing for prevention of atrial fibrillation: assessment of simultaneously implemented algorithms
aCardiology Department, Brest University Hospital Brest, France; bCardiology Department, UCL Mont-Godinne Namur, Belgium; cEla Medical, Le Plessis-Robinson France; dCardiology Department, Annonay Hospital Annonay, France; eCardiology Department, Universitätsklinikum Heidelberg, Germany; fCardiology Department, La Pitié-Salpétrière Hospital Paris, France; gCardiology Department, General Hospital Aix-En-Provence, France
Manuscript submitted 19 December 2003. Accepted after revision 9 May 2004.
*Corresponding author. Cardiology Department, Hôpital de la Cavale Blanche, Bld Tanguy Prigent, 29609 Brest, France. Tel.: +33-(0)2-98-34-73-92; fax: +33-(0)2-98-34-78-03. E-mail address: jean-jacques.blanc{at}chu-brest.fr (Y. Poezevara).
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionConclusionAppendix AAcknowledgementsReferences |
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AIMS: Several preliminary studies indicated that right atrial pacing could prevent atrial tachyarrhythmias (ATA). We sought to compare the safety and the efficacy of atrial-based pacing supplemented by dedicated combined algorithms with conventional atrial pacing in the prevention of ATA.
METHODS: Fifty-five patients with a history of recurrent paroxysmal ATA implanted with a dual-chamber pacemaker were studied during two randomized cross-over pacing periods (conventional DDD and DDD with ATA prevention algorithms) of 6 months duration. The primary endpoint was the burden of ATA episodes recorded by the device mode switch algorithm.
RESULTS: The cross-over analysis did not demonstrate any significant difference between the two pacing modes: 254±533 h of ATA during the control period versus 238±518 h during the ATA prevention period. Analysis of a subgroup of patients found that those with the lower percentage of ventricular pacing benefited from ATA prevention algorithms (120±182 h versus 225±350 h during the control period; P<0.04).
CONCLUSION: When compared with DDD pacing at 70 bpm, ATA prevention algorithms have not demonstrated significant efficacy. However, a subgroup of patients with preserved native AV conduction (low percentage of ventricular pacing) responded to ATA prevention algorithms.
Key Words: atrial fibrillation, right atrial pacing, prevention algorithms
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAcknowledgementsReferences |
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In patients with sinus node disease it has been demonstrated that atrial-based pacing, when compared with ventricular pacing, is associated with a reduction in the occurrence of atrial fibrillation [1–
6]. However, it is unclear, based on current data, whether atrial pacing prevents atrial tachyarrhythmia (ATA) recurrences by itself or if it is ventricular pacing that exerts pro-arrhythmic effects. Up to now, very few data are available to evaluate the isolated effect of atrial-based pacing in reducing recurrences of ATA episodes in patients with or without bradycardia. In the Canadian Atrial Pacing Peri-ablation for Paroxysmal Atrial Fibrillation Study [7], pacing from the right atrial appendage in patients without bradycardia did not exhibit any benefit. Several preliminary studies indicated that right atrial pacing could prevent atrial fibrillation, however, these results were obtained from small groups of patients followed for short periods after pacemaker implantation [8–12]. Recently, the results of randomized trials available as a paper [13] or abstract [14] gave arguments for prevention of ATA by pacing. The purpose of the present study was to compare the effects of atrial-based pacing supplemented by combined algorithms with conventional atrial pacing on the incidence of ATA.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAcknowledgementsReferences |
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The Pacing in Prevention of Atrial Fibrillation (PIPAF) Study, which has been described previously [15]
, consisted of different sub-studies assessing algorithms dedicated to ATA prevention. All these studies were multicentre, prospective, single-blinded, with a randomized cross-over design. We report the results of the study comparing DDD pacing at 70 bpm, with DDD pacing implementing algorithms dedicated to ATA prevention from a mono-site right atrial pacing configuration. This study was approved by the Ethical Committee of enroling centres, and all patients gave informed written consent before inclusion.
Entry criteria
Patients were eligible for enrolment in the study if they had a history of paroxysmal and sustained ATA, in the presence of a pacing indication, provided that ablation therapy had not been considered appropriate or was not effective. ATA consisted of symptomatic or asymptomatic atrial fibrillation, typical or atypical atrial flutter, or other types of atrial tachycardia. At least three episodes of ATA had to be electrocardiographically documented in the year preceding enrolment, and at least one episode within the last 3 months.
In approximately half of the patients (Table 1) the only pacing indication was ATA prevention without associated sinus dysfunction, which was a class IIb indication according to the ACC/AHA guidelines [16] published at time of study initiation.
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Antiarrhythmic drug therapy had to remain unchanged for at least 1 month, except for amiodarone which was kept stable for at least 2 months before entry into the study. No change in pharmacological treatment was allowed after randomization. Patients were not enroled if: (1) they were less than 18 years old or pregnant; (2) had known sustained ventricular tachyarrhythmias, severe coronary artery disease, unstable angina pectoris, or advanced dilated or hypertrophic cardiomyopathy; (3) had myocardial infarction or cardiac surgery within 3 months before inclusion; (4) had a life-expectancy of less than 1 year.
Study protocol
Following implantation of a dual-chamber pacemaker, an observational period of at least 1 month was allowed to stabilize the drug regimen and to check pacing and sensing parameters.
An echocardiogram was systematically performed in the week following implantation. For the purpose of the present study only the left atrial diameter measured in the long axis view was analyzed.
Patients were randomly assigned to 6 months of DDD pacing, or 6 months of DDD pacing with the implementation of the ATA prevention algorithms. After the completion of the first 6-month period, patients crossed over for a 6-month period to the alternative pacing modality. Each period was initiated only in patients in sinus rhythm.
Follow-up visits were performed every 3 months for control of correct functioning of the pacing system and interrogation of the device memories. A customized questionnaire, including 14 questions measuring frequency and intensity of ATA-related symptoms was completed at baseline and at the end of each of the 6-month treatment periods.
In case of persistent atrial arrhythmias at the time of follow-up visits, patients were excluded as the primary outcome measurement, i.e. total duration of paroxysmal ATA, could not be determined.
At the time of study design, no data or estimations (means, standard deviations) on the clinical measurements of the primary endpoint of the study were published and, from both the clinical and quantitative point of view, expected improvements could not be anticipated. Therefore, sample size was planned to ensure normality assumptions of statistical models.
Pacing system and baseline programming
Implanted pacemakers, Chorum 7334 or Talent DR 213 (ELA Medical, Montrouge, France), were connected to a conventional bipolar atrial lead located in the right appendage or the lateral wall. Ventricular lead polarity was left to the investigator's choice. The ventricular lead was located in all cases in the right apex. Implanted pacemakers stored the number and cumulative duration of automatic mode switch (AMS) episodes, and the percentage of atrial and ventricular pacing (calculated over time free of AMS). Fourteen marker chains documenting the beginning of the last AMS episodes were also available.
Before randomization the following parameters were required: (1) atrial and ventricular pacing thresholds 
2.5 V at a 0.5 ms pulse duration; and (2) atrial signal amplitude during sinus rhythm 
1.5 mV. These values were selected to avoid loss of atrial capture during atrial overdrive and to allow good detection of ATA. For patients in ATA at the randomization visit, the randomization was postponed until recovery of sinus rhythm, and atrial sensing was considered satisfactory provided proper recognition of the arrhythmia by AMS algorithm.
For the purpose of the study, stored AMS events were considered as potential ATA episodes. To eliminate ATA artifacts such as far-field sensing, all stored AMS marker chains were individually validated in every patient by the same blinded expert. In case of detection of far-field sensing, refractory periods were reprogrammed and if crosstalk persisted the patient was excluded from the study.
Standard programming included: DDD mode, basic rate at 70 bpm, AMS, rate smoothing, hysteresis at 0%, rate responsive function (programmed only in case of chronotropic incompetence) and maximal bipolar atrial sensitivity (0.4 mV). Programming of AV delay was left to the investigators’ discretion.
ATA prevention algorithms
Three algorithms specially designed for ATA prevention and previously described [15] were downloaded into the pacemaker memory.
Sinus rhythm overdrive (SRO) was developed to provide permanent atrial pacing at a rate just above the spontaneous sinus rate. This is achieved by pacing at an interval 50 ms shorter than any sensed (non-premature) sinus cycle. SRO features a specific window designed to discard atrial events that might induce undesirably steep accelerations. Atrial events sensed in this window are considered non-sinus and do not induce acceleration. Following an accelerated plateau of 16 cycles, SRO gradually decreases in rate until sensing a new sinus beat. SRO conception allowed dynamic adaptation to exercise or to any other variations in sinus rate, but this function is immediately inhibited on sensing the onset of ATA, and reactivated on sensing its termination.
Post-extrasystolic pause suppression (PEPS) prevents the occurrence of prolonged post extrasystolic pauses (with the pacemaker models used in this study, a premature event is defined as a spontaneous event approximately 25% shorter than the ongoing rhythm) by delivering (1) an early AV pacing sequence after a premature atrial event, or (2) an early synchronous atrial pacing pulse when a premature ventricular event is sensed. PEPS is inactivated during ongoing ATA.
Acceleration after premature atrial complexes (APAC) increases the atrial pacing rate by 5 bpm when repetitive premature atrial complexes (PAC) are detected. Successive accelerations are allowed until PAC disappearance or until an increment of 25 bpm higher than the previously ongoing rate was reached. Upon PAC disappearance, the atrial pacing rate remains at a plateau during 24 cycles, before gradually returning to the ongoing sinus rate. APAC is automatically inactivated if the pacing rate increase results in an increase in PAC frequency.
Study endpoints
The primary endpoint of the study was the cumulative duration of ATA recurrences validated as AMS episodes during each 6-month period.
Secondary endpoints included the number of ATA recurrences, and the severity of the symptoms collected in the patient questionnaire. Number of ATA recurrences has been considered a secondary objective rather than primary because patients with long lasting episodes may experience a small number of recurrences and still be severely exposed to ATA.
To assess more precisely the efficacy of the ATA prevention algorithms, three retrospective analyses were performed: (1) influence of the pacing indication; (2) influence of the proportion of ventricular paced beats; and (3) influence of the increase of atrial pacing percentage provided by activation of ATA prevention algorithms.
Statistical analysis
Results regarding primary endpoints are expressed as mean±standard deviation and as median in square brackets.
Baseline characteristics were assessed with the use of the chi-square test or Fisher's exact test for dichotomous variables and Student's t-test or Wilcoxon rank sum test (non-parametric) for quantitative variables.
The responses obtained for all criteria assessing primary clinical objectives were compared using the Wilcoxon rank sum test according to a two-period and two-treatment cross-over design. Absence of period and carry-over effects was checked prior to assessment of treatment efficacy. In some patients a slight departure from planned exposure time was observed, so a normalization of ATA cumulative duration and number was performed in order to homogenize differences between patients. All statistical tests were two-sided and the threshold of significance was set at 5%. A significance threshold superior to 20% is reported as NS in the tables.
Moreover, we present parallel and subgroup analysis to study the effect of the algorithm in various categories of patients. As they were not planned in the study protocol, they are not to be interpreted as a claim of superiority of algorithm but rather as exploratory analyses to give further understanding of the mechanism of atrial-based pacing supplemented by combined algorithms.
Consequently, for all additional analyses, one-sided tests of significance were retained to ensure that the probability of an erroneous conclusion concerning potential superiority of the algorithm arm was less than or equal to the specified alpha level of 5%.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAcknowledgementsReferences |
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Patient population
During the study period 95 patients were recruited in the 21 participating centres. Forty patients were excluded due to: (1) far-field ventricular sensing despite refractory periods reprogramming (4 cases); (2) atrial undersensing (9 cases); (3) modification of the anti-arrhythmic drug regimen (10 cases); (4) inappropriate pacemaker programming (8 cases); and (5) persistent ATA during follow-up (9 cases, 5 during the control period and 4 during the ATA prevention period). Finally, the study group included the 55 patients (41 males, mean age 68±11 years, left atrial diameter 43.1±6.0 mm) who completed the protocol. Their main clinical characteristics are summarized in Table 1. Anti-arrhythmic medication was prescribed in 51 patients: Class I (13 cases), Class II (7 cases), Class III (Amiodarone 27 cases, Sotalol 9 cases), Class IV (3 cases). A combination of anti-arrhythmic drugs was prescribed in eight patients.
Atrial arrhythmias recurrences
As expected the percentage of the time during which the atrium was paced was significantly higher (P<0.0001) in the DDD+ATA prevention algorithms pacing period (98±2%) than in the control DDD period (86±18%), mainly due to SRO algorithm activation.
The primary endpoint, i.e. duration of ATA episodes, was similar (NS) during the two randomized 6-month periods: 254±533 [53] h during the control DDD 70 bpm period and 238±518 [57] h during the ATA prevention period (DDD 70 bpm+algorithms).
The number of episodes was also similar (NS) during the two pacing periods: 152±234 [17] during the control period and 128±201 [31] during the ATA prevention period (Fig. 1).
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Seven patients remained free of ATA during the control period, and ten during the ATA prevention period. Four patients did not experience any ATA during the whole study follow-up.
The intensity of ATA-related symptoms reported in the questionnaire was analyzed; minimal and maximal potential scores were from 0 (most severe symptoms) to 2 (absolutely no symptom). Observed scores were not different during the two periods of pacing (1.45±0.34 in the control period versus 1.49±0.27 in the treatment period, NS), and when compared with baseline (1.47±0.43, NS). Patients did not complain about symptoms clearly related to pacing algorithms and none asked for deactivation of those algorithms.
Influence of the pacing indication
The above-mentioned results are not significantly modified when the analysis is performed according to the indication for pacing (Table 2).
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Influence of the ventricular pacing
In the study group the mean and median proportion of paced ventricular beats were 67% and 70%, respectively. Patients were stratified into two subgroups according to the median of the proportion of paced ventricular beats: Group 1, patients with a "low" percentage of ventricular pacing (29 patients, V=42±25%, AV delay 261±32 ms), and Group 2, patients with a "high" percentage of ventricular pacing (26 patients, V=99±4%, AV delay 176±23 ms), P<0.0001. ATA prevention algorithms are significantly effective in Group 1 on ATA duration (225±350 [50] h during the control period versus 120±182 [48] h, P=0.04) and on ATA recurrences (129±242 [9] during the control period versus 96±208 [8], P=0.03) whereas there is no significant difference in Group 2 on ATA total duration (287±688 [71] h during the control period versus 366±715 [101] h, P=NS) and ATA episodes (179±227 [74] versus 164±191 [45], P=NS) (Fig. 2).
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Influence of atrial pacing percentage increment
Activation of ATA prevention algorithms resulted in an increase of percent of atrial pacing by a mean value of 12%. The study group was divided according to the median increment of atrial pacing (+6%) in the ATA prevention period. The first subgroup (28 patients) with similar percentage of atrial pacing in both pacing modes (mean increment was +1%) had no significant difference in terms of ATA duration (152±290 [32] h during the control period versus 169±323 [52] h, NS) and ATA recurrences (77±130 [7] during the control period versus 73±107 [24], NS). The other subgroup (27 patients) with substantial increment in the percentage of atrial pacing in the ATA prevention period (+22%) had significant decrease of the ATA duration (360±692 [122] h in the control period versus 307±665 [67] h, P<0.04) and ATA recurrences (231± 290 [78] in the control period versus 185±257 [35], P<0.03).
Comparison of the first 6-month periods in the two groups (parallel analysis)
The 27 patients randomly assigned to the control period were compared with the 28 patients assigned to the ATA prevention period. These two groups have similar baseline clinical characteristics (Table 3). Of interest, the duration of ATA in the ATA prevention group was lower (P=0.07) than in the control group (113±156 [47] h versus 319±691 [53] h, respectively).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAcknowledgementsReferences |
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The main result of the present study is that the use of sophisticated pacing algorithms does not seem to exert a substantial improvement in the prevention of paroxysmal ATA.
The purpose of the present study was to assess the incremental benefit of dedicated ATA prevention algorithms over optimized DDD pacing. It was therefore decided to set the basic rate at 70 bpm; as a result the majority of patients were consistently paced in the atrium whatever the pacing mode. The consequence is that the percentage of atrial pacing could hardly be increased by the activation of ATA algorithms in some patients. A clear ATA prevention effect might have been observed with a lower basic rate. A strong argument to support this hypothesis is that better results were observed in the subgroup of patients with an important increase in atrial pacing percentage.
Methodology
Studies dedicated to ATA prevention have to overcome many limitations. Selection of patients is a major difficulty as many different groups could be included: patients with only ATA and no indication for pacing, patients with bradycardia due either to atrio-ventricular block or sinus node disease, patients with paroxysmal or persistent ATA converted to sinus rhythm prior to implantation, patients with or without cardiac disease, .... Consequently it is likely that pacing can prevent atrial arrhythmias in some patients but not in others. In addition to the selection of patients, the site of atrial pacing might have some influence: right atrial appendage, inter-atrial septum [17], coronary sinus ostium [18], biatrial [19] or dual-site pacing [20].
Endpoints to evaluate effectiveness of treatment are also difficult to determine: time elapsed to first recurrence, ATA burden (cumulative duration of ATA), symptoms, number of episodes, occurrence of persistent or permanent ATA, stroke, mortality. It is clear that the "hard" endpoints (severe morbidity or mortality) are not adequate for studies with sophisticated pacing algorithms as they need very large populations and long-term follow-up. "Soft" endpoints (ATA burden, symptoms), on the contrary, are more adapted to pacing therapy but the outcome is less relevant and also requires a large population. It should be noted that a retrospective statistical estimation of the sample size with the current data shows that a population of more than 5000 patients would have been necessary to show a significant difference in the primary endpoints between the two pacing modalities.
Although endpoints are difficult to select, it must be stressed that ATA burden is certainly the most accurate parameter in paced patients as AMS algorithms demonstrated a very good specificity and sensitivity in detecting episodes of atrial arrhythmias. This was well demonstrated with the pacemaker used in this study as a comparison between Holter monitoring and automatic mode switch appeared highly concordant [21]. However, the atrial function of the pacemaker must be carefully checked at each follow-up, in order to correct oversensing or undersensing which may significantly bias the results by ATA over (or under-) counting.
At the time of study conception, a cross-over experiment was thought appropriate for the initial evaluation of ATA prevention algorithms, as each patient acts as his/her own control. Of interest in the present study, the result of the "parallel analysis" was almost significant (P=0.07) whereas the "crossover analysis" was not (NS). Although the test for a carry-over effect was not significant, which makes the cross-over analysis applicable, it must be underlined that this test lacks power [22]. The possibility that a parallel design is more suitable for this pathological area cannot be excluded by observation of our data.
Influence of ventricular pacing
Although we included a limited number of patients with atrio-ventricular block, more than 60% on average of ventricular beats were paced in our study group. It has been shown that the right apical ventricular pacing has haemodynamically deleterious effects [23,24] which may have caused the higher ATA burden in patients with a high percentage of ventricular pacing [25]. Even though this post-hoc analysis was not part of the primary objective, we observed that ATA prevention algorithms were significantly more effective in patients with less frequent ventricular pacing compared with patients predominantly paced in the ventricle. The explanation of such a side-effect remains questionable. One possible hypothesis refers to the Wolff Parkinson White syndrome. It is well known that in this case, pre-excitation of the ventricle favours the occurrence of ATA even in young patients with normal hearts [26,27]. Pacing the right ventricle in patients with near normal AV conduction induces fusion beats with a partial pre-excitation of some part of the ventricle. Even if the mechanism is not totally understood and if our study does not allow definitive conclusions, these data give rationale for new prospective trials.
Study limitations
The following limitations must be underlined, which may partially explain the lack of significance of our results.
Almost half of the patients enroled have been excluded from the analysis of primary objectives, which limits the included population and the power of the statistical analysis.
AMS events were documented by AV marker chains, but no synchronous atrial electrograms were provided by the pacemakers. This may limit the efficacy of the ATA episode validation.
The devices under study trigger an AMS after 15–30 s of ATA, according to tachycardia rate; this may be too short to correspond to episodes presenting with clinical significance.
Nothing is known about optimal programming of preventive pacing algorithms. It cannot be excluded that with different algorithms or different programming of the present algorithms the study results would have been different.
As suggested by the post-hoc analysis of ventricular pacing, AV delay programming may have a significant impact on the efficacy of ATA algorithms. However, no specific guidelines for AV delay programming were proposed in the study protocol.
Finally, the counter data on the percentage of ventricular pacing may have also included ventricular pseudo-fusion (ineffective ventricular spike in the ascending limb of the R wave) without any haemodynamic effect.
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Conclusion |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAcknowledgementsReferences |
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Implementation of different sophisticated and well functioning algorithms in pacemakers implanted to prevent ATA recurrences has not demonstrated positive results when compared with the usual DDD pacing at 70 bpm. Native AV conduction seems to be an important condition for the effectiveness of ATA prevention by pacing. Further devices specially designed to avoid unnecessary ventricular pacing featuring ATA prevention algorithms might demonstrate some effectiveness.
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Appendix A |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAcknowledgementsReferences |
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The following PIPAF investigators participated in this study:
France: C Barnay, JJ Blanc, S Cazeau, JM Dupuis, R Franck, D Galley, H Garnier, P Graux, F Hidden-Lucet, C Juin, D Lamaison, G Lascault, T Lavergne, J Mansourati, JL Marcon, J Taieb, J Victor.
Germany: W Schoels, J Michaelsen.
Italy: E Occhetta, F Zolezzi, G Saccomano.
United Kingdom: V Paul, T Levy.
Belgium: L De Roy, J Vijgen.
Co-ordinators: Y Poezevara, B Hallier, D Contardi, E Boulogne, D Bouchez.
Statistics: MC Vandrell.
Data management: JM Torralba.
Data monitoring: H Ranaivoson.
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Acknowledgements |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAcknowledgementsReferences |
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This study was supported by a grant from Ela Medical, Montrouge, France.
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Footnotes |
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1The other investigators who participated to this study, part of the PIPAF study, are listed in Appendix A.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAcknowledgementsReferences |
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C. W. Israel What is the role of the pacing rate in the prevention of atrial tachyarrhythmias? Europace, November 1, 2007; 9(11): 999 - 1001. [Full Text] [PDF]
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Writing Committee Members, V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: full text: A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society Europace, September 1, 2006; 8(9): 651 - 745. [Full Text] [PDF]
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 V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation--Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society J. Am. Coll. Cardiol., August 15, 2006; 48(4): 854 - 906. [Full Text] [PDF]
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V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society J. Am. Coll. Cardiol., August 15, 2006; 48(4): e149 - e246. [Full Text] [PDF]
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 V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society Circulation, August 15, 2006; 114(7): e257 - e354. [Full Text] [PDF]
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V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, et al. ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation--Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society Circulation, August 15, 2006; 114(7): 700 - 752. [Full Text] [PDF]
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 Authors/Task Force Members, V. Fuster, L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation executive summary: A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients with Atrial Fibrillation) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society Eur. Heart J., August 2, 2006; 27(16): 1979 - 2030. [Full Text] [PDF]
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P. Azzolini, G. Critelli, V. De Giorgi, G. B. Del Giudice, G. Ibba, D. Melissano, A. Scaccia, and A. Puglisi Atrial tachyarrhythmia burden modelling by some electrophysiological parameters in pacemaker-recipient patients with Brady-Tachy syndrome Europace, July 1, 2006; 8(7): 474 - 481. [Abstract] [Full Text] [PDF]
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E. Hoffmann, N. Sulke, N. Edvardsson, J. Ruiter, T. Lewalter, A. Capucci, A. Schuchert, S. Janko, J. Camm, and on behalf of the Atrial Fibrillation Therapy (AFT) 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, April 25, 2006; 113(16): 1933 - 1941. [Abstract] [Full Text] [PDF]
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 Additional Information JAMA, March 15, 2006; 295(11): E7 - E14. [Full Text] [PDF]
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G. Frohlig, D. Gras, J. Victor, P. Mabo, D. Galley, A. Savoure, G. Jauvert, P. Defaye, P. Ducloux, and A. Amblard Use of a new cardiac pacing mode designed to eliminate unnecessary ventricular pacing. Europace, February 1, 2006; 8(2): 96 - 101. [Abstract] [Full Text] [PDF]
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C. W. Israel The role of pacing mode in the development of atrial fibrillation. Europace, February 1, 2006; 8(2): 89 - 95. [Abstract] [Full Text] [PDF]
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N. Musilli and L. Padeletti Pacemaker selection: time for a rethinking of complex pacing systems? Eur. Heart J., January 2, 2006; 27(2): 132 - 135. [Abstract] [Full Text] [PDF]
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