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(Circulation. 1999;99:2553-2558.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Atrial Pacing Periablation for Prevention of Paroxysmal Atrial Fibrillation
From the Division of Cardiology, The University of Calgary, Calgary, Alberta, Canada.
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionAppendix 1References |
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Background—This study tested the hypothesis that rate-adaptive atrial pacing would prevent paroxysmal atrial fibrillation (PAF) in patients with frequent PAF in the absence of symptomatic bradycardia.
Methods and Results—Patients (n=97) with antiarrhythmic drug-refractory PAF received a Medtronic Thera DR pacemaker 3 months before planned AV node ablation. Patients were randomized to no pacing (n=48) or to atrial rate-adaptive pacing (n=49). After a 2-week stabilization period, patients were followed up for an additional 10 weeks. The time to first recurrence of sustained PAF, the interval between successive episodes of PAF, and the frequency of PAF were compared between the 2 groups in intention-to-treat analysis. Time to first episode of sustained PAF was similar in the no-pacing (4.2 days; 95% CI, 1.8 to 9.5) and the atrial-pacing (1.9 days; 95% CI, 0.8 to 4.6; P=NS) groups. PAF burden was lower in the no-pacing (0.24 h/d; 95% CI, 0.10 to 0.56) than in the atrial-pacing (0.67 h/d; 95% CI, 0.30 to 1.52; P=0.08) group. Paired crossover analysis in 11 patients revealed that time to first PAF was shorter during atrial pacing (1.6 days; 95% CI, 0.6 to 4.9) than with no pacing (6.0 days; 95% CI, 2.4 to 15.0; P=0.13), and PAF burden was greater during atrial pacing (1.00 h/d; 95% CI, 0.35 to 2.91) than with no pacing (0.32 h/d; 95% CI, 0.09 to 1.13; P<0.016).
Conclusions—Atrial rate-adaptive pacing does not prevent PAF over the short term in patients with antiarrhythmic drug-resistant PAF without symptomatic bradycardia.
Key Words: fibrillation • pacemakers • tachyarrhythmias
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Some clinical data suggest that atrial pacing might prevent paroxysmal atrial fibrillation (PAF).1 2 3 4 5 Atrial pacing could prevent PAF by preventing bradycardia-induced dispersion of repolarization.3 6 7 Overdrive atrial pacing might also reduce at least 1 potential trigger for PAF, frequent supraventricular premature beats (SVPBs).3 5 8 Finally, atrial pacing preserves atrioventricular (AV) synchrony, which might prevent stretch-induced changes in atrial repolarization predisposing to PAF.7 9 10 11 12 This last mechanism might explain the many retrospective studies13 14 15 16 and 1 prospective study17 reporting that atrial pacing reduces the incidence of chronic atrial fibrillation compared with ventricular pacing in patients with sinus node disease. Atrial pacing as a primary therapy for the prevention of PAF has not been evaluated previously in patients without an indication for cardiac pacing.
The present study was designed to test the hypotheses that (1) atrial-based pacing reduces the time to first recurrence of sustained PAF and (2) atrial-based pacing reduces the frequency and duration of PAF.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Study Population
Patients with a history of PAF who had experienced at least 3 episodes of PAF within the year before study were enrolled. The most recent episode occurred within 3 months of entry. At least 1 of these episodes of PAF was documented electrocardiographically. Patients were refractory to or intolerant of medical therapy and were being considered for total AV node ablation.
Study Protocol
The study design is outlined in Figure 1
. Consenting patients received a
Medtronic Thera DR pacemaker 3 months before planned AV node ablation.
This device can store information on the time, date, and duration of up
to 15 consecutive episodes of an atrial
tachyarrhythmia. This information can be retrieved
during follow-up visits. After implantation of the pacemaker, patients
were randomly assigned to no pacing or to atrial pacing. The DDI mode
at a rate of 30 bpm was used for no pacing. The DDI mode allowed the
high-rate atrial episode diagnostic feature used for
detection of PAF. The DDIR mode with a lower rate of 70 bpm was used
for atrial pacing. This mode likewise activated the high-rate
atrial episode diagnostic feature, and the lower rate and
rate responsiveness were chosen to ensure that the atrium would be
paced most of the time. Detailed pacemaker programming
parameters used are shown in Table 1.
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Patients completed a 2-week stabilization phase to reduce the probability that short-term lead placement might increase arrhythmia frequency and to permit stabilization of antiarrhythmic drug therapy. High-rate atrial episode diagnostic data were retrieved and the counters cleared at 2 weeks. The next follow-up visit was scheduled 3 months after pacemaker implantation. At that visit, high-rate atrial episode data were retrieved. These data were used to determine the primary outcome event. Patients in the no-pacing group could cross over to a trial of atrial pacing after the 3-month follow-up period or earlier if they experienced intolerable recurrent symptomatic PAF. On completion of the 3-month follow-up, patients either proceeded to AV node ablation or could defer the procedure. Ambulatory ECGs were obtained at baseline and at 3 months.
Study Outcome Events
The primary study outcome was the time to first
recurrence of PAF lasting 
5 minutes occurring 2 weeks after
randomization. Because the time course of recurrence may not be
completely random, the interval between the first and second episodes
of PAF was also determined.18 Other outcome measures
included intervals between successive episodes of PAF, frequency of
PAF, and proportion of patients who chose to defer ablation.
PAF Detection
The Thera DR high-rate atrial tachycardia detection
feature was used for PAF detection in this study. This feature has been
reported to have a high sensitivity and specificity for the detection
of atrial tachyarrhythmias.19 The
programming parameters for PAF detection (Table 1
)
were selected to reduce the likelihood that nonsustained PAF would fill
the diagnostic counters and to ensure that intermittent
sense failure of atrial events during PAF would not be inappropriately
classified as PAF.19 No PAF episodes <1 minute long were
detected as an episode of PAF. To maximize collection of sequential
episodes of PAF, the atrial electrogram storage feature was not used.
Validation of appropriate detection of PAF was carried out in 28
patients by use of an enhanced marker channel feature of the device
combined with ambulatory ECG. One channel of the ambulatory ECG and
downloaded marker signals representing what the device
interpreted as atrial and ventricular electrograms were
recorded simultaneously. Appropriate detection of all
episodes of PAF was observed in 10 patients who experienced PAF during
ambulatory ECG monitoring.
False-positive detection of PAF by the Thera DR could occur because of oversensing of near-field P waves or far-field R waves or competitive atrial pacing when the atrial rate is high and the postventricular atrial refractory period is long.20 21 22 To exclude false-positive detections of PAF, all episodes of PAF detected by the pulse generator were reviewed by 2 observers who were blinded to the programmed pacing modality.22 Episodes designated as oversensing or competitive atrial pacing were then reviewed by an additional 2 observers for a final classification. Of 1636 episodes of PAF detected in the study population, 48 (2.9%) were inappropriately detected as PAF. There were 25 inappropriate detections (1.5%) due to oversensing; 2 of 3 patients with oversensing had unipolar atrial leads. Twenty-three episodes of competitive atrial pacing (1.4%) occurred in 7 patients. False-positive detections were not included in the final data analysis.
Data Analysis
Analysis was performed according to the
intention-to-treat principle. The times to occurrence of the first and
second episodes of PAF were determined by the Kaplan-Meier
method.23 Differences in the curves were compared by the
log-rank test.24 Differences between curves for paired
data were compared by a Cox proportional hazards model incorporating
the cluster term. PAF burden was calculated as the total duration of
atrial fibrillation during the follow-up period. When the event
counters were filled, PAF burden was calculated as the total duration
of atrial fibrillation during the time available for analysis.
Geometric mean data were calculated after log transformation, and
differences were compared by a nonpaired t test. Differences
in proportions were compared a 
2
analysis. Data are presented as mean±SD or geometric
mean and 95% CIs when log transformation was used. A value of
P<0.05 for 2-sided comparisons was considered
significant.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Study Population
Forty-eight patients were randomized to the no-pacing group and 49 to the atrial-pacing group. The characteristics of the 2 groups were similar and are shown in Table 2
. At the
3-month follow-up visit, pacing had not occurred in either chamber in
the no-pacing group, whereas the atrium was paced 67±34% of the time
and the ventricle was paced 64±31% of the time in the atrial-pacing
group. Ambulatory ECG recordings indicated that 67% of
pacing in the ventricle was competitive.
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Early Crossovers to Atrial Pacing or AV Node Ablation
Twelve patients randomized to no pacing crossed over to atrial
pacing before completion of the 2-week stabilization period. AV node
ablation was performed before completion of the 3-month follow-up
period in 12 patients (25%) randomized to no pacing and in 17 patients
(35%) randomized to atrial pacing. Eleven patients completed trials of
no pacing and subsequent atrial pacing. AV node ablation was deferred
in 14 patients (29%) in each group.
Intention-to-Treat Analysis
Survival free of recurrent PAF after the 2-week stabilization
period is shown in Figure 2. No
significant differences were observed between the 2 groups
(P=0.26). Event-free survival of the interval between the
first and second episodes of sustained AF was also compared and was
similar between the 2 groups (Figure 3).
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The characteristics of PAF are shown in Table 3. The majority of patients (84%)
experienced PAF, and most patients experienced multiple episodes. No
significant differences in the time to first episode of PAF, the
interval between first and second episodes of PAF, the number of
episodes of PAF, or the rate of PAF were observed. The total PAF burden
tended to be lower in the no-pacing group than in the atrial-pacing
group (P=0.08). The interval between the first and second
episodes of PAF was significantly shorter than the time to first
episode of PAF in both groups (P<0.05).
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Analysis of PAF recurrence immediately after pacemaker implantation was also performed. The time to first episode of PAF occurring during the 2-week stabilization period before the occurrence of any patient crossovers to atrial pacing was similar in the no-pacing (4.6 days; 95% CI, 2.4 to 7.1) and the atrial-pacing (2.4 days; 95% CI, 1.7 to 3.0; P=0.16) groups. The interval between first and second episodes of PAF occurring during the 2-week stabilization period was also similar in the 2 groups.
Ambulatory ECG monitoring demonstrated that atrial pacing reduced the frequency of SVPBs (3.8/h; 95% CI, 1.4 to 10.9 at baseline, to 0.5/h; 95% CI, 0.2 to 1.1 at 3-month follow-up; P<0.01), whereas SVPB frequency was unchanged in the no-pacing group over time (3.2 SVPB/h; 95% CI, 0.9 to 11.9 at baseline and 3.2 SVPB/h; 95% CI, 0.8 to 12.6 at 3-month follow-up; P=NS).
Paired Crossover Data
Eleven patients completed the 3-month follow-up in the no-pacing
limb and then crossed over to a 3-month trial of atrial pacing.
Event-free survival to the first episode of PAF and between the first
and second episodes of PAF is shown in Figure 4. PAF tended to recur earlier during
atrial pacing than with no atrial pacing. The characteristics of PAF
during follow-up in the 2 treatment modes are shown in Table 4. The time to first PAF tended to be
shorter during atrial pacing than with no pacing (P=0.13).
The total PAF burden was significantly greater during atrial pacing
than with no pacing (P=0.016).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Present therapeutic strategies for the management of PAF are unsatisfactory for many patients. Recently, atrial-pacing modalities have been proposed for the prevention of PAF.3 4 5 To the best of our knowledge, the present study is the first to test the hypothesis that atrial pacing might prevent or reduce the burden of PAF in patients without symptomatic bradycardia. The results show that atrial rate-adaptive pacing does not prevent PAF recurrence, nor does atrial pacing reduce the frequency or duration of PAF over the short term after implantation of a DDDR pacemaker in patients without symptomatic bradycardia.
Coumel et al1 reported that atrial pacing prevented vagally mediated PAF in 4 of 6 patients as long as a sufficient pacing rate was maintained. Attuel et al2 reported that DDD pacing with the lower rate programmed to exceed the diurnal mean heart rate prevented PAF in 10 patients with sinus node disease in whom PAF was associated with bradycardia or atrial pauses. Other such data have been reviewed.3 Saksena et al4 reported that single- and dual-site right atrial pacing prolonged the PAF-free interval compared with the preimplant interval in patients with sinus node disease and PAF. Some of these studies were not prospective, drug therapy before and after pacing was not carefully controlled, and therapy was not randomly assigned. Moreover, all patients had bradycardia as an indication for pacing. In the present study, a no-pacing treatment group was possible because the study population did not require pacing for bradycardia and patients were stabilized on antiarrhythmic drug therapy during the 2-week run-in phase.
Mechanisms for Pacing Prevention of PAF
Atrium-based pacing might prevent PAF by preventing
bradycardia-dependent episodes of PAF. Bradycardia-induced increased
dispersion of atrial repolarization may provide a substrate for
PAF.3 6 7 25 We hypothesized that atrial pacing might
prevent PAF by preventing "relative" bradycardia-induced changes in
atrial electrophysiology. In our study population randomized to atrial
pacing, the atrium was paced 67% of the time. If consistent
atrial activation is important, selection of a higher lower rate
for pacing would have increased the proportion of time the atrium was
paced and might have altered the time course of PAF recurrence.
However, other investigators evaluating an algorithm that ensures
almost constant atrial pacing have not shown a significant reduction in
the frequency of PAF.26 Furthermore, episodes of PAF
documented during ambulatory ECG monitoring were frequently observed
during atrial pacing in our patients.27
Atrial overdrive suppression of SVPBs has also been postulated to be a mechanism for prevention of PAF.3 5 8 A pacing algorithm to suppress SVPBs in patients with PAF has been reported to prevent PAF in some patients but to increase PAF recurrence in other patients.5 In our study population, atrial pacing did suppress SVPB frequency, but this did not correlate with a reduction in PAF.27
More rapid atrial pacing might provoke atrial arrhythmias, as has been suggested by the paired crossover data analysis in the present study. It is possible that an aggressive rate-response algorithm could initiate episodes of rapid atrial pacing, leading to atrial fibrillation. During ambulatory ECG monitoring, we never observed episodes of atrial pacing at the upper sensor rate provoking atrial fibrillation.27 Competitive atrial pacing resulting in short atrial-pacing intervals due to programming a long postventricular atrial refractory period might initiate PAF. However, we saw no evidence of this during ambulatory ECG monitoring.
It may be that atrial pacing per se has no direct antiarrhythmic effects. Atrioventricular pacing may allow more aggressive antiarrhythmic therapy, because symptomatic sinus bradycardia or high-grade AV block is no longer a concern. Furthermore, it is possible that ventricular pacing may be proarrhythmic by virtue of the deleterious effects of ventricular pacing on cardiac hemodynamics, which might cause asynchronous ventricular activation,28 valvular regurgitation,11 12 and stretch-induced changes in atrial repolarization that might predispose to PAF.7 9 10
Possible Limitations
The high proportion of early crossovers to atrial-pacing therapy
reduces the power of this study. Thus, it is possible that a modest
treatment effect of atrial pacing would not be detected. However,
because patients in the atrial-pacing group were experiencing PAF
earlier than the no-treatment group, such an outcome is unlikely.
The majority of atrial leads were positioned in the right atrial appendage. It is possible that stimulation in this site results in delayed activation of some areas in the atria that are important in the initiation of PAF. Site-specific atrial pacing, eg, Bachmann's bundle,29 30 left atrial, or dual-site atrial pacing,4 31 might be more efficacious by virtue of shortening total atrial activation times. These modalities are currently being tested. As discussed, it is possible that more continuous atrial pacing might prevent PAF, because the patients in the present study were not paced in the atrium 33% of the time. Other studies are currently testing algorithms to promote more continuous pacing. The present study compared no pacing with atrial pacing in the DDIR mode. In the DDIR mode, ventricular rate acceleration is not dependant on the atrium. Hence, the present study results cannot necessarily be extrapolated to other pacing modalities. The primary study outcome depended on reliable detection of PAF by the device. It is possible that undersensing of PAF occurred in some patients; however, the frequency should have been similar in both groups. The study design did not discriminate between symptomatic and asymptomatic episodes of PAF.
Conclusions
Atrial rate-adaptive pacing does not prevent recurrence of
PAF over the short term, nor does it reduce PAF frequency or duration
in patients with PAF in the absence of symptomatic
bradycardia.
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Acknowledgments |
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This study was supported by a grant in aid from Medtronic, Inc, Minneapolis, Minn. Dr Gillis is a Senior Scholar of the Alberta Heritage Foundation for Medical Research. The authors thank Ken Riff, MD, and Nick Jensen, DVM, Medtronic, Inc, for their advice on study design; Rahul Mehra, PhD, Michael Hill, PhD, and Stephanie Fitts, PhD, Medtronic, Inc, for help with validating the high-rate atrial episodes; Margot McDonald, Karen Hillier, Andrew Mah, and Catherine St George, study coordinators; and Karen Burrell for help with manuscript preparation.
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Footnotes |
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Reprint requests to Anne M. Gillis, MD, Division of Cardiology, The University of Calgary, 3330 Hospital Dr NW, Calgary, Alberta, Canada T2N 4N1.
All the authors have been involved in the clinical evaluation of Medtronic investigational devices in the past. Dr Gillis has been a member of a Medtronic Physician Advisory Board. Dr Yee is currently a member of the Medtronic Physician Advisory Board.
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Appendix 1 |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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The following institutions and individuals participated in this study (listed in descending order of number of patients randomized).
Hamilton General Hospital, Hamilton, Ontario: Stuart J. Connolly,
Wesley James, Catherine LeFeuvre, Maryann Menard. Foothills Medical
Centre, Calgary, Alberta: Anne M. Gillis, D. George Wyse, John M.
Rothschild, L. Brent Mitchell, Henry J. Duff, Karen Hillier, Charlotte
Hale. Institut de Cardiologie, Montreal, Quebec: Marc Dubuc, Mario
Talajic, Dennis Roy, Eric Lavallee. Institut de Cardiologie,
Hôpital Laval, Quebec City, Quebec: François Philippon,
Marcel Gilbert, Gilles O'Hara, Johanne Rompré. University
Hospital, London, Ontario: Raymond Yee, George Klein, Caro Norris.
Hôpital Notre Dame, Montreal, Quebec: Pierre Lacombe, Diane
Therrin, Claude Proven
al, Louise Patry. St Paul's Hospital,
Vancouver, British Columbia: Charles D. Kerr, John Boone, John
Yeung-Wai-Lah, Sheila Flavelle, Susan Mooney. University Hospital,
Edmonton, Alberta: Katherine M. Kavanagh, Shane Kimber, Ingrid Scott.
QE II Health Sciences Centre, Victoria General Hospital, Halifax, Nova
Scotia: Martin J. Gardner, Laurence Sterns, Marcia Shields. University
of Ottawa Heart Institute, Ottawa, Ontario: Anthony S. L. Tang,
Clare Carey. Hôpital du Sacre-Coeur, Montreal, Quebec: Teresa
Kus, Franck Molin, Ginette Gaudette. St Michael's Hospital,
Toronto, Ontario: David Newman, Paul Dorian, Jane Laslop, Linda
DeBelias. Kingston General Hospital, Kingston, Ontario: Hoshiar
Abdollah, Sharon Fair.
Received October 16, 1998; revision received February 3, 1999; accepted February 23, 1999.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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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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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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M. E.W. Hemels, A. C.P. Wiesfeld, B. Inberg, P. F.H.M. Van Dessel, W. Nieuwland, E. S. Tan, H. Mulder, D. J. Van Veldhuisen, and I. C. Van Gelder Right atrial overdrive pacing for prevention of symptomatic refractory atrial fibrillation. Europace, February 1, 2006; 8(2): 107 - 112. [Abstract] [Full Text] [PDF]
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C. R. Kerr, S. J. Connolly, H. Abdollah, R. S. Roberts, M. Gent, S. Yusuf, A. M. Gillis, A. S.L. Tang, M. Talajic, G. J. Klein, et al. Canadian Trial of Physiological Pacing: Effects of Physiological Pacing During Long-Term Follow-Up Circulation, January 27, 2004; 109(3): 357 - 362. [Abstract] [Full Text] [PDF]
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J.-J. Blanc, L. De Roy, J. Mansourati, Y. Poezevara, J.-L. Marcon, W. Schoels, F.ço. Hidden-Lucet, C. Barnay, and for the PIPAF investigators Atrial pacing for prevention of atrial fibrillation: assessment of simultaneously implemented algorithms Europace, January 1, 2004; 6(5): 371 - 379. [Abstract] [Full Text] [PDF]
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C. W. Israel Is there a role for pacing in the prevention of atrial tachyarrhythmias? Europace, January 1, 2004; 6(5): 380 - 383. [Full Text] [PDF]
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A. Schuchert Contributions of permanent cardiac pacing in the treatment of atrial fibrillation Europace, January 1, 2003; 5(s1): S36 - S41. [Abstract] [Full Text] [PDF]
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A. G. Manolis, A. G. Katsivas, C. Vassilopoulos, D. Koutsogeorgis, and N. E. Louvros Prevention of atrial fibrillation by inter-atrial septum pacing guided by electrophysiological testing, in patients with delayed interatrial conduction Europace, January 1, 2002; 4(2): 165 - 174. [Full Text] [PDF]
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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 and Policy Conferences (Committee to develop guidelines for the management of patients with atrial fibrillation) developed in collaboration with the North American Society of Pacing and Electrophysiology Eur. Heart J., October 2, 2001; 22(20): 1852 - 1923. [PDF]
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V. Fuster, L. E. Ryden, R. W. Asinger, D. S. Cannom, H. J. Crijns, R. L. Frye, J. L. Halperin, G. N. Kay, W. W. Klein, S. Levy, et al. ACC/AHA/ESC 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 and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology J. Am. Coll. Cardiol., October 1, 2001; 38(4): 1266 - 1266. [Full Text] [PDF]
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M. M. Scheinman and F. Morady Nonpharmacological Approaches to Atrial Fibrillation Circulation, April 24, 2001; 103(16): 2120 - 2125. [Abstract] [Full Text] [PDF]
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S. Saksena Implantable defibrillators in the third millennium: increasingly relegated to a standby role? J. Am. Coll. Cardiol., September 1, 2000; 36(3): 828 - 831. [Full Text] [PDF]
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A. M. Gillis, S. J. Connolly, P. Lacombe, F. Philippon, M. Dubuc, C. R. Kerr, R. Yee, M. S. Rose, D. Newman, K. M. Kavanagh, et al. Randomized Crossover Comparison of DDDR Versus VDD Pacing After Atrioventricular Junction Ablation for Prevention of Atrial Fibrillation Circulation, August 15, 2000; 102(7): 736 - 741. [Abstract] [Full Text] [PDF]
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K. Fan, K. L. Lee, C. S.W. Chiu, J. W.T. Lee, G.-W. He, D. Cheung, M. P. Sun, and C.-P. Lau Effects of Biatrial Pacing in Prevention of Postoperative Atrial Fibrillation After Coronary Artery Bypass Surgery Circulation, August 15, 2000; 102(7): 755 - 760. [Abstract] [Full Text] [PDF]
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C. T. F. Lam, C.-P. Lau, S.-K. Leung, H.-F. Tse, K. L. F. Lee, M.-O. Tang, and V. Tsang Efficacy and tolerability of continuous overdrive atrial pacing in atrial fibrillation Europace, January 1, 2000; 2(4): 286 - 291. [Abstract] [PDF]
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