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Circulation. 2000;102:1382-1387

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(Circulation. 2000;102:1382.)
© 2000 American Heart Association, Inc.


Clinical Investigation and Reports

Randomized Controlled Study Investigating the Effect of Biatrial Pacing in Prevention of Atrial Fibrillation After Coronary Artery Bypass Grafting

T. Levy, MRCP; G. Fotopoulos, MD; S. Walker, MRCP; S. Rex, MRCP; M. Octave, BSc; V. Paul, FRCP; M. Amrani, FRCS

From the Department of Cardiology (M.A.) and Department of Cardiac Surgery (T.L., G.F., S.W., S.R., M.O., V.P.), Royal Brompton and Harefield NHS Trust, Harefield Hospital, Harefield, Middlesex, UK.

Correspondence to Dr T. Levy, MRCP, Specialist Registrar Cardiology, Royal Brompton and Harefield NHS Trust, Harefield Hospital, Harefield, Middlesex, UB9 6JH UK. E-mail terry{at}levy77.freeserve.co.uk


*    Abstract
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*Abstract
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Background—Atrial fibrillation (AF) is a common problem after CABG. Prevention with prophylactic drug therapy has had limited success, therefore alternative approaches are required. This study investigated the role of biatrial pacing compared with no pacing on AF incidence after isolated first-time CABG.

Methods and Results—During surgery, temporary pacing leads were placed in the lateral wall of the right atrium and at the roof of the left atrium in Bachmann’s bundle to allow bipolar pacing and sensing at each site. After surgery, all patients were connected to an external pacemaker (Chorum ELA) that also acted as a Holter monitor. Patients were consecutively randomized to either 4 days of biatrial pacing at a base rate of 80 bpm or to no pacing (control group, base rate 30 bpm). End points included an episode of AF lasting >1 hour on pacemaker Holter, clinically detected AF, intensive care unit (ICU) and hospital stay, and postoperative complications. One hundred thirty patients were randomized. Biatrial pacing significantly reduced both monitored (13.8% versus 38.5%, P=0.001) and clinical (10.8% versus 33.8%, P=0.002) episodes of AF. Median ICU (19 versus 24 hours, P=NS) and mean hospital stay (7.7±6.9 versus 9.7±10, P=NS) did not significantly change. The number of postoperative complications was lower in the biatrial group (13 versus 35, P=0.001).

Conclusions—Biatrial pacing after CABG significantly decreases the incidence of AF. This is associated with reduced postoperative complications and a trend toward reduced ICU and hospital stay.


Key Words: pacing • bypass • grafting • fibrillation


*    Introduction
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up arrowAbstract
*Introduction
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Atrial fibrillation (AF) is common after CABG, with development in up to one third of patients within the first 4 to 5 postoperative days.1 2 Furthermore, its incidence is increasing as the age of patients undergoing CABG rises.3 The development of AF is associated with an increased incidence of postoperative complications, prolonged intensive care unit (ICU) and hospital stay, with an additional cost to the patients care estimated at $1600 to $10 000.1 2

Prophylactic drug treatment to prevent AF after CABG has had limited efficacy, is contraindicated in many patients, and requires discontinuation in others because of side effects.4 5 6 7 Therefore, alternative nonpharmacological strategies are required.

Biatrial pacing is a technique of simultaneous activation of the right atrium and left atrium. It has been reported to prevent the recurrence of AF in paced patients with marked intra-atrial conduction delay.8 In patients undergoing bypass surgery, the baseline occurrence of intra-atrial conduction delay has been associated with an increased incidence of AF after CABG.9 10 Therefore, it may be postulated that preexistent intra-atrial conduction delay can precipitate the onset of AF in vulnerable patients and that biatrial pacing may be effective in its prevention.

The aim of our randomized controlled study was to further investigate the role of biatrial pacing in the prevention of AF after CABG.


*    Methods
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up arrowAbstract
up arrowIntroduction
*Methods
down arrowResults
down arrowDiscussion
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Patient Population
Between May 1998 to May 1999, all patients under the care of a single surgeon at our institution were screened for participation in this study. Inclusion criteria were first isolated CABG requiring cardiopulmonary bypass, age >18 years, sinus rhythm before surgery, and written informed consent. Exclusion criteria were implantation of a permanent pacemaker, permanent atrial fibrillation, and other planned concurrent surgical procedure. Of 146 suitable patients, 144 consented, with 130 included (89%). Fourteen patients (9.7% of those consenting) were excluded because severe aortic calcification prevented safe placement of left atrial pacing leads. Baseline characteristics were matched in the biatrial and control groups (Table 1Down). The local ethics committee approved the study.


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Table 1. Baseline Characteristics of Patients

Study Protocol
All patients underwent isolated CABG with the standard techniques used at our institution (details of surgical procedure, Table 1Up). Before surgery, {approx}60% of patients were taking ß-blockers. These were withdrawn in all patients at the time of surgery and for the duration of the study, in keeping with our local policy. During surgery, all patients had temporary atrial epicardial pacing leads placed at both the lateral wall of the right atrium and the roof of the left atrium at Bachmann’s bundle. Pacing leads used were either 4 unipolar leads (n=98, Medtronic 6500/6491, 2 at each atrial site) or 2 bipolar leads (n=32, Medtronic 6495, 1 at each atrial site) to allow separate bipolar pacing and sensing at each atrial site.

After surgery on the ICU, the temporary atrial leads were connected and screwed to a pacing Y-adapter (Osypka GmbH) through their pin electrodes within 6 hours. Two unipolar leads (1 pin electrode per lead) were required from each atrial site to connect to the anodal and cathodal ports of the Y-adapter, whereas only 1 bipolar lead was required (2 pin electrodes per lead). The Y-adapter was connected to the atrial port of a permanent pacemaker (Chorum ELA Medical) that acted as a temporary external pacemaker. This connection allowed bipolar sensing and pacing threshold to be performed individually at each site, with baseline measurements recorded by use of the pacemaker. Alternatively, connection of 2 electrode pins (1 from each atrial site) to each Y-adapter port gave biatrial pacing and sensing. The ventricular port was not connected routinely.

Patients remained connected to the pacemaker for 4 days and were randomized to 1 of 2 pacing programs: (1) DDD with base rate of 30 bpm, the lowest programmable rate (control group). Pacing would only occur at sinus rates <30 bpm. (2) DDD with base rate of 80 bpm with activation of an atrial-resynchronized algorithm to produce biatrial pacing. With sinus rates <80 bpm, simultaneous pacing occurred at both atrial sites. For sinus rates >80 bpm, the atrial-resynchronized algorithm (developed by ELA medical) ensured biatrial pacing. It works by sensing from either lead and causing near immediate pacing (3-ms delay) of both leads when atrial activity is detected. In practice, the site where atrial activity is sensed first leads to triggered pacing into the refractory period at this site but to earlier activation at the other atrial site compared with normal intrinsic conduction.

Atrial sensitivity (0.4 mV) and pacing output were programmed to their maximum (5 V at 0.98 ms). After connection and programming, the pacemaker was placed in a small bag that was either pinned to the patient’s clothing or adhered to the skin. It required no monitoring until 4 days after CABG, when sensing and pacing thresholds were reevaluated. At this stage, the pacemaker was removed and interrogated to determine if AF had occurred, and pacing leads were extracted.

The pacemaker acted as our Holter monitor. It is able to detect episodes of AF by responding to nonphysiological atrial acceleration, which has been validated elsewhere.11 The pacemaker records the number of mode switching episodes (atrial arrhythmic events), the total duration of all episodes, and the duration of the last 8 episodes with time of onset. Stored intracardiac electrograms of the last 8 episodes allow confirmation of arrhythmia type (Figure 1Down).



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Figure 1. Example of pacemaker Holters in patient from control group. Top image gives information on percentage of atrial pacing at base rate. P indicates sensed atrial event; A, paced atrial event; V, paced ventricular event; and R, sensed ventricular event. In this control patient there should be 100% sensed atrial activity (P) and 100% ventricular pacing because ventricular port was not connected (PV: 100%). Number of mode-switching episodes (2 FMS indicates fallback mode switching, periods of sustained nonphysiological atrial acceleration), and their total duration (12 hours and 40 minutes) in addition to 24-hour heart rate profile are also shown. Bar chart (top left) shows percentage (6%) of total time spent in FMS mode. Middle image shows 4-day heart rate profile, with 2 periods of higher atrial rates during FMS clearly seen (*). These may be due to episodes of AF. Ventricular rate during FMS episodes was slow because pacemaker mode switches to VDI mode at its base rate (30 bpm in control patient). Lower image shows atrial intra-cardiac signal during FMS episode. As can be seen, P-to-P timing intervals are irregularly irregular, indicating AF. In this example, clinical AF was documented simultaneously. Intracardiac signals were available for up to 8 separate episodes, with precise onset and duration of each episode also stored (data not shown).

Temporary bradycardic pacing was performed in the control group as required with pacing leads from one atrial site, whereas the other site was connected to the Chorum pacemaker. In the biatrial group, pacing-dependent patients relied on the Chorum pacemaker for pacing. Checks were done every 24 hours until patients were pacing independent or until day 4, when they were transferred to a conventional external pacemaker. In complete heart block, patients could have ventricular pacing only or alternatively, DDD pacing by a further Y-adapter placed in the Chorum.

Patients and the surgical team involved in postoperative care were blinded to treatment. Furthermore, this independent surgical team, which was not involved directly with the study, undertook all post-CABG treatment decisions and documentation of postoperative complications into a surgical database. This database was used for our secondary outcomes.

Primary Outcome
The primary outcome was an episode of AF lasting >1 hour detected from the pacemaker Holter.

Secondary Outcomes
Secondary outcomes were clinical episodes of AF (any length) recorded by the surgical team in the first 4 days while connected to the pacemaker and subsequently until discharge; duration of ICU and hospital stay; complications; and pacing lead performance.

Statistical Analysis
Data were analyzed on the basis of intention to treat. Values are given as mean±SD, and median values were stated. Continuous mean variables were analyzed by the use of the Mann-Whitney test, a nonparametric test for 2 independent samples, whereas median values were analyzed by the use of the Kruskal-Wallis test, a nonparametric test for independent samples. Noncontinuous variables were analyzed by the use of {chi}2. Kaplan-Meier analysis was used to compare the probability of remaining in sinus rhythm in the biatrial group compared with the control.


*    Results
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*Results
down arrowDiscussion
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Primary Outcome
Incidence of AF lasting >1 hour was 13.8% (9 of 65 patients) in the biatrial group compared with 38.5% (25 of 65) in the control group (P=0.001, relative reduction 64%, absolute 24.7%). The Kaplan-Meier (Figure 2Down) of percentage patients remaining in sinus rhythm showed a significant difference (P=0.001). Mean duration of AF was not significantly different (biatrial, 26±27 hours versus control, 14.5±20 hours, P=NS).



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Figure 2. Kaplan-Meier curve of percentage of patients remaining in SR after CABG. Bi indicates biatrial group; Con, control group.

Secondary Outcomes
Clinical AF
Incidence of clinical AF while connected to the pacemaker was 10.8% (7 of 65) in the biatrial group compared with 32.3% (21 of 65) in the control group (P=0.003, relative reduction 67%, absolute 21.5%). Only 1 clinical episode (54 minutes) was not a primary end point, which occurred in a patient from the biatrial group.

There was only 1 further episode of clinical AF after pacemaker disconnection that occurred in the control group (day 9). Therefore, before discharge, clinical AF occurred in 10.8% (7 of 65) of the biatrial group compared with 33.8% (22 of 65) of the control group (P=0.002, relative reduction 68%, absolute 23%).

Incidence of any AF (primary and secondary) was 15.4% (10 of 65) in the biatrial group compared with 40% (26 of 65) in the control group (P=0.001, relative reduction 61.5%, absolute 24.6%).

AF was managed by antiarrhythmic medication (intravenous amiodarone) in 6% (4 of 65) in the biatrial group compared with 20% (13 of 65) in the control group (P=0.03). In addition, 1 of these patients (1.5%) from each group also required DC cardioversion. A further patient (1.5%) in each group was treated with oral digoxin. At hospital discharge, 4.5% (3 of 65) in the biatrial group and 18.5% (12 of 65) in the control group were taking oral amiodarone (P=0.01).

ICU Stay
The mean and median ICU stay in the biatrial group was 80±329 hours and 19 hours, respectively, compared with 68±185 hours and 24 hours in the control group (P=NS for mean and median).

In the control group, those with AF (n=26) spent longer in the ICU compared with those remaining in sinus rhythm (SR) (mean 131±280 versus 27±41 hours, P=0.001, median 36 versus 19 hours, P=0.0001). There was no such difference in the biatrial group (AF, n=10; SR, n=55; mean 50±100 versus 86±355 hours, P=NS, median 21 versus 19 hours, P=NS).

Hospital Stay
The mean and median hospital stay in the biatrial group was 7.7±6.9 days and 6 days, respectively, compared with 9.7±10 days and 7 days in the control group (P=NS for mean and median). In the control group, those with AF spent longer in the hospital compared with those remaining in SR (mean 13±14 versus 7.5±5.3, P=0.03, median 7 versus 6 days, P=0.05). There was no such difference in the biatrial group (mean 10±12 versus 7.2±5.5 days, P=NS, median 7 versus 6 days, P=NS).

Complications
There were no serious complications related to pacemaker use or implantation and extraction of the pacemaker leads. No patient in the biatrial group had to have pacing discontinued. Temporary pacing was required in the control group in 11 patients (18.5%; 24 hours n=10; sinus bradycardia n=9; complete heart block n=1; 4 days: n=1, sinus arrest). One patient (1.5%) died in the biatrial group (78-year-old man after 10 days, perioperative stroke) compared with 2 (3%) in the control group (76-year-old woman after 30 days, perioperative stroke, and 78-year-old man after 6 days, perioperative myocardial infarction) (P=NS). Other complications are shown in Table 2Down. Overall, there were significantly fewer complications in the biatrial group compared with the control group (13 versus 35 complications, P=0.001). Proportionately more complications occurred in those with AF compared with those maintaining SR (48 complications in total, 31 [65%] occurred in the 36 patients [28%] in whom AF developed, P<0.0001).


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Table 2. Complications Occurring after CABG in Biatrial and Control Groups

Lead Performance
Lead failure defined as either loss of atrial sensing and/or pacing capture at either site by day 4 occurred in 26 patients (20%, right atrium n=13, left atrium n=13). These were caused by loss of atrial sensing at 1 site in 14 patients (10.8%, right atrium n=8, left atrium n=6). This was combined with loss of capture at the same site in 6 patients. No patient had failure to sense at both sites. There was a further isolated failure of atrial capture in 12 patients (9.2%, right atrium n=5, left atrium n=7). Leads used were unipolar in 22 patients (22 of 98, 22.5%) and bipolar in 4 (4 of 32, 12.5%, P=NS). Failure related to experience of the implanting surgeon, with rates varying from 4% (3 of 70) to 40% (4 of 10, P<0.05).

Lead failure occurred in 12 patients from the biatrial group compared with 14 from the control group (P=NS). The primary end point in the biatrial group was significantly increased in those with lead failure 25% (3 of 12) compared with those without (11%, 6 of 53, P=0.04). This was not observed in the control group (lead failure 36% [5 of 14] versus no lead failure 39% [20 of 51], P=NS).


*    Discussion
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
We showed that 4 days of biatrial pacing significantly reduces the incidence of both monitored and clinical episodes of AF after isolated CABG surgery. There were fewer post-CABG complications in the biatrial group and a significant reduction in the use of both inpatient and outpatient antiarrhythmic treatment with amiodarone. A trend toward reduced ICU and hospital stay was also identified.

Our study was underpowered to evaluate ICU or hospital stay, being primarily designed to test for reduction in monitored AF. However, consistent with previous studies,1 2 3 we demonstrated that the development of AF within our control group was associated with prolonged ICU and hospital stay, suggesting that a larger study may demonstrate significant reductions in these end points with biatrial pacing.

Four days of pacing was chosen because the majority of AF episodes occur within this time period.12 After pacemaker disconnection, there were no new clinical AF episodes in the biatrial group, suggesting that biatrial pacing prevented the development of AF rather than delayed its occurrence. Further advantages of the technique include its applicability to the majority of patients undergoing isolated CABG and that patients could be rehabilitated normally as pacemaker monitoring was not required.

Biatrial pacing was achieved with a permanent pacemaker (Chorum ELA Medical) containing a specific triggered algorithm acting as a temporary external device. It was possible that triggered pacing may have occasionally occurred after normal intrinsic conduction, thus causing pacing into the refractory period. To limit this, our site for left atrial pacing was chosen at Bachmann’s bundle because it is an area of potential conduction block. Furthermore, this site may be involved in AF initiation, and pacing at this site has antifibrillatory properties.13 It is also a relatively accessible site where leads can be placed at the end of surgery off bypass by retracting the aorta, except in {approx}10% of patients with severe aortic calcification, in whom retraction is potentially dangerous. We had no serious complications related to either placement or extraction at this site or any diaphragmatic pacing.

The efficacy of our technique was reduced if lead failure occurred, implying that biatrial pacing was not achieved for the entire 4-day period. Failure rate was kept limited by careful surgical technique while placing the leads and the use of high-quality temporary epicardial pacing leads and a pacemaker with good atrial sensing capabilities (0.4 mV). Despite this, we still had a failure rate of 20%. However, in no case did we have sensing failure at both sites, which causes asynchronous pacing that is proarrhythmic.14

This is the first published randomized study on biatrial pacing to prevent AF after CABG. The only other report is a pilot study of 61 patients comparing 3 treatment options of either biatrial, right atrial, or no pacing. This showed no significant difference between any of these treatments on the incidence of AF after CABG.15 This study was underpowered but did suggest a positive interaction between ß-blocker use combined with biatrial pacing in preventing AF. ß-Blockers were stopped in our patients. The site of left atrial pacing also differed from our study. It was at the left posterior aspect of the left atrium, which led to diaphragmatic pacing in a proportion of patients requiring pacing discontinuation.

The mechanism for AF development after CABG is unclear but must involve proarrhythmic electrophysiological changes in the atrium, including slowing in conduction velocity and or shortening of the refractory period. Possible culprits include sterile pericarditis, which develops with a time course similar to the occurrence of AF and causes slowing in conduction velocity.16 Baseline measurements indicative of slow atrial conduction such as prolonged P-wave duration on the surface electrogram, intra-atrial conduction delay at electrophysiological studies, and prolonged signal-averaged P-wave duration are all predisposing factors for AF development after CABG.9 10 17 A role for atrial ischemia has also been postulated as a further mechanism of AF through increased dispersion of refractoriness.18 Finally, increased sympathetic activation causing shortening of atrial refractory periods may be important.19

The initial report of an antiarrhythmic effect from biatrial pacing was from a prospective study in patients with atrial arrhythmias requiring permanent pacemakers for conventional indications.8 However, the antifibrillatory mechanisms of biatrial pacing have mainly been investigated with temporary pacing leads placed either within the coronary sinus or at the ostium, combined with a high right atrial lead. These studies have shown that biatrial pacing in response to extrastimuli from the high right atrium increases atrial conduction velocity, preventing areas of conduction block needed to initiate AF, prolonging the refractory period, and improves the recovery of excitable tissue, thus having an antifibrillatory role.20 21

Study Limitations
Our study was underpowered to assess ICU and hospital stay. We also excluded patients requiring redo-operations, valvular procedures, and MIDCAB (minimally invasive CABG). Further studies are required to assess whether this technique can be applied to all types of cardiovascular surgery.

The optimal site for left atrial pacing and the optimal mechanism for biatrial pacing has not been assessed in this study.

The withdrawal of ß-blockers is not universally practiced, and it is standard practice in many institutions to continue them after surgery. Their withdrawal may increase the incidence of AF. However, biatrial pacing appears to be effective even in their absence. Furthermore, the percentage of patients taking ß-blockers at baseline was not greater in those with AF compared with those remaining in SR for both groups (control: AF 52% versus SR 65%, biatrial: AF 55% versus SR 59%). However, the role of biatrial pacing combined with ß-blockers requires further evaluation.

The increased number of complications in the control group may have been a chance finding rather than a genuine reduction from biatrial pacing. AF has consistently been shown to be associated with complications; however, it remains unclear which is cause and effect in this situation. It is possible that patients with AF are more prone to postoperative complications. Further studies are required to confirm our finding of a reduced complication rate with AF prevention.

Lead failures remain a constant problem and reduce the efficacy of this technique. The incidence of AF, however, was still lower with biatrial pacing even if there was lead failure compared with the control patients. With a dedicated and experienced surgeon, a failure rate of <10% should be achievable. Furthermore, our results, which showed a significant benefit, were analyzed by intention to treat and included a failure rate of 20%.

Holter episodes were chosen as the primary end point because Holter monitoring has been used in the majority of previous studies. A 1-hour duration of AF was selected to try and ensure clinical relevance. All bar 1 of the 28 clinical episodes (96%) were longer than this. Furthermore, with the use of the pacemaker Holters, there were 9 further AF episodes with a duration <1 hour (mean duration 26±17 minutes, biatrial n=5, control n=4), which were all asymptomatic. However, the importance of AF duration, its clinical detection, and its relation to complications in this setting are unknown. Therefore, any duration of AF is arbitrarily selected. However, our technique remains effective if we include all AF episodes regardless of duration (biatrial 23% versus control 45%, P=0.009).

We were also reliant on a pacemaker Holter that has been validated previously as a permanent implant but not as a temporary device, as used in this study. However, of the 28 patients with clinical episodes of AF (81% of total), all correlated with information from our pacemaker Holter. In the remaining clinically undetected episodes, intracardiac electrograms stored in the pacemaker showed a fast, irregular atrial intracardiac signal consistent with the electrograms seen during the clinical episodes of AF. These were interpreted as AF. Atrial tachycardia or flutter was believed to be unlikely because of the irregular signal, and neither of these arrhythmias was observed clinically. There does, however, remain a small possibility of arrhythmia misclassification of these clinically silent episodes.

Conclusions
Biatrial pacing for 4 days significantly reduces the incidence of monitored and clinical episodes of AF after isolated CABG. This is associated with a significant reduction in postoperative complications. There was also a trend toward reduced ICU and hospital stay.


*    Acknowledgments
 
This study was supported by Pacemakers (Chorum ELA) donated by ELA Medical. Temporary pacing wires were supplied by a sponsorship from Medtronic Ltd.

Received January 25, 2000; revision received April 18, 2000; accepted April 20, 2000.


*    References
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowMethods
up arrowResults
up arrowDiscussion
*References
 
1. Mathew JP, Parks R, Savino JS, et al, for the Multicenter Study of Perioperative Ischaemia Research Group. Atrial fibrillation following coronary artery bypass graft surgery: predictors, outcomes, and resource utilization. JAMA. 1996;276:300–306.[Abstract/Free Full Text]

2. Aranki SF, Shaw DP, Adams DH, et al. Predictors of atrial fibrillation after coronary artery surgery: current trends and impact on hospital resources. Circulation. 1996;94:390–397.[Abstract/Free Full Text]

3. Creswell LL, Schuessler RB, Rosenbloom M, et al. Hazards of postoperative atrial arrhythmias. Ann Thorac Surg. 1993;56:539–549.[Abstract]

4. Andrews TC, Reimold SC, Berlin JA, et al. Prevention of supraventricular arrhythmias after coronary artery bypass surgery: a meta-analysis of randomized trials. Circulation. 1991;84(suppl III):III-236–III-244.

5. Kloter Weber U, Osswald S, Huber M, et al. Selective versus non-selective antiarrhythmic approach for prevention of atrial fibrillation after coronary surgery: is there a need for pre-operative risk stratification? A prospective placebo-controlled study using low-dose sotalol. Eur Heart J. 1998;19:794–800.[Abstract/Free Full Text]

6. Suttrorp MJ, Kingma JH, Joe Gin MT, et al. Efficacy and safety of low and high dose sotalol versus propranolol in the prevention of supraventricular tachyarrhythmias early after coronary artery bypass operations. J Thorac Cardiovasc Surg. 1990;100:921–926.[Abstract]

7. Daoud EG, Strickberger SA, Man KC, et al. Preoperative amiodarone as prophylaxis against atrial fibrillation after heart surgery. N Engl J Med. 1997;337:1785–1791.[Abstract/Free Full Text]

8. Daubert C, Berder V, Gras D, et al. Atrial tachyarrhythmias associated with high degree interatrial conduction block: prevention by permanent atrial resynchronization. Eur J Card Pacing Electrophysiol. 1994;1:35–44.

9. Capucci CA, Frabetti L, Turinetto B, et al. Fibrillazione atriale nei post operati de bypass aorto-coronarica. G Ital Cardiol. 1987;17:575–582.[Medline] [Order article via Infotrieve]

10. Buxton AE, Josephson ME. The role of P wave duration as a predictor of postoperative atrial arrhythmias. Chest. 1981;80:68–73.[Abstract/Free Full Text]

11. Defaye P, Dournaux F, Mouton E, for the AIDA Multicentre Study Group. Prevalence of supraventricular arrhythmia from the automated analysis of data stored in the DDD pacemakers of 617 patients: the AIDA study. Pacing Clin Electrophysiol. 1998;21:250–255.[Medline] [Order article via Infotrieve]

12. Olshansky B. Management of atrial fibrillation after coronary artery bypass graft. Am J Cardiol. 1996;78:27–34.[Medline] [Order article via Infotrieve]

13. Niwano S, Yamaura M, Washizuka T, et al. Comparison of arrhythmogenicity of atrial pacing at several right atrial pacing sites: evaluation of canine atrial electrograms during atrial pacing and arrhythmogenicity for atrial fibrillation. Pacing Clin Electrophysiol. 1998;21:1918–1926.[Medline] [Order article via Infotrieve]

14. Kurz DJ, Naegeli B, Kunz M, et al. Epicardial, biatrial synchronous pacing for prevention of atrial fibrillation after cardiac surgery. Pacing Clin Electrophysiol.. 1999;22:721–726.[Medline] [Order article via Infotrieve]

15. Gertstenfeld EP, Hill MRS, French SN, et al. Evaluation of right atrial and biatrial temporary pacing for the prevention of atrial fibrillation after coronary artery bypass surgery. J Am Coll Cardiol. 1999;33:1981–1988.[Abstract/Free Full Text]

16. Waldo AL. Atrial fibrillation after surgery. In: Olsson SB, Allessie MA, Campbell RWF, eds. Atrial Fibrillation Mechanisms and Therapeutic Strategies.. Armonk, NY: Futura Books; 1994:211–224.

17. Stafford PJ, Kolvekar S, Cooper J, et al. Signal averaged P wave compared with standard electrocardiography or echocardiography for prediction of atrial fibrillation after coronary bypass grafting. Heart. 1997;77:417–422.[Abstract/Free Full Text]

18. Kolvekar S, D’Souza A, Akhatar P, et al. Role of atrial ischaemia in development of atrial fibrillation following coronary artery bypass surgery. Eur J Cardiothorac Surg. 1997;11:70–75.[Abstract]

19. Kalman JM, Munawar M, Howes LG, et al. Atrial fibrillation after coronary bypass grafting is associated with sympathetic activation. Ann Thorac Surg. 1995;60:1709–1715.[Abstract/Free Full Text]

20. Papageorgiou P, Anselme F, Kirchhof CJHJ, et al. Coronary sinus pacing prevents induction of atrial fibrillation. Circulation. 1997;94:1893–1898.

21. Papageorgiou P, Monahan K, Boyle NG, et al. Site-dependent intra-atrial conduction delay: relationship to initiation of atrial fibrillation. Circulation. 1996;94:384–389.[Abstract/Free Full Text]




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Ann. Thorac. Surg., January 1, 2005; 79(1): 117 - 126.
[Abstract] [Full Text] [PDF]


Home page
EuropaceHome page
T. Hakala, A. J.M. Valtola, A. K. Turpeinen, A. E. Hedman, R. E.U. Vuorenniemi, J. M. Karjalainen, I. S. Vajanto, J. Kouri, P. A. Jaakkola, and J. E.K. Hartikainen
Right atrial overdrive pacing does not prevent atrial fibrillation after coronary artery bypass surgery
Europace, January 1, 2005; 7(2): 170 - 174.
[Abstract] [Full Text] [PDF]


Home page
HeartHome page
R A Archbold and R J Schilling
Atrial pacing for the prevention of atrial fibrillation after coronary artery bypass graft surgery: a review of the literature
Heart, February 1, 2004; 90(2): 129 - 133.
[Abstract] [Full Text] [PDF]


Home page
Eur. J. Cardiothorac. Surg.Home page
M. Debrunner, B. Naegeli, M. Genoni, M. Turina, and O. Bertel
Prevention of atrial fibrillation after cardiac valvular surgery by epicardial, biatrial synchronous pacing
Eur. J. Cardiothorac. Surg., January 1, 2004; 25(1): 16 - 20.
[Abstract] [Full Text] [PDF]


Home page
J Am Coll CardiolHome page
D. Amar, H. Zhang, S. Miodownik, and A. H. Kadish
Competing autonomic mechanisms precedethe onset of postoperative atrial fibrillation
J. Am. Coll. Cardiol., October 1, 2003; 42(7): 1262 - 1268.
[Abstract] [Full Text] [PDF]


Home page
Asian Cardiovasc. Thorac. Ann.Home page
W.-K. Au, S.-W. Chiu, M.-P. Sun, L.-C. Cheung, and L.-C. Cheng
Biatrial Pacing to Prevent Atrial Fibrillation After Coronary Artery Bypass
Asian Cardiovasc Thorac Ann, September 1, 2003; 11(3): 222 - 225.
[Abstract] [Full Text]


Home page
Ann. Thorac. Surg.Home page
J.F. M. Bechtel, J. F. Christiansen, H.-H. Sievers, and C. Bartels
Low-energy cardioversion versus medical treatment for the termination of atrial fibrillation after CABG
Ann. Thorac. Surg., April 1, 2003; 75(4): 1185 - 1188.
[Abstract] [Full Text] [PDF]


Home page
Eur. J. Cardiothorac. Surg.Home page
H. Shin, K. Hashizume, Y. Iino, K. Koizumi, T. Matayoshi, and R. Yozu
Effects of atrial fibrillation on coronary artery bypass graft flow
Eur. J. Cardiothorac. Surg., February 1, 2003; 23(2): 175 - 178.
[Abstract] [Full Text] [PDF]


Home page
HeartHome page
A D Taylor, J G Groen, S L Thorn, C T Lewis, and A J Marshall
New insights into onset mechanisms of atrial fibrillation and flutter after coronary artery bypass graft surgery
Heart, December 1, 2002; 88(5): 499 - 504.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
E. Crystal, S. J. Connolly, K. Sleik, T. J. Ginger, and S. Yusuf
Interventions on Prevention of Postoperative Atrial Fibrillation in Patients Undergoing Heart Surgery: A Meta-Analysis
Circulation, July 2, 2002; 106(1): 75 - 80.
[Abstract] [Full Text] [PDF]


Home page
NEJMHome page
J. M. Cooper, M. S. Katcher, and M. V. Orlov
Implantable Devices for the Treatment of Atrial Fibrillation
N. Engl. J. Med., June 27, 2002; 346(26): 2062 - 2068.
[Full Text] [PDF]


Home page
Journals of Gerontology Series A: Biological Sciences and Medical SciencesHome page
W. S. Aronow
Management of the Older Person With Atrial Fibrillation
J. Gerontol. A Biol. Sci. Med. Sci., June 1, 2002; 57(6): M352 - 363.
[Abstract] [Full Text]


Home page
Cardiovasc ResHome page
A. Shimizu and O. A. Centurion
Electrophysiological properties of the human atrium in atrial fibrillation
Cardiovasc Res, May 1, 2002; 54(2): 302 - 314.
[Abstract] [Full Text] [PDF]


Home page
HeartHome page
M. R Gold
ELECTROPHYSIOLOGY: Permanent pacing: new indications
Heart, September 1, 2001; 86(3): 355 - 360.
[Full Text] [PDF]


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