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Ann Thorac Surg 2000;69:1057-1063
© 2000 The Society of Thoracic Surgeons
a Department of Cardiology, The Cleveland Clinic Foundation, Cleveland, Ohio, USA
b Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, Cleveland, Ohio, USA
Address reprint requests to Dr Chung, Department of Cardiology, The Cleveland Clinic Foundation, 9500 Euclid Ave, Desk F-15, Cleveland, OH 44195-5245
e-mail: chungm{at}ccf.org
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Abstract |
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Methods. To determine whether atrial overdrive pacing reduces atrial fibrillation and atrial ectopy after coronary artery bypass grafting, 100 patients were randomized to no atrial pacing (Control) versus AAI pacing at 10 beats/min or more above the resting heart rate (Paced), started by postoperative day 1 and continued through day 4. Major end points were new atrial fibrillation and frequency of atrial ectopy during the first 4 days after coronary artery bypass grafting.
Results. Atrial fibrillation occurred by day 4 in 13 of 51 (25.5%) Paced and in 14 of 49 (28.6%) Control patients, p = 0.90. Control patients who developed atrial fibrillation had significantly more atrial ectopy than those who did not. Atrial ectopy was paradoxically more frequent in the Paced group (2,106 ± 428 versus 866 ± 385 per 24 hours, p = 0.0001). Loss of capture, sensing, and consistent atrial pacing occurred frequently during atrial pacing.
Conclusions. Contrary to prevailing opinion and practice, postoperative atrial overdrive pacing significantly increases atrial ectopy and does not reduce the likelihood of atrial fibrillation.
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Introduction |
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The occurrence of frequent atrial ectopy after operation has often been perceived to herald the potential onset of atrial fibrillation. In practice this often triggers use of atrial overdrive pacing to suppress this ectopy. In patients with permanent pacemakers, dual-chamber or atrial pacing, which maintains atrioventricular synchrony, does appear to reduce the incidence of atrial fibrillation when compared to single-chamber ventricular pacing [9–12]. However, this practice has not been proved to reduce atrial fibrillation after cardiac operation, when the mechanisms producing atrial fibrillation may differ from that of chronic forms of atrial fibrillation.
In this study we aimed to test the hypothesis that atrial pacing after coronary artery bypass grafting (CABG) reduces postoperative atrial fibrillation and atrial ectopy. Using temporary pacing leads that are routinely placed at the time of CABG, we studied the effect of atrial overdrive pacing in the most clinically used mode (AAI) on atrial premature depolarization frequency and incidence of atrial fibrillation after operation.
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Material and methods |
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Eligibility for randomization and inclusion into the study was assessed 6 to 24 hours after operation (on postoperative day 0 or early postoperative day 1) to allow evaluation of hemodynamic stability. Patients were excluded from randomization for any of the following: development of atrial fibrillation during the time between operation and randomization; resting native heart rate more than 100 beats/min that would then preclude atrial overdrive pacing at a maximum rate of 110 beats/min; hemodynamic instability at the time of assessment for randomization (hypotension with systolic blood pressure less than 90 mm Hg or cardiac index less than 2.2 L · min-1 · m-2 ); atrial threshold of temporary pacing wires more than 10 mA; or postoperative pacemaker dependency (no intrinsic rhythm more than 50 beats/min or requiring atrial pacing for hemodynamic reasons with baseline systolic blood pressure < 90 mm Hg or cardiac index < 2.2 L · min-1 · m-2 and improvement with atrial pacing).
Eligible patients were randomized to AAI pacing at 10 or more beats/min faster than the native heart rate at rates of 90 to 110 beats/min (Paced) versus no pacing (Control). A computerized random number generation program was used.
Pacing protocol
At the time of operation, pairs of atrial and ventricular temporary epicardial pacing wires (A & E Medical Corporation, Farmingdale, NJ) were placed. For the Paced group, atrial pacing was achieved through a DDD temporary pacemaker pulse generator (Medtronic model 5345 or 5346; Medtronic, Minneapolis, MN) programmed in the AAI mode with outputs at least twofold over the diastolic pacing threshold (maximum, 20 mA) and sensitivity with at least a twofold safety margin. Antibradycardia pacing in the VVI mode only at 60 beats/min was allowed in the Control group at the discretion of the primary physicians. Pacing threshold, sensitivity, and native heart rates were assessed daily and pulse generators adjusted accordingly. Pacing was continued for 4 days unless pacing wires were nonfunctional or discontinued as clinically indicated. Pacing was also discontinued if the native resting heart rate exceeded the maximum pacing rate of 110 beats/min. If the primary end point occurred, then atrial pacing was discontinued and the arrhythmia was treated at the discretion of the primary physician. Primary physicians were allowed to use all medications other than class I or III antiarrhythmic agents at their discretion including ß-adrenergic blockers, digoxin, calcium-channel blockers, and aspirin during the protocol. If the primary clinical end point was observed, then use of any antiarrhythmic agent was permitted.
End points
The primary end point of the trial was the development of atrial fibrillation/flutter requiring pharmacologic or electrical therapy. Pharmacologic therapy included rate-controlling AV nodal blocking agents and Vaughan Williams class I or III antiarrhythmic agents. Electrical therapy included direct current cardioversion or atrial overdrive pacing for the termination of atrial fibrillation/flutter. Atrial fibrillation that was brief enough not to warrant pharmacologic or electrical treatment was not considered an end point. Atrial premature depolarization frequency was quantitated and normalized per 24-hour period.
Data collection and analysis
Baseline data collection and initial evaluation included (1) complete history, physical examination, and laboratory testing as was standard for all patients undergoing CABG at our institution; (2) selective coronary angiography, and (3) assessment of left ventricular function by echocardiography, contrast or nuclear left ventriculography obtained within 6 months of operation. Continuous taped telemetry or Holter monitoring was performed during the 4 days after randomization to quantify atrial premature depolarization (APD) frequency and the occurrence of clinical tachyarrhythmias. Ectopy counts were normalized per 24-hour period, after exclusion of nonanalyzable data due to monitor artifact and censoring of counts during atrial fibrillation and after the development of the primary atrial fibrillation end point.
Statistical analysis
Demographic and clinical variables, effect of ß-adrenergic blocker use, and atrial fibrillation incidence were analyzed using the 
2 test or Fisher’s exact test for categorical variables and t tests for continuous variables. Atrial ectopy frequency was analyzed using nonparametric Mann-Whitney tests due to the skewness of the data. Statistical analysis was performed using SAS (Cary, NC) and SPSS (Chicago, IL) software. Variables were considered significant at p values less than 0.05. Patient and perioperative characteristics were reported as mean ± standard deviation unless otherwise stated. APD frequency was reported as mean ± standard error of the mean.
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Results |
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Patient characteristics
As shown in Table 1, baseline clinical characteristics in the two groups were similar except for a trend (p = 0.07) toward younger age in the Paced group (62.5 ± 9.1 years) compared to the Control group (65.7 ± 8.0 years). There were no significant differences between Paced and Control groups detected in perioperative characteristics (Table 2), including inotrope, ß-adrenergic blocker, calcium-channel blocker, or digoxin use, aorta cross-clamp time, or cardiopulmonary bypass time, although there was a trend toward more perioperative inotrope use in the Control group.
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Pacing had no effect on the incidence of atrial fibrillation when patients were grouped by age. By day 4, atrial fibrillation occurred in 3 of 16 (18.8%) Control and 2 of 25 (8%) Paced patients less than 65 years old (p = 0.36). Atrial fibrillation occurred in 11 of 33 (33.3%) Control and 11 of 26 (42.3%) Paced patients 65 years of age or older (p = 0.59).
Effect of ß-blockers and pacing on atrial fibrillation
The incidence of atrial fibrillation was not significantly different overall in patients on preoperative ß-blockers (15 of 43 patients, 34.9%) compared to those who were not on preoperative ß-blockers (12 of 57 patients, 21.1%), p = 0.17. The incidence of atrial fibrillation tended to be lower in patients who received postoperative ß-blockers (3 of 17 patients, 17.6%) compared to those who did not receive postoperative ß-blockers (24 of 83 patients, 28.9%), but this was not statistically significant (p = 0.55).
In the Control group, atrial fibrillation tended to occur more frequently in patients on preoperative ß-adrenergic blockers (10 of 23 patients, 43.5% versus 4 of 26 patients, 15.4%) than on no ß-adrenergic blockers, p equal to 0.056. This trend was not observed in Paced patients in whom atrial fibrillation occurred in 5 of 20 patients (25%) on ß-blockers versus 8 of 31 patients (25.8%) on no ß-blockers, p value greater than 0.95. There were no significant differences in atrial fibrillation incidence in Control or Paced groups when stratified by postoperative ß-blocker use, although only 17% of patients received postoperative ß-blockers. The incidence of atrial fibrillation was 12 of 40 (30.0%) in Control patients not receiving postoperative ß-blockers, 2 of 9 (18.4%) in Control patients who did receive ß-blockers (p > 0.95), 12 of 43 (27.9%) in Paced patients not receiving ß-blockers, and 1 of 8 (12.5%) in Paced patients receiving ß-blockers (p = 0.66).
Incidence of atrial fibrillation by efficacy analysis
Intermittent loss of atrial capture was detected in 8 patients and intermittent atrial undersensing was detected in 20 patients. Periods of sinus rhythm or sinus tachycardia at rates above the programmed atrial pacing rate, resulting in intermittent loss of atrial overdrive pacing, were detected in 27 patients. Of the 13 Paced patients who developed atrial fibrillation, review of telemetry taping revealed 5 were not paced at the time of atrial fibrillation onset.
Pacing was discontinued before postoperative day 4 because of lead failure in 3 patients, sinus tachycardia in 3 patients, and in 7 patients because of other clinical indications dictated by the primary physicians. Atrial overdrive pacing was completed for the duration of the protocol in 38 of 51 patients (74.5%).
By efficacy analysis, accounting for discontinuation of pacing in the Paced group, the incidence of atrial fibrillation in the Paced group was not significantly different from that in the Control group. The cumulative incidence of atrial fibrillation by postoperative day 4 was 24% in the Paced group and 29% in the Control group (p = 0.72). The incidence of atrial fibrillation in the patients in the Paced group who completed the protocol and had no atrial undersensing, undercapture, or override by sinus rhythm or sinus tachycardia was 8 of 28 (29%), which was not different from that of the Control group (p = 1.0).
Atrial premature depolarization frequency
Telemetry or Holter monitor tapes were analyzed for APD frequency. APD frequency was normalized over 24-hour periods for postoperative days 1 through 4. A total of 244 patient-days of monitoring was available for review (with 155,349 minutes of analyzable data after censoring of atrial fibrillation).
For the control group (Fig 3), patients who developed postoperative atrial fibrillation had a 10-fold higher APD frequency when compared to patients who did not develop atrial fibrillation (2,715 ± 1,405 versus 232 ± 72 APDs/24 hours, p = 0.023). Overall increased APD frequency in the atrial fibrillation patients was not seen in the Paced group (2,204 ± 665 APDs/24 hours with atrial fibrillation versus 2,075 ± 529 APDs/24 hours without atrial fibrillation), although on postoperative day 2, APD frequency was significantly higher in the Paced patients who developed atrial fibrillation (4,756 ± 1,450 versus 1,794 ± 607 APDs/24 hours, p = 0.019).
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Comment |
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TopAbstractIntroductionMaterial and methodsResultsCommentReferences |
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Previous studies
In patients with permanent pacemakers, dual-chamber or atrial pacing, which maintains atrioventricular synchrony, may reduce the long-term incidence of atrial fibrillation when compared to single-chamber ventricular pacing [9, 10, 12]. Atrial fibrillation that occurs by a vagally mediated mechanism has been successfully controlled by atrial overdrive pacing [13]. However, Mathew and colleagues [5] suggested that postoperative atrial, although not atrioventricular, pacing was marginally associated with an increase in postoperative atrial fibrillation. A smaller study of 61 patients after CABG also showed that right or biatrial pacing did not prevent atrial fibrillation, although a trend toward benefit was observed in patients treated with ß-adrenergic blockers [14].
This failure to prevent postoperative atrial fibrillation may be due to differences in triggers of atrial fibrillation occurring after cardiac operation compared to chronic forms of atrial fibrillation. Factors that may promote atrial fibrillation in the postoperative period include atrial trauma, inflammation, infarction, edema, and pericarditis [15–17]. Also, patients with coronary artery disease undergoing CABG are often on ß-adrenergic blockers. Subsequent withdrawal in the postoperative period may lead to increased vulnerability to atrial fibrillation [18]. The peak occurrence of postoperative atrial fibrillation during the second and third postoperative day suggests that an inflammatory mechanism or ß-blocker withdrawal may be important.
Although subsequent reports have suggested a benefit to chronic biatrial or dual site pacing [11], these were small in study size and studies have yet to be published applying this to patients after cardiac operation. At the time of this study, dual or left atrial overdrive pacing was not routine. In addition, an adequate examination of single site overdrive atrial pacing had not yet been performed. As single right atrial temporary pacing lead placement is currently the routine during cardiac operations, using this existing practice might be more practical, if effective, than pursuing pacing through the left atrium. The left atrial leads may be technically slightly more difficult to place or remove. Single site temporary AAI mode of pacing was chosen because in our experience this has been the mode most commonly used clinically to suppress APDs and atrial fibrillation after cardiac operation.
We had hoped that if effective, this mode of pacing might supplant the use of ß-adrenergic blockers in the prophylaxis of postoperative atrial fibrillation. Therefore, the use of ß-adrenergic blockers was not required or promoted during the study. Although ß-blockers have been shown to be effective in the prevention of postoperative atrial fibrillation [7, 8, 19], in our experience, they are not often used because of perceived or real contraindications in postoperative patients.
Effect of atrial pacing on atrial fibrillation and atrial premature depolarizations
The importance of APD frequency to vulnerability to postoperative atrial fibrillation was demonstrated by the more than 10-fold increase in APD frequency in control patients who developed atrial fibrillation. Although not associated with an increase in atrial fibrillation, atrial pacing was associated with an overall increase in APD frequency, when compared to the control group, which was in the range of control patients that experienced atrial fibrillation.
Potential mechanisms of atrial ectopy proarrhythmia from atrial pacing could include (1) inappropriate premature atrial paced beats due to atrial undersensing or noncapture; (2) sinus rates increasing above atrial paced rates that might predispose to competitive atrial pacing in patients with marginal atrial sensing; and (3) proarrhythmic increase in APDs triggered by the higher heart rate. All three mechanisms were observed frequently in the paced group during this study.
The inability to achieve consistent atrial overdrive pacing, using the AAI mode, was detected frequently upon review of taped telemetry tracings and Holter monitors. Atrial undersensing and loss of capture, often occurring concomitantly, led to an increase in pacing-induced APDs in several patients. This occurred despite at least daily vigilance of pacing thresholds, sensing, outputs, and rates. Upon ambulation, many patients reached heart rates that exceeded the programmed atrial pacing rate. Indeed, this study demonstrated that atrial pacing in the AAI mode was ineffective in achieving consistent overdrive pacing in 50% of the atrially paced patients. This may have resulted in competitive atrial pacing and an increase in pacing-induced APDs that could have diminished the efficacy of pacing. Our results thus underscore the potential for APD proarrhythmia with temporary pacemakers, not only those that are programmed with atrial insensitivity or that could promote competitive atrial pacing (eg, in the atrial asynchronous or DVI mode), but also in standard AAI modes.
The potential proarrhythmic effect of atrial pacing at faster heart rates could also have promoted an increase in APD frequency and diminished the usefulness of atrial overdrive pacing at the 90 to 110 beat/min range that was used in this study. Atrial ischemia may not have been directly alleviated by the coronary artery bypass grafts that are generally targeted toward relief of ventricular ischemia. In addition, postoperative atrial fibrillation is unlikely to be due to bradycardia- or vagally-mediated mechanisms. If this form of atrial fibrillation is more adrenergically mediated, atrial pacing may be more likely to augment rather than suppress triggering atrial ectopy. No different effects were noted among patients who received postoperative ß-adrenergic blockers, although conclusions are limited by the small number of patients treated with postoperative ß-blockers.
Study limitations
Because of the difficulties in maintaining consistent atrial pacing, the increase in APD frequency, and the absence of a clinically significant effect seen on atrial fibrillation incidence, the trial was not continued past 100 patients, as it was unlikely to show a potential benefit of pacing on atrial fibrillation and the increase in APD frequency with pacing indicated potential harm. Nevertheless, the sample size was comparable to those used in other trials of drug prophylaxis for postoperative atrial fibrillation.
Interpretation of atrial ectopy counts from later postoperative days, particularly days 3 and 4, should be limited, as patients who were removed from monitoring after the development of atrial fibrillation could bias results on these days. Lastly, despite frequent clinical use, which led to the selection of this mode for this study, pacing in the AAI mode did not achieve consistent atrial overdrive pacing. Difficulties in maintaining atrial pacing and variability in native heart rates particularly during activity limit the potential efficacy of this clinically used mode of atrial pacing.
In conclusion, contrary to prevailing opinions and common practice after CABG, atrial overdrive pacing in the AAI mode using temporary wires did not prevent postoperative atrial fibrillation. A 10-fold increase in atrial premature depolarization frequency was noted in control patients who developed atrial fibrillation. Paradoxically, atrial overdrive pacing did not suppress but promoted atrial ectopy. Future efforts to determine whether atrial overdrive pacing is effective in suppressing atrial fibrillation and atrial ectopy should address the technical limitations in temporary atrial pacing. Unless efficacy of atrial pacing is established in the future, the routine use of atrial overdrive pacing in the AAI mode to suppress atrial ectopy in the postoperative period may be proarrhythmic and should be avoided.
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Acknowledgments |
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