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Ann Thorac Surg 1995;60:1709-1715
© 1995 The Society of Thoracic Surgeons
Departments of Cardiology, Clinical Pharmacology, and Cardiac Surgery, Austin Hospital, Melbourne, Australia
Accepted for publication July 24, 1995.
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Methods. Continuous ambulatory monitoring was performed for 80 hours in 131 patients after coronary artery bypass grafting. Right atrial plasma norepinephrine levels were assessed preoperatively and every 4 hours for 48 hours postoperatively.
Results. Of the 131 patients, 50% (65) had development of atrial fibrillation and 36% (47) required treatment. Onset of atrial fibrillation was preceded by a significant increase in sinus rate and atrial ectopic activity. On multivariate logistic regression, elevated mean postoperative norepinephrine levels (5.78 ± 2.83 versus 3.57 ± 1.31 nmol/L; p = < 0.0001), increased age (68.9 ± 5.7 versus 63.8 ± 8.7 years; p = 0.02), and decreased postoperative magnesium levels (0.79 ± 0.09 versus 0.83 ± 0.10 mmol/L; p = 0.02) were independently associated with the occurrence of atrial fibrillation.
Conclusions. Elevated norepinephrine levels suggest that sympathetic activation may be important in the pathogenesis of atrial fibrillation after coronary artery bypass grafting, and this underlines the importance of ß-adrenoceptor blockade as prophylaxis.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Numerous studies, many of which have been retrospective, have attempted to determine possible etiologic factors in the pathogenesis of atrial fibrillation after coronary artery bypass grafting [1, 2]. However, only two factors have been related to the development of postoperative atrial fibrillation with any consistency. These were advanced age and preoperative withdrawal of ß-adrenoceptor antagonist therapy [3, 4], although even here conflicting evidence exists [5].
It has been demonstrated that advancing age is associated with increasing circulating norepinephrine level, and one postulated reason for this is increasing sympathetic outflow [6]. Several clinical studies have examined the role of ß-adrenoceptor antagonists in the pathogenesis of atrial fibrillation after coronary artery bypass grafting [2, 7]. White and associates [7] and Salazar and colleagues [2] both found a twofold to fivefold increase in incidence of atrial fibrillation in patients in whom administration of ß-adrenoceptor antagonists was ceased when compared with those whose drug treatment was continued postoperatively. These observations may be due to the effects of ß-adrenoceptor antagonist withdrawal on the sensitivity of ß-adrenoceptor-mediated responses [8, 9]. It is also noteworthy that atrial arrhythmias are more likely to occur 20 to 60 hours postoperatively at the time of maximal rebound effect from ß-adrenoceptor antagonist withdrawal [1]. Furthermore, a number of randomized, controlled studies have found that ß-adrenoceptor antagonists given prophylactically significantly reduce the incidence of postoperative atrial fibrillation [7].
However, despite this wealth of data, the specific precipitants and pathophysiology of atrial fibrillation after coronary artery bypass grafting are poorly defined, and a better understanding would have obvious implications regarding prophylaxis. We have prospectively investigated the pathophysiology of this arrhythmia and examined the particular hypothesis that postoperative sympathetic activation may play an important role.
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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All of the study subjects gave their written, informed consent, and the study was approved by the Hospital Ethics Review Committee.
Anesthetic induction was performed using medium-dose fentanyl, and anesthesia was maintained by an intermittent inhalational agent, either halothane or enflurane. Two-stage right atrial venous cannulation was used. All patients received warm blood cardioplegia for induction and reperfusion, which in the majority of patients was given both anterogradely and retrogradely. Early postoperative analgesia was by intravenous morphine either as an infusion or by incremental bolus.
Norepinephrine Sampling
Samples for measurement of right atrial plasma norepinephrine levels were taken before institution of cardiopulmonary bypass and postoperatively every 4 hours for 48 hours. Samples were drawn from the proximal port of a Swan-Ganz catheter during the initial 24 hours postoperatively and subsequently from the distal port after the catheter had been pulled back to the right atrium. Samples were taken with the patient resting comfortably for 20 minutes at approximately a 30- to 45-degree incline and were transferred immediately to ice-chilled tubes and then centrifuged at 4°C. The plasma was then separated for storage at -70°C until assayed. Analysis of norepinephrine levels was by high-performance liquid chromatography with electrochemical detection [10]. Norepinephrine samples taken after onset of sustained atrial fibrillation were excluded from analysis as atrial fibrillation may be associated with hypotension and secondary increase in sympathetic activity.
Holter Monitoring
Monitoring was performed using a two-channel electrocardiography monitor (Cardiodata) connected in the immediate postoperative period and continued for 80 hours. Tapes were analyzed manually by freezing the monitor when an arrhythmia was detected during tape scanning, and details of the arrhythmia were noted by review of a hard copy electrocardiography print out. Tapes were analyzed by an experienced cardiac technician and reviewed independently by two cardiologists. All analyses were performed blinded to the results of other investigations.
Definitions
Atrial fibrillation was defined as an irregular narrow complex rhythm (in the absence of bundle branch block) with absence of discrete P waves (Fig 1
). Atrial flutter was defined by the presence of coarse ``saw-tooth'' flutter waves with an atrial rate of 250 to 350 beats/min. Atrial tachycardia was defined as an atrial rate greater than 120 beats/min, with sudden onset, and a P wave morphology distinctly different from that of the sinus P wave, to make the distinction from sinus tachycardia. Atrial arrhythmias were arbitrarily defined as nonsustained if lasting between ten beats and 10 minutes, and sustained if persisting for more than 10 minutes.
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Pulmonary infection was defined as the development of purulent sputum associated with a fever and chest roentgenographic signs consistent with consolidation. Hypertension was a history of hypertension requiring treatment during the 12 months before operation.
Left ventricular hypertrophy was defined from the preoperative electrocardiogram using standard voltage criteria [11]. Left ventricular end-diastolic pressure was measured before the left ventriculogram at preoperative cardiac catheterization. Left ventricular ejection fraction was digitized from a preoperative single-plane left ventriculogram in the right anterior oblique projection.
Other Investigations
Serum levels of sodium, potassium, creatinine, and creatine phosphokinase-MB fraction were measured preoperatively and daily postoperatively for 3 days. Serum magnesium level was sampled preoperatively and at 48 hours postoperatively. A chest roentgenogram and a 12-lead electrocardiogram were performed preoperatively and daily postoperatively for 3 days.
Statistical Analysis
All analyses were performed between patients in whom atrial fibrillation developed and those in whom it did not. Patients with other atrial arrhythmias such as atrial flutter or atrial tachycardia were not included in the group with atrial fibrillation as the mechanism of these atrial arrhythmias differs [12].
Data were analyzed in the following stepwise manner, and all comparisons, regardless of the statistical significance, are reported to allow assessment of the potential for finding significant association due to chance.
We first performed univariate analysis on nine prospectively defined variables, selected on the basis of several considerations, including previously demonstrated or biologically plausible association with postoperative atrial fibrillation. Second, we included these variables in a multivariate stepwise logistic regression analysis to determine which were independent predictors of atrial fibrillation. The following variables were included in these analyses: age at operation, preoperative use of a ß-adrenoceptor antagonist, left ventricular ejection fraction, preoperative norepinephrine level, number of bypass grafts, aortic cross-clamp time, previous coronary operation, mean postoperative norepinephrine level, and postoperative magnesium level. Subsequently, analysis was performed on ten further variables considered by other previous investigators to have a possible association with postoperative atrial fibrillation [5]. We selected these as ``secondary'' variables as they were considered less likely to be important in the development of atrial fibrillation and because the inclusion of multiple statistical comparisons increases the possibility of chance association, thereby negatively influencing the validity of a positive finding. These ``secondary'' variables are defined above and included sex, a history of hypertension, diabetes, left ventricular hypertrophy, left ventricular end-diastolic pressure, recent myocardial infarction, perioperative infarction, cardiopulmonary bypass time, the development of pulmonary infection, and postoperative serum potassium level (sampled at 48 hours postoperatively). Univariate analysis on these ``secondary'' variables was performed, followed by a multivariate analysis that included all 19 variables.
Baseline comparisons between the above groups and all other statistical analyses were performed using Student's unpaired t test for continuous data and the 
2 statistic or Fisher exact test where appropriate for categoric data. All statistical tests were two-sided, and significance was accepted at the 0.05 level. Data are presented as mean ± one standard deviation in tables and as mean ± one standard error in the figure of norepinephrine levels.
All statistical analyses were performed using the SPSS statistical software (version 4.0.1; Microsoft Corp, Redmond, 1990).
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Incidence of Arrhythmias
The incidence of atrial arrhythmias (overall 55%) is presented in Table 1. Atrial fibrillation as the predominant arrhythmia developed in 65 patients (50%) within 80 hours postoperatively. In 52 (40%) the arrhythmia was sustained (duration, >10 minutes) and in 13 (10%) it was nonsustained (duration, 10 beats to 10 minutes). Forty-seven patients (36%) required treatment for atrial fibrillation as determined by the managing physician. In many patients with atrial fibrillation, short episodes of atrial flutter could be detected; however, atrial flutter as the predominant atrial arrhythmia was relatively uncommon, occurring in only 5 patients (4%). Of these, only 2 patients had sustained atrial flutter. Atrial tachycardia as the sole atrial arrhythmia occurred in only 2 patients. However, atrial tachycardia was present in an additional 13 patients, all of whom also developed atrial fibrillation.
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In the 3 minutes immediately before onset of sustained atrial fibrillation, there was a pattern of increasing sinus rate (96.4 ± 14.9 versus 87.7 ± 9.1 beats/min; p < 0.05) and an increase in the frequency of atrial ectopic activity (11.7 ± 7.3 per 3 minutes versus 5.7 ± 5.6; p = 0.0001) when compared with the 3 hours before onset. Of the 52 patients in whom sustained atrial fibrillation developed, only 4 (7.7%) remained in atrial fibrillation at the time of discharge.
Norepinephrine Levels
Plasma norepinephrine levels increased significantly in the immediate postoperative period. Mean postoperative levels were significantly higher in patients developing atrial fibrillation (p < 0.0001 by univariate analysis). In addition, at every 4-hour postoperative sampling interval there was a significant increase in right atrial norepinephrine levels in patients in whom atrial fibrillation developed (Fig 2). Norepinephrine levels were not statistically different in patients with nonsustained versus sustained atrial fibrillation.
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Other Variables
Table 2 shows the nine prospectively identified variables considered to have a possible influence on development of atrial fibrillation. On univariate analysis, increasing age, preoperative treatment with ß-adrenoceptor antagonist therapy, and lower postoperative serum magnesium levels, in addition to elevated postoperative norepinephrine levels, were associated with the development of atrial fibrillation.
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Multivariate Analysis
Using multivariate logistic regression, only elevated mean postoperative plasma norepinephrine levels (p < 0.0001), increased age (p = 0.03), and decreased postoperative serum magnesium level (p = 0.04) were found to be independently associated with atrial fibrillation.
Serum Magnesium
Magnesium levels decreased significantly after operation (0.86 ± 0.08 mmol/L preoperatively versus 0.81 ± 0.09 mmol/L postoperatively; p < 0.001). Although, as already noted, lower postoperative serum magnesium levels were associated with atrial fibrillation, there was no such association between preoperative magnesium level and the development of atrial fibrillation (No atrial fibrillation: 0.86 ± 0.08 mmol/L versus atrial fibrillation: 0.85 ± 0.08 mmol/L; p = not significant).
Preoperative ß-Adrenoceptor Antagonist Therapy
Preoperative norepinephrine levels were higher in patients receiving preoperative ß-adrenoceptor antagonists than in patients receiving other antianginal agents, although the difference did not reach statistical significance (1.86 ± 2.41 versus 1.25 ± 1.36 nmol/L, respectively; p = 0.09). However, mean postoperative norepinephrine levels were significantly higher in those patients receiving ß-adrenoceptor antagonists before operation (5.34 ± 2.89 versus 4.16 ± 2.22 nmol/L; p = 0.01). The difference persisted to 48 hours postoperatively even though ß-adrenoceptor antagonists were not given in the postoperative period.
The mean time of onset of sustained atrial fibrillation was significantly later for patients who had received preoperative ß-adrenoceptor antagonists (53.3 ± 17.1 hours) than for those who had not (39.7 ± 19.0 hours; p < 0.01).
Analysis of Secondary Variables
None of the secondary variables were found to be significantly associated with atrial fibrillation by univariate analysis, and when included in the multivariate analysis, again only the three above-mentioned variables were significant.
Duration of Intensive Care and Hospital Stay
The duration of hospital stay was significantly longer in the 47 patients with atrial fibrillation requiring treatment (9.5 ± 4.9 days) compared with patients either without atrial fibrillation or those with clinically insignificant (untreated) atrial fibrillation (8.1 ± 3.2 days; p < 0.05). The duration of intensive care stay was, however, not prolonged in those patients with atrial fibrillation requiring treatment compared with those who did not (2.3 ± 1.9 versus 2.2 ± 0.5 days, respectively; p = 0.53).
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Arrhythmia Incidence
The incidence of atrial arrhythmias in this study (50% atrial fibrillation and 55% overall) is in the upper range of that previously reported [1, 3, 7]. This relatively high incidence may reflect our use of continuous Holter monitoring and the inclusion of nonsustained atrial fibrillation (although only 10%) in the analysis. Also, the exclusion of patients less than 50 years of age would be expected to produce an artificially increased incidence of atrial fibrillation.
Norepinephrine Levels
Although the pattern of onset of atrial fibrillation provides indirect evidence as to the pathogenesis of postoperative atrial fibrillation, measurement of plasma norepinephrine level allows a more direct analysis of the level of sympathetic activation. Using this method we have demonstrated significantly increased levels in patients in whom atrial fibrillation developed after coronary artery bypass grafting, suggesting a possible causative role.
The predominant sources of circulating norepinephrine in humans derives largely from sympathetic nerve endings and in particular from the sympathetic innervation to vascular walls, especially of small arteries and arterioles [15]. The relative contribution of a particular organ to peripheral venous norepinephrine levels depends both on the amount of norepinephrine released and on the regional blood flow to that particular organ. Although sampling norepinephrine from a peripheral vein may predominantly reflect norepinephrine release in peripheral musculature, central mixed venous norepinephrine levels are more likely to provide an accurate picture of ``overall'' sympathetic nervous activity. Thus mixed venous norepinephrine reflects the averaged contributions from various vascular beds and provides a reasonable if indirect index of sympathetic neural activity [15]. For this reason we chose to sample norepinephrine from the right atrium. Although pulmonary artery sampling would provide a better mixed venous estimate, we did not have the facility to monitor a pulmonary artery catheter for 48 hours.
There are two limitations with this approach to assessment of sympathetic activation. First, plasma levels of norepinephrine depend not only on the rate of release of norepinephrine but also on the rate of clearance from the plasma pool. However, within relatively homogeneous population groups plasma norepinephrine levels have been shown to correlate strongly with norepinephrine spillover. Second, it has been elegantly demonstrated, using tritiated norepinephrine to measure organ specific norepinephrine spillover rates, that sympathetic nervous outflow to individual organs may not be activated or suppressed uniformly in different disease states [16]. We postulate that in patients who have had coronary artery bypass grafting, sympathetic activation is likely to be generalized and therefore the right atrial norepinephrine level would adequately reflect cardiac sympathetic activity.
A marked elevation in norepinephrine levels after coronary artery bypass grafting has previously been demonstrated and has been shown to be associated with postoperative hypertension [17]. We have demonstrated a significant association between mixed venous norepinephrine levels and the development of postoperative atrial fibrillation, suggesting that sympathetic activation may be an important factor in the majority of patients in whom this arrhythmia develops. Our hypothesis is that within the spectrum of sympathetic activation in response to a cardiac operation, those patients whose norepinephrine levels fall in the upper range have a higher risk of atrial fibrillation. An important issue is why the time of peak norepinephrine levels, which occurred in most patients at 4 hours postoperatively (and probably earlier), did not coincide with the time of onset of atrial fibrillation (mean, 42.7 ± 19.7 hours postoperatively). There may be a number of explanations. First, in those patients taking ß-adrenoceptor antagonists preoperatively, a rebound phenomenon after withdrawal would account for the timing of atrial fibrillation onset. This phenomenon has its peak effect at 20 to 60 hours after discontinuation of drug administration, which correlates well with the time of onset of postoperative atrial fibrillation. Indeed, we found that in those patients receiving ß-adrenoceptor antagonists before operation, onset of atrial fibrillation was significantly later than in patients not receiving these agents. Second, by sampling norepinephrine levels at 4-hour intervals we would not have detected more frequent fluctuations, which might occur in response to interventions such as physiotherapy, insertion of intravenous lines, or in association with early ambulation. However, it is also possible that high levels of sympathetic activation may interact with another as yet unidentified factor to precipitate atrial fibrillation.
Preoperative ß-Adrenoceptor Antagonist Therapy
As was usual practice in this unit, administration of ß-adrenoceptor antagonists was stopped on the day before operation and not routinely recommenced in the early postoperative phase, thus producing a withdrawal effect. It has previously been demonstrated that patients taking ß-adrenoceptor antagonists may have elevated circulating norepinephrine levels [18], which may persist for up to 14 days after their cessation and which can be accentuated by operation. In this study, both the incidence of atrial fibrillation and postoperative norepinephrine levels were significantly higher in patients who were receiving ß-adrenoceptor-blocking agents in the preoperative period. However, when entered into the multivariate analysis, there was no independent effect of preoperative ß-adrenoceptor-blocking agents on incidence of atrial fibrillation. This suggests that the effect of these drugs on atrial fibrillation may be mediated, at least in part, via increased norepinephrine levels.
Magnesium Levels
In this study a lower serum magnesium level was independently associated with postoperative atrial fibrillation. The high frequency of hypomagnesemia after coronary artery bypass grafting is well established [19], and recent studies have demonstrated that prophylactic administration of magnesium sulfate decreased the incidence of atrial fibrillation after coronary artery bypass grafting [20].
The only other variable shown in our study to be significantly associated with development of postoperative atrial arrhythmias was increasing age, which has been shown to be a risk factor for postoperative atrial fibrillation in a number of earlier studies [3]. Although increased age has been associated with elevated norepinephrine levels, we found an independent effect from both variables.
Limitations of the Study
Due to the logistic and ethical contraindications to leaving a Swan-Ganz catheter in situ when no longer clinically indicated, we did not measure right atrial norepinephrine levels beyond 48 hours postoperatively. As 42% of atrial arrhythmias occurred between 48 and 80 hours postoperatively, these data would have provided a more complete picture of the relationship between atrial fibrillation and plasma norepinephrine.
Although we have demonstrated an independent relationship between postoperative atrial fibrillation and elevated norepinephrine levels, the reason for the elevation is uncertain, and we have not established cause and effect. Cardiac operation and admission to the intensive care unit are clearly potent activators of the sympathetic nervous system, but this does not explain why norepinephrine levels were higher in those patients in whom atrial fibrillation developed. We found no significant relationship between plasma norepinephrine level and analgesic requirement, but this is a rather crude measure of postoperative pain.
Magnesium levels were sampled only once in the postoperative period, precluding any correlation of the time of maximal hypomagnesaemia with the time of onset of atrial fibrillation. Therefore, cause and effect have not been clearly established and this result should be viewed with caution. This preliminary observation warrants further study.
Conclusions
We have demonstrated a significant and independent difference in right atrial norepinephrine levels in patients in whom atrial fibrillation developed after coronary artery bypass grafting compared with those in whom it did not. This difference was maintained throughout the 48 hours of sampling, and was independent of left ventricular function and immediate preoperative ß-adrenoceptor antagonist therapy. The results provide circumstantial evidence that atrial fibrillation after coronary artery bypass grafting may be mediated at least in part by activation of the sympathetic nervous system. Furthermore, the development of an increase in sinus rate before the onset of atrial fibrillation coupled with increasingly frequent atrial extrasystoles and episodes of atrial tachycardia is further evidence suggesting sympathetic activation.
These findings suggest that the most logical approach to prevention of atrial fibrillation in patients after coronary artery bypass grafting would be by methods that blunt sympathetic activation or effects. In spite of clinical trials demonstrating benefit, the use of prophylactic ß-blockade is not widespread [1]. In those patients receiving preoperative treatment with ß-adrenoceptor antagonists, there is a particularly strong argument for continuing administration of these agents in the early postoperative period. In view of the significantly prolonged duration of hospital stay in those patients in whom atrial fibrillation develops, the economic impact of effective prophylaxis could be considerable.
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Acknowledgments |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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We gratefully acknowledge the expert technical assistance of Ms Jane Tippett and Ms Tracy Muir. This study could not have been performed without the support and cooperation of the nursing and medical staff of the intensive care, coronary care, and cardiothoracic units.
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