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Ann Thorac Surg 2000;69:1064-1069
© 2000 The Society of Thoracic Surgeons

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ORIGINAL ARTICLES: CARDIOVASCULAR

Tachyarrhythmias and triggering factors for atrial fibrillation after coronary artery bypass operations

^a Department of Thoracic and Cardiovascular Surgery, University Hospital, Uppsala, Sweden
^b Department of Cardiology, University Hospital, Uppsala, Sweden
^c Department of Clinical Chemistry, University Hospital, Uppsala, Sweden
^d Department of Physiology, University of Uppsala, Uppsala, Sweden

Address reprint requests to Dr Jidéus, Department of Thoracic and Cardiovascular Surgery, University Hospital, S-751 85 Uppsala, Sweden
e-mail: lena.jideus{at}kirurgi.uu.se

	Abstract

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Background. We evaluated the role of supraventricular arrhythmias and assessed clinical predictors of atrial fibrillation (AF) that developed after coronary artery bypass operations.

Methods. Eighty patients, with a mean age of 65.8 years, underwent 24-hour Holter monitoring preoperatively and for 4 consecutive days postoperatively, or until clinically documented AF, for analysis of the number of premature beats and tachyarrhythmias. Atrial areas and atrial peptides were measured preoperatively and postoperatively.

Results. Twenty-nine of 80 (36.3%) patients had postoperative AF. Preoperatively, the maximal supraventricular premature beats per minute were higher in the AF group (p = 0.02). The body mass index and total amount of cardioplegia were lower (p = 0.02 and p = 0.006, respectively), and withdrawal of ß-blockers postoperatively more frequent (p = 0.001) in the AF group, but atrial areas and atrial peptides did not differ.

Conclusions. Frequent supraventricular premature beats preoperatively may indicate a propensity for AF. A larger amount of cardioplegia during the cross-clamp period may reduce the risk of postoperative AF. Further studies are mandatory to clarify why patients with lower body mass index were more prone to AF.

	Introduction

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Atrial fibrillation (AF) is a common complication after cardiac operations with an incidence that has remained unchanged for some years despite improvements in surgical techniques and drug therapy. It is frequently associated with increased morbidity and discomfort, requiring treatment with antiarrhythmic drugs or electrical cardioversion, resulting in prolonged hospitalization [1].

The mechanism of postoperative AF after cardiac operations has long been a subject of speculation. Triggering factors, such as atrial wall stretch, ischemia, inflammation, or imbalance in the autonomic nervous system, can result in changes in conduction and refractoriness, previously shown to be related to the propensity for AF [2, 3]. In several studies age has been suggested to be the most important independent risk factor [1, 4, 5]. Because more patients are undergoing coronary artery bypass grafting (CABG) at an older age, the incidence of postoperative AF will continue to increase, leading to prolonged hospital stays, which has considerable financial implications [1, 4].

The aim of this study was to evaluate the role of supraventricular arrhythmias by continuous 24-hour Holter electrocardiogram recordings and to identify other clinical predictors of postoperative AF after CABG. We also hypothesized that postoperative fluid retention and postoperative stress might contribute to increased atrial vulnerability to arrhythmias.

	Material and methods

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Ninety-six patients who had elective CABG at the Department of Thoracic and Cardiovascular Surgery, University Hospital, in Uppsala, Sweden, between October 1994 and May 1997 were included in the study. Patients with a clinical history of documented supraventricular tachyarrhythmias (SVT), heart valve disease, cardiomyopathy, diabetes mellitus, chronic obstructive pulmonary disease, chronic renal disease, severe reduced ejection fraction, thyroid disorders, or treatment with anti-arrhythmic drugs were not included to obviate disorders that could be associated with an increased incidence of AF [2, 6]. Eight patients were excluded because abnormal surgical procedures were used or because of complications occurring during or after the operation. The reasons for exclusion were a different surgical technique (n = 2), reexploration because of bleeding (n = 3), inotropic support for 6 hours or more due to markedly reduced ejection fraction postoperatively (n = 2), and treatment with antiarrhythmic drugs immediately after CABG because of ventricular arrhythmia (n = 1). Another 8 patients were excluded because of severe anxiety postoperatively, leading to incomplete 24-hour Holter recordings. The clinical characteristics of the remaining 80 patients (67 men, 13 women) are summarized in Table 1. All patients had given their informed oral consent to the study, which was approved by the local ethics committee.

View larger version (15K): [in this window] [in a new window]   Fig 1. Results of analysis of atrial areas. Data are shown as mean values and error lines indicate one standard deviation. Open bars are patients maintaining sinus rhythm and black bars are patients developing atrial fibrillation. All p values are less than 0.05 within the groups, preoperatively and on Day 2, but all p values are not significant between the two patients groups. (Preop = preoperative.)

View larger version (14K): [in this window] [in a new window]   Fig 2. Results of analysis of atrial peptides. Data are shown as mean values and error lines indicate one standard deviation. Open bars are patients maintaining sinus rhythm and black bars are patients developing atrial fibrillation. All p values are less than 0.05 within the groups, preoperatively and on Day 2, but all p values are not significant between the two patients groups. (pg/mL = picogram per milliLiter; pmol/L = picomol per Liter; preop = preoperative.)

Arrhythmia definitions and analysis
A SVT was defined as a narrow and regular or irregular QRS complex tachycardia with three or more consecutive beats with a heart rate above or equal to 100 beats per minute. Atrial fibrillation was defined as the absence of consistent P waves before each QRS complex and an irregular ventricular rate. Sustained AF was defined as an episode of AF lasting at least 30 seconds. A supraventricular premature beat (SPB) was defined as a narrow QRS complex occurring with 20% prematurity and differentiated from sinus arrhythmia on the basis of P-wave morphology, cyclic changes in preceding RR intervals, or both. Bradycardia was defined as a three-interval heart rate less than 50 bpm. The following variables were analyzed for each 24-hour period recorded: maximal number of SPB and ventricular premature beats (VPB) per minute, maximal number of SPB and VPB per hour, mean number of SPB and VPB per hour, the number of episodes of SVT, SVT with nn sequential SPBs, and SVT with nn maximal beats per minute (SVT maximum rate).

Echocardiography and atrial peptides
Two-dimensional echocardiographic examinations were performed with a Hewlett-Packard Sonos 1500 or 2500 cardiac ultrasound unit (Hewlett-Packard, Andover, MA). A 2.5-MHz transducer was used for most of the two-dimensional examinations. The right and left atrial areas were measured in the apical four-chamber view at atrial end diastole during sinus rhythm preoperatively and on day 2, in the morning at rest. The same technician took all of the measurements. Absolute values and values corrected for body surface area, using the Boyd formula, were calculated. Blood samples were taken at the same time for the echocardiographic examination and collected from a decubital vessel in ethylenediaminetetraacetic acid and aprotinin-treated (atrial natriuretic peptide [ANP] analysis) or heparin-containing (N-terminal pro-ANP analysis) tubes on ice. Atrial natriuretic peptide in plasma was measured by a commercial radioimmunoassay (RPA512; Amersham, United Kingdom). N-terminal pro-ANP was measured by a two-site Delfia immunoassay. The method is described in detail elsewhere [7].

Postoperative complications
Early death was defined as death from any cause within 30 days postoperatively, perioperative myocardial infarction as the development of new Q waves on the surface by 12-lead electrocardiogram, and neurologic deficit as symptoms for 6 hours or longer and verified by computed tomography. No patient required postoperative pacing.

Statistical analysis
The associations of all preoperative, perioperative, and postoperative factors with postoperative AF were analyzed using an unpaired t test and ² test, as required. Double-checking was done using relevant nonparametric methods. Continuous variables are presented as mean ± standard deviation. Logistic regression was used when the dependent variable is dichotomous and represents an event or a presence/absence relation. Such an event or relation has a probability of occurrence that can also be stated as odds. The probability of the event, p, has the following relation to the concept of odds: odds (event) = p/(1 - p). However, to get a linear relationship between the dependent variable, the event, and the predictors, we have to take the natural log of the odds. Our model then becomes: 1n[p/(1 - p)] = b₀ + b₁X₁ + ... + b_kX_k. This can easily be rewritten as p = 1/(1 + e^-Z), where Z is the linear combination of all the predictors: Z = b₀ + b₁X₁ + ... + b_kX_k. Values of p less than 0.05 were considered significant. Discriminant analysis was also used but had some limitations because some of the variables were dichotomous and not suitable as predictors.

	Results

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Postoperative sustained AF occurred in 29 of 80 patients (36.3%), of whom 26 were symptomatic. Three were diagnosed by Holter recordings. Atrial fibrillation started on average 2.2 days (52.84 ± 20.8 hours) postoperatively. All 26 patients with clinically recognized AF were treated with sotalol and converted to sinus rhythm before discharge, whereas in the remaining 3 patients, AF terminated spontaneously after 7 to 189 minutes. The patients’ demographics, surgical, and postoperative data are summarized in Table 1. There were no statistically significant differences between patients who had AF and those who maintained sinus rhythm postoperatively, with regard to clinical variables, except for BMI, the total amount of cardioplegia, and the withdrawal of ß-blockers postoperatively. The patients who had AF postoperatively had a lower BMI (p = 0.02), received less cardioplegia (p = 0.006), and were taken off ß-blockers more frequently postoperatively (p = 0.001) than those maintaining sinus rhythm. Heart-specific biochemical markers did not differ significantly between patients remaining in sinus rhythm and those who had postoperative AF; serum aspartate aminotransferase (1.19 ± 0.5 µkat/L versus 1.16 ± 0.5 µkat/L), serum creatinine kinase-MB (25.0 ± 18.8 µg/L versus 23.9 ± 21.4 µg/L), and serum troponin-t (0.52 ± 0.6 µg/L versus 0.38 ± 0.4 µg/L). There were no early deaths, and no patient had perioperative myocardial infarction or neurological deficit.

Arrhythmia analysis
A total of 20 of 29 (70%) patients with postoperative AF had SVT runs recorded preoperatively compared with 23 of 51 (45%) patients who maintained sinus rhythm, which was a significant difference (p = 0.03). The maximum SPB per minute and the recorded SVT maximum rate were significantly higher preoperatively in patients who had AF compared with those who remained in sinus rhythm (Table 2), whereas the other preoperative variables did not differ between the patient groups. Patients who had AF had significantly more postoperative SPBs than patients who maintained sinus rhythm (Table 2). There was no significant difference regarding episodes of bradycardia and VPBs recorded preoperatively and postoperatively between the two patient groups (Table 2).

Logistic regression
Presence of AF was considered the dependent variable, and three variables were found to be predictors, including BMI, total amount of cardioplegia, and maximum SPB per minute. The model obtained had a likelihood ratio ² statistic of 18.64, which, with four degrees of freedom, gave a p value of 0.00032. The classification table shows that 88% of the patients without AF were classified correctly, and the model correctly classified 51.72% of the patients with AF. The overall odds ratio was 7.86, and the overall classification rate was 74.68%, which is substantially greater than the naive classification rate, which was 42.29%. If a test statistic Z is calculated, a p value less than 0.001 is obtained, which also serves to consolidate the foundation on which the classification rests (Table 3).

	Comment

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The observation that preoperative maximum SPB per minute and the SVT maximum rate were significantly higher in patients who had postoperative AF than in those remaining in sinus rhythm can be explained by an anatomic substrate that is already present preoperatively. The P-wave duration, measured preoperatively, was recently reported to predict postoperative AF independently [10]. An increased P-wave duration could indicate left atrial enlargement or prolonged intra-atrial conduction, thus an anatomic substrate. The use of anti-arrhythmic drugs in the patients studied and the use of different methods of measuring P-waves in the various studies, however, make the results difficult to evaluate [10–12].

The observed increase in right and left atrial areas in both patient groups was probably secondary to an increased volume overload postoperatively, triggering the secretion of atrial peptides. Atrial dilatation is the main regulatory mechanism for atrial secretion of ANP and N-terminal pro-ANP, the plasma concentration of which might be a marker for increased atrial pressures [13]. Moreover, ANP is also reported to have effects on the autonomic nervous system [13], which might contribute to the development of postoperative AF.

Another explanation for increased frequency of arrhythmias preoperatively in patients who had postoperative AF might be an imbalance in the autonomic nervous system. Moreover, advanced age has been associated with increased levels of circulating norepinephrine [14]. These patients could be more vulnerable to withdrawal of ß-blockers postoperatively, which may be supported by the finding of significantly more frequent SPBs and the increase in the number of SVT runs postoperatively. Increased sympathetic stimulation secondary to the postoperative trauma might also be important [3]. In our study, 37.5% of the patients who had AF discontinued ß-blockade postoperatively compared with only 7.1% of those remaining in sinus rhythm. This is in accordance with the reported twofold to fivefold increased incidence of postoperative AF when ß-blockade was discontinued after CABG [3]. Several other studies have also supported the benefit of postoperative ß-adrenergic blockade [8]. Unfortunately, in our study, ß-blockers were not reinstituted consistently. Therefore, it is not possible to conclude anything without a randomized trial, which ensures that patients continuing with ß-blocking agents are similar to patients in whom these drugs are discontinued postoperatively.

Although the operative technique was consistent among the surgeons, the total amount of cardioplegia was significantly lower in the AF group than in the patients remaining in sinus rhythm, which is a novel finding. It is therefore possible that the atria were not sufficiently protected during the cross-clamp period. None of our patients had perioperative myocardial infarction, and the heart-specific biochemical markers were low and did not differ between the two groups, indicating that the ventricles were well protected. Many authors have speculated whether perioperative protection of the atria is important for subsequent postoperative AF. A strong correlation was found between the duration of atrial activity during the cross-clamp period and the incidence of postoperative SVTs, suggesting inadequate atrial protection during global myocardial ischemia [15]. Smith and colleagues [16] found that atrial regions received significantly less cardioplegic solution compared with the ventricles, resulting in electrophysiologic alterations in atrioventricular conduction and, consequently, more postoperative supraventricular arrhythmias. Moreover, ultrastructural and morphometric studies of mitochondria obtained from biopsy specimens of patients who had cardiac operations showed significantly poorer preservation of the atrium compared with the ventricle [17]. Conversely, topical cardiac cooling during the cross-clamp period, to improve atrial protection by bringing atrial temperature in line with that of the ventricles, resulted in even more frequent supraventricular arrhythmias postoperatively [18]. That study, however, also included patients with a history of supraventricular arrhythmia. An attempt to decrease the atrial temperature by using double caval cannulation with snaring, to avoid the return of warm venous blood to the right atria, resulted instead in a reactivation of the right atria during the cross-clamp period in 61% of the patients [19]. When mild hypothermia was used before the adoption of cold hyperkalemic cardioplegia, the incidence of postoperative supraventricular arrhythmias was only 15% in a study including only elective coronary artery bypass [20]. The low incidence may, however, in part be related to the patients’ young age, which was more than a decade less than in our study. The very low incidence of postoperative AF in patients undergoing cardiac transplantation [1, 4] may also be related to the patient’s young age, which probably makes them less vulnerable to atrial ischemia than those who have CABG. It should, however, be emphasized that old noncardioplegic procedures with short ischemia time [21] and new operation techniques such as off-pump procedures, ie, CABG but without cardiopulmonary bypass and cardioplegic technique, have the same frequencies of postoperative AF as conventional techniques [22]. Nevertheless, a larger amount of cardioplegia given during the cross-clamp period might reduce the risk of postoperative AF. Surprisingly, in our study, patients who had postoperative AF had significantly lower BMI. Even though the total amount of cardioplegia given to the patients with lower BMI was less, BMI was an independent risk factor for postoperative AF. Therefore, further studies are mandatory. It is still not known why postoperative AF occurs 2 to 3 days after the operation and not earlier. A possible explanation is the time needed for the above-mentioned triggering factors to develop and cause electrophysiologic abnormalities required to elicit postoperative AF [4].

Moreover, it is still not known whether postoperative AF increases the risk of developing AF in the future. Further studies are mandatory to identify patients at risk and to target these patients with more intensive prophylactic measures to reduce the incidence of postoperative AF.

	Acknowledgments

 
Grants for this study were received from the Swedish Heart and Lung Foundation.

	References

Top Abstract Introduction Material and methods Results Comment References

 

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