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Ann Thorac Surg 2007;84:1878-1884. doi:10.1016/j.athoracsur.2007.07.014
© 2007 The Society of Thoracic Surgeons
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Right arrow Lung - transplantation

Original Articles: General Thoracic

Atrial Fibrillation After Lung Transplantation: Timing, Risk Factors, and Treatment

David P. Mason, MDa,*, Dale H. Marsh, MDa, Joan M. Alster, MSb, Sudish C. Murthy, MD, PhDa, Ann M. McNeill, RNa, Marie M. Budev, DOc, Atul C. Mehta, MDc, Gösta B. Pettersson, MD, PhDa, Eugene H. Blackstone, MDa,b

a Department of Thoracic and Cardiovascular Surgery, Cleveland Clinic, Cleveland, Ohio
b Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, Ohio
c Department of Pulmonary, Allergy, and Critical Care Medicine, Cleveland Clinic, Cleveland, Ohio

Accepted for publication July 6, 2007.

* Address correspondence to Dr Mason, Department of Thoracic and Cardiovascular Surgery, Cleveland Clinic, 9500 Euclid Ave/Desk F24, Cleveland, OH 44195 (Email: masond2{at}ccf.org).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background: Atrial fibrillation (AF) is common after lung transplantation and can be challenging to manage. Objectives of this study were to determine prevalence and timing of perioperative AF, identify its risk factors, evaluate treatment strategies, assess return to sinus rhythm by hospital discharge, and investigate its impact on outcomes.

Methods: From March 1995 to January 2005, 333 patients underwent primary lung transplantation (exclusive of heart and lung transplantation). Data on timing, prevalence, management, and outcome were extracted from the Unified Transplant Registry and Cardiothoracic Anesthesia databases, supplemented with medical record review. Risk factors for AF were identified by logistic regression analysis, and bootstrap bagging was used for variable selection.

Results: AF developed postoperatively in 68 patients (20%), with the peak incidence 2 days after operation. Risk factors were older age (p = 0.0004), primary pulmonary hypertension (5 of 12 [42%] versus 63 of 321 [20%] for others, p = 0.006), and extremes of weight (p = 0.04). Pharmacologic treatment consisted of rate control agents only in 18 patients (27%), antiarrhythmics only in 5 (7.5%), and both in 44 (66%). Cardioversion was required in 24 (36%). Rhythm was recorded for 59 patients, and 55 (93%) were in sinus rhythm at discharge. Postoperative AF had no short-term or long-term survival impact.

Conclusions: AF after lung transplantation is common, with occurrence peaking 2 days postoperatively. Older patients and those with primary pulmonary hypertension are at elevated risk. Treatment requires a combination of multiple pharmacologic agents and electrical cardioversion. Almost all patients are discharged in sinus rhythm, and prognosis is unaffected.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Atrial fibrillation (AF) after lung transplantation presents an important challenge. It can produce hemodynamic instability, dyspnea, and pulmonary congestion, which can mimic or mask other serious postoperative conditions such as pneumonia or acute rejection and add to treatment and diagnostic uncertainty [1, 2]. It has been shown to increase hospital stay and perioperative mortality [3]. Few data are available on its treatment strategies and return to sinus rhythm [3–6]. Our own experience with AF after lung transplantation has been that it is common, difficult to manage, and frequently requires multiple pharmacologic agents or electrical cardioversion to control. Therefore, to improve its management, we set out to (1) determine prevalence and timing of perioperative AF, (2) identify its risk factors, (3) evaluate treatment strategies, (4) assess return to sinus rhythm by hospital discharge, and (5) investigate its impact on outcomes.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 Acknowledgments
 References
 
Patients
From March 1995 to January 2005, 333 patients underwent primary single-lung or double-lung transplantation for end-stage lung disease at Cleveland Clinic, exclusive of heart and lung transplantation. Data were extracted from the Unified Transplant Registry and Cardiothoracic Anesthesia databases, which have been approved for use in research by the Institutional Review Board (IRB), with patient consent waived. The IRB approved supplemental review of medical records.

End Points
The primary end point was development of atrial arrhythmias. All patients had continuous electrocardiographic monitoring in the intensive care unit (ICU) and were subsequently discharged to a monitored unit throughout their hospital stay. Atrial arrhythmias were identified according to the Society of Thoracic Surgeons definition as those that were clinically documented or treated. These were ascertained through review of ICU records, charts, and electrocardiograms. Observed atrial arrhythmias were AF and atrial flutter (AFL), and unless otherwise stated, we use "AF" to mean either. All-cause mortality was determined by patient follow-up. Mean follow-up for survivors was 3.7 ± 2.3 years, and 27% were followed up for more than 5 years.

Secondary end points included treatment strategies, discharge rhythm, length of postoperative stay, and survival. Discharge rhythm was identified as normal sinus rhythm (NSR), AF, or AFL.

Timing and Risk Factors
Timing of AF was calculated as the interval from the date of transplantation to the date of developing AF. Time-related risk of AF was estimated parametrically by a multiphase hazard decomposition method [7], which was also used to identify donor, recipient, and transplant factors (Table 1 and Appendix) associated with AF. (For additional details, see http://www.clevelandclinic.org/heartcenter/hazard.) Data were screened to ensure that at least five AF events were associated with each dichotomous variable. Bagging was used for variable selection [8]. Briefly, automated stepwise variable selection with p = 0.05 for inclusion was performed on 1000 bootstrap samples, and the results were aggregated by both individual factors and clusters of related factors. Those appearing in 50% or more of the analyses (median rule) were considered reliably statistically significant at p ≤ 0.05.


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  		Table 1 Recipient, Donor, and Surgical Procedure Characteristics According to Presence or Absence of Postoperative Atrial Fibrillation
 

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  		Appendix Risk Factors Considered in Multivariable Analysis
 
Survival
A log-rank test was used to compare survival of patients in whom posttransplant AF developed with those in whom it did not. Because all but one AF event occurred within 2 weeks of transplant, "time zero" for this survival comparison was set at 15 days after transplant. This eliminated 6 patients who died before day 15 (2 experienced AF before death; 4 did not). Also eliminated from the comparison was a patient in whom AF developed 37 days after transplant.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 Acknowledgments
 References
 
Prevalence and Timing
Postoperative atrial arrhythmias developed in 68 patients (20%). Five had preoperative atrial arrhythmias, 54 (79%) had AF, 2 (2.9%) had AFL, 11 (16%) had both, and 1 had an unspecified atrial arrhythmia assumed to be AF or AFL. Incidence of AF peaked 2 days after the procedure and declined steadily thereafter (Fig 1).


Figure 1
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  		Fig. 1. Incidence of atrial fibrillation or flutter (AF) after lung transplantation (hazard function). Solid line is the parametric estimate, and dashed lines are 68% confidence limits, equivalent to ±1 standard error.

 
Risk Factors
Risk factors for AF or AFL after lung transplantation included older age (Fig 2A), diagnosis of primary pulmonary hypertension (5 of 12 [42%] versus 63 of 321 [20%] for other indications for transplantation), and extremes of weight (Fig 2B, Table 2).


Figure 2
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  		Fig. 2. Occurrence of atrial fibrillation or flutter (AF) within 10 days of lung transplantation. Nomogram from multivariable analysis with indication for transplant other than primary pulmonary hypertension. (A) Occurrence according to age at transplantation for a patient weighing 68 kg. (B) Occurrence according to weight at transplantation of a patient age 48 years. The solid line in each figure is the parametric estimate, and the dashed lines are 68% confidence limits, equivalent to ±1 standard error.

 

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  		Table 2 Incremental Risk Factors for Atrial Fibrillation or Flutter After Lung Transplantation
 
Treatment
Pharmacologic treatment consisted of rate-control agents only in 18 of the 68 patients (26%), antiarrhythmics only in 5 (7.4%), and both in 45 (66%). Rate-control agents included metoprolol, diltiazem, and digoxin; rhythm-control agents included amiodarone and procainamide. Electrical cardioversion was used in 24 patients (36%), of whom 18 (75%) required one cardioversion, 4 (17%) required two, 1 (4.2%) required three, and 1 (4.2%) had an unknown number. Cardioversion was begun at 200 J according to American College of Cardiology recommendations [9], and transesophageal echocardiography was performed when hemodynamic stability permitted. Warfarin was used to treat 13 patients (19%; Fig 3).


Figure 3
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  		Fig. 3. The percentage of patients who underwent respective treatments of postoperative atrial fibrillation or flutter after lung transplantation is indicated by black bars.

 
Restoration of Normal Sinus Rhythm
Rhythm at discharge was available from the records of 59 of the 68 patients; of these, 55 (93%) were in NSR at discharge, 1 was in AF, 2 were in AFL, and 1 was discharged paced for a junctional rhythm. Fifteen patients (23%) were discharged with antiarrhythmic therapy only, 24 (38%) with rate-control medications only, and 15 (23%) with both.

Impact on Outcomes
Patients in whom AF developed had a longer median length of postoperative stay (17 days) than those who did not have AF (14 days; p = 0.0004). There was no short-term or long-term survival difference between those patients who developed AF and those who did not (log-rank p = 0.5; Fig 4).


Figure 4
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  		Fig. 4. Survival after transplantation according to whether (filled circles, dashed line) or not (open circles, solid line) postoperative atrial fibrillation or flutter (AF) occurred. Starting point is 15 days posttransplantation (see Methods). Each symbol represents a death, vertical bars are 68% confidence limits equivalent to ±1 standard error, and numbers in parentheses are patients remaining at risk.

 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
Acknowledgments
 References
 
Atrial arrhythmias occur commonly after lung transplantation, but despite the management challenge they present, few studies have described their prevalence or focused on treatment strategies for restoring sinus rhythm. Therefore, we evaluated our own single-institution experience, focusing on prevalence and timing, risk factors, treatment, and outcome.

Prevalence and Timing
AF was common after lung transplantation. Our prevalence was similar to the 28% and 40% observed in two previous studies [3, 4] as well as to that observed after other thoracic and cardiac procedures: 10% to 40% after pulmonary resection for cancer, 10% to 30% after coronary artery bypass grafting (CABG), and nearly 60% after CABG and concomitant valve surgery [10–12].

Its etiology after lung transplantation, as well as after other cardiac and thoracic procedures, likely includes operative trauma and surgical dissection of the atrium, local inflammation and pericarditis, and catecholamine production produced by postoperative pain and anxiety. In addition, intrapericardial dissection around the superior vena cava and pulmonary arteries and mobilization of the atrium may alter autonomic innervation of the heart, predisposing patients to AF [13].

The early peak in AF incidence in our study occurred 2 days postoperatively, a time frame similar to that observed for postoperative AF after other thoracic and cardiac surgical procedures. It typically occurs on postoperative day 2 or 3 after these procedures, with 70% occurring in the first 4 postoperative days [10, 11]. This period corresponds to the early peaks in pain and fluid shifts that occur immediately after transplantation, with the added confounding factors of hypoxia and graft dysfunction.

Identifying the timing of AF after lung transplantation provides a target for strategies aimed at prevention. Factors that may contribute to early postoperative AF should be prevented to the extent possible. Pain causes increased catecholamine release, and its control should be optimized; we believe that thoracic epidurals provide optimal pain control and should be used whenever possible [14]. Sympathetic blockade by using bupivacaine through a thoracic epidural has been shown in some studies to decrease prevalence of AF after lung resection, possibly by reducing the sympathotonic condition caused by injury to cardiac parasympathetic nerves [15]. Catecholamines should be weaned rapidly, and arrhythmogenic agents such as dopamine should be avoided whenever possible [16].

Careful attention should be paid to fluid balance to prevent atrial dilatation and activation of the renin-angiotensin-aldosterone system, which has been implicated in the genesis of AF [17, 18]. Similarly, overdiuresis should be avoided because it can produce hypotension, tachycardia, hypomagnesemia, and hypokalemia, all of which predispose patients to AF [19, 20].

In addition, the early peak of AF 2 days after surgery suggests that pharmacologic prophylaxis against AF must begin preoperatively or immediately postoperatively to be effective.

Risk Factors
Risk factors for AF after lung transplantation that we identified correspond to those identified in other studies after general thoracic and cardiac operations. Older age was the strongest, corresponding to the consistent observation that prevalence of AF increases with age. This is true in both the general population and in patients undergoing cardiac and thoracic operations [10, 11, 21]. The reason AF is more common in older patients is generally considered to be age-related atrial structural changes [22]. In a study by Hoffman and colleagues [6] of pediatric lung transplantation, no postoperative AF or AFL developed, highlighting the importance of older age in development of AF [6].

We found that AF was more likely to develop in patients with primary pulmonary hypertension (PPH) than those who received a transplant for other diagnoses. This was an unexpected finding, because AF is not described as being directly associated with PPH. We hypothesize that right atrial enlargement occurring in PPH predisposes patients to AF: echocardiographic studies reveal that 80% of patients with PPH have moderate-to-severe tricuspid regurgitation and 92% have right atrial enlargement [23, 24]. This is similar to the mechanism by which elevated left-sided pressures with mitral valve disease lead to left atrial enlargement and AF [25]. In addition, patients with PPH and right heart failure have relative volume overload preoperatively. Correcting pulmonary hemodynamics improves right ventricular function, resulting in reverse cardiac remodeling, volume shifts, and diuresis after transplantation [26, 27]. These volume shifts likely contribute to postoperative AF.

We also found that postoperative AF was more likely to develop in patients at extremes of weight. Those who weighed 60 kg had the lowest likelihood of AF, and prevalence increased with both lower and higher weights. The finding that increased weight increases risk of AF is consistent with previous reports that obesity increases the prevalence of AF. This may be due to increased left atrial size in obese patients [28]. However, the pathogenesis of AF patients with lower body weight is unclear. Of interest was that body mass index (BMI) did not prove to be a predictor of postoperative AF. We speculate that global deconditioning may cause weight loss that predisposes patients to operative trauma and catecholamine surge that induce AF. Smaller patients may also have greater relative fluid shifts in the perioperative period that predispose them to AF. The pathogenesis remains conjecture, however.

Older age and diagnosis of PPH are not modifiable risk factors for AF, although identifying patients at highest risk for AF may help direct prophylactic therapy to those most likely to benefit. Weight, however, may be a modifiable risk factor. Goals for target weights before transplantation may serve to reduce risk of AF and may also produce ancillary benefits by reducing other complications. Elevated BMI has been shown to increase perioperative risk after lung transplantation, and very low BMI has been shown to increase mortality after transplantation [29, 30]. Achieving an "optimal" preoperative weight may help improve outcomes. We are aggressive in our own transplant program about addressing weight loss in obese patients before listing and in providing nutritional supplementation to patients we believe are malnourished.

An interesting finding was that the choice of single-lung versus double-lung transplantation did not affect risk of postoperative AF, even though double-lung transplantation produces complete surgical pulmonary vein isolation. Ectopic beats in most patients with intermittent AF have been shown to initiate spontaneously in the pulmonary veins [31]. This finding provides the scientific basis for surgical pulmonary vein isolation introduced with the Cox-Maze procedure [32]. Excision of the recipient’s pulmonary veins, with anastomosis of the donor lung to the heart with a left atrial suture line, provides a natural experiment in surgical pulmonary vein isolation. The recipient pulmonary veins are totally excised and the donor veins are completely isolated in each lung after transplantation. Our finding that double-lung transplant recipients are just as likely to develop AF postoperatively as those who receive a single lung suggests that genesis of AF in this setting is in the recipient atrium itself.

The finding that AF occurs commonly in the immediate postoperative period despite surgical therapy that theoretically should prevent it mimics the finding that AF develops within the first 2 postoperative weeks after surgical AF ablation procedures in as many as 46% of patients. This prevalence declines over time [33]. Because most patients in our study were treated and returned to NSR before discharge, it is unlikely that further surgical intervention at the time of transplant aimed at preventing AF will be valuable; rather, prophylaxis must be pharmacologic. Currently, we universally initiate prophylaxis for AF with metoprolol starting in the immediate postoperative period.

Finally, similar to the fact that off-pump coronary surgery has not been clearly demonstrated to decrease prevalence of AF compared with on-pump coronary surgery, AF was similarly prevalent with or without the use of cardiopulmonary bypass during lung transplantation [34].

Treatment
Debate continues over optimal treatment of postoperative AF; however, guidelines have been established for its management [35]. The first step for the stable patient is attempted control of rapid ventricular response rate with β-blockers or other rate control agents such as calcium-channel blockers and digoxin. Once ventricular response rate to AF has been controlled, antiarrhythmics can be considered. The primary antiarrhythmics used are amiodarone and procainamide, although amiodarone has recently become the medication of choice for many [36, 37].

We reserve cardioversion for those patients who are unstable and those in whom rate control has proven refractory to medical management. In our study, managing AF after lung transplantation proved challenging, with multiple agents often required. Combination therapy, including rate-control agents as well as antiarrhythmics, was necessary in two-thirds, and more than one-third required electrical cardioversion. Use of multiple medications and cardioversion in such a large proportion of patients reflects both the challenge of AF in this patient population and our aggressive treatment of AF that targets tight rate control and restoration of NSR [13].

Restoring Normal Sinus Rhythm
The importance of restoring NSR after postoperative AF develops has been debated [38, 39]; however, it is the bias of our lung transplant program that restoration of NSR is particularly important. In our experience, rate control is difficult to establish, and shortened cardiac filling contributes to dyspnea and pulmonary congestion that is poorly tolerated in the early period after lung transplantation. In addition, the risk of thromboembolism increases if AF persists, raising the possible need for anticoagulation. Yet, anticoagulation poses a risk for bleeding early postoperatively, and the threshold for its use is unclear [40]. It also presents a logistic problem for surveillance bronchoscopic biopsies, for which anticoagulation must be held. Our study has shown that with aggressive treatment, NSR can be restored in almost all patients and anticoagulation largely avoided.

Impact on Outcomes
Nielsen and colleagues [3] found that the development of postoperative AF resulted in a longer perioperative stay, as did we; however, they also found that mortality was increased. We did not find that postoperative AF affected survival up to at least 6 years, which may reflect results of our aggressive treatment strategy.

Limitations
The primary limitation of this study is that it represents the clinical experience of a single center with relatively few patients. In addition, treatment was empiric, nonrandomized, and evolved over time. It was not possible to compare one treatment strategy with another because almost all resulted in NSR. Finally, criteria were not carefully defined for when a single agent had failed, a second agent was required, or electrical cardioversion was indicated. However, we believe that it represents an accurate "real-life" description of treatment challenges produced by AF after lung transplantation.

Conclusions
Prevalence of AF is high after lung transplantation and its management challenging. Adequate treatment often requires multiple pharmacologic agents combined with electrical cardioversion. NSR can almost always be reestablished before discharge. Risk factors for AF and its timing have been identified and can help direct targeted prophylaxis. Interesting questions regarding the pathophysiology of AF after lung transplantation have been raised that deserve further investigation. A prospective study focusing on preventing AF after lung transplantation seems warranted.


   Appendix
 


   Acknowledgments
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
References
 
We acknowledge and appreciate the expert editing and manuscript preparation by Tess Parry.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 

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