Arrhythmias and conduction disturbance
Frequency of Atrial Flutter After Adult Lung Transplantation

https://doi.org/10.1016/j.amjcard.2010.10.076Get rights and content

Lung transplantation, which involves an anastomosis of the graft to the native left atrium, may increase the risk of left-side atrial flutter (AFL). Our aim was to evaluate the incidence, predisposing conditions, and course of AFL after lung transplantation in adults. Two hundred sixty-nine consecutive patients who underwent lung transplantation were studied retrospectively. All patients received a preoperative echocardiogram and postoperative electrocardiographic monitoring. All 12-lead electrocardiograms were reviewed. Typical or atypical AFL was diagnosed by 2 independent reviewers based on accepted criteria. Predictors of AFL were investigated separately using univariate and multivariate logistic regression analyses. AFL occurred in 35 of 269 patients (13%) over a mean of 12 days after transplantation. All patients who developed AFL had no previous atrial arrhythmia. Of these 35 patients, 24 (68.6%) had atypical AFL by electrocardiographic criteria. In multivariate logistic regression analysis, patients with idiopathic pulmonary fibrosis (IPF) were 2.9 times more likely to have AFL than those patients with lung transplant without IPF (p = 0.009). Other independent risk factors for AFL were advanced age and preoperative left atrial enlargement. Only 3 of 35 patients (8.6%) with AFL had persistent atrial arrhythmia and needed electrophysiologic study and ablation. In conclusion, AFL is common soon after lung transplantation. Those with IPF, advanced age, or left atrial enlargement are at increased risk. In most cases, AFL is a self-limited arrhythmia that resolves spontaneously with no need for ablation.

Section snippets

Methods

We retrospectively reviewed records of all patients undergoing lung transplantation at the University of California, San Francisco, from April 1998 through June 2010. Patients with uni- or bilateral lung transplantation were included in the study.

Patients' demographic and medical characteristics including age, gender, preoperation diagnosis, and date of transplantation were identified from their hospital records. A 12-lead electrocardiogram (ECG) was obtained before surgery. Patients underwent

Results

Two hundred sixty-nine patients 15 to 76 years of age who underwent lung transplantation were included for study. These patients were followed serially for the rest of their lives. Baseline characteristics of patients at time of transplantation are listed in Table 1. Preoperative echocardiograms of the study population revealed right ventricular hypertrophy in 59 (22%), right atrial enlargement in 78 (29%), and left atrial enlargement in 27 (10%). Eighty-two percent (n = 222) underwent

Discussion

Our study demonstrates that AFL and atypical AFL in particular are common after lung transplantation. Overall incidence of AFL in patients after lung transplantation was 13%, which is much higher than the rate in an age-matched population (rate 0.05).9 None of the patients in our cohort had previous AFL, suggesting that the transplantation procedure was responsible for the arrhythmia. Most of these diagnosed AFLs resolved without ablation.

Several studies have suggested that atrial arrhythmias

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    Our cumulative incidence of post-operative AA was also similar to other previous studies that reported a cumulative incidence of post-operative AA at 19% to 28% before hospital discharge (4,13–16), 39% within 14 days (3), and 34% by 4 weeks (5,16). In our study, the peak incidence of post-operative AA was at 5 days post-transplantation, which was consistent with the previous studies that reported the peak incidences of combined AA between 2 and 5 days after transplantation (3,4,15) but earlier than the peak incidence of pure AFL, which was between 10 and 12 days (17). In this study, we found invasive mPAP to be inversely associated with post-operative AA.

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    The higher incidence of AF in the Nielsen et al series may be explained, at least in part, by the large number of patients with AF before lung transplantation as well as the use of inotropes. The incidence of AFL in our cohort (5.7%) was much lower than that reported in two previous, both smaller studies by Gandhi et al6 (11.3% in a pediatric population) and Azadani et al9 (13% in adults). The reason for this significant difference is unclear, but we speculate that the use of calcium channel blockers or beta-blockers in about a third of our cohort of patients before transplant prevented the development of either AF or AFL.

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