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a Division of Thoracic Surgery, Massachusetts General Hospital, Boston, Massachusetts
b Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts
c Division of Pathology, Massachusetts General Hospital, Boston, Massachusetts
d Division of Pulmonary Medicine, Massachusetts General Hospital, Boston, Massachusetts
Accepted for publication June 19, 2008.
* Address correspondence to Dr Gaissert, Division of Thoracic Surgery, Massachusetts General Hospital, Blake 1570, 55 Fruit St, Boston, MA 02114 (Email: hgaissert{at}partners.org).
| Abstract |
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| Introduction |
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A 58-year-old woman presented 6 years earlier with atrial fibrillation and congestive heart failure. Echocardiography was normal. Normal sinus rhythm was restored with cardioversion, and medical treatment was instituted. Three years later, she experienced symptomatic, paroxysmal atrial fibrillation and underwent circumferential radiofrequency ablation of both left pulmonary veins. Paroxysmal atrial fibrillation refractory to medical therapy recurred after 5 weeks. A transesophageal echocardiogram 2 months after ablation showed a left atrial thrombus and anticoagulation with warfarin was begun. Magnetic resonance imaging demonstrated 70% stenosis of the left inferior pulmonary vein and uncertain visualization of the superior vein. An electrophysiologic study 2 years later found the left veins isolated, but high frequency electrical activity was present at the left atrial appendage and around the right-sided veins. Repeat circumferential ablation of the right-sided veins restored sinus rhythm. Transeptal left atrial catheterization showed an occluded left superior vein and a 70% stenosis of the inferior vein without pressure gradient. Right-sided veins were patent. Ventilation-perfusion scintigraphy demonstrated 17% perfusion to the left lung (Fig 1A). Anticoagulation was continued. Over the ensuing months, additional cardioversions were administered for recurrent episodes of symptomatic atrial fibrillation associated with progressive exertional dyspnea.
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Computed tomography demonstrated occlusion of both left pulmonary veins. The right veins were normal (Fig 2). Echocardiography demonstrated an ejection fraction of 62%. During cardiac catheterization, right ventricular pressure was 55/3, pulmonary artery pressure 55/25 (mean, 40), and right lower pulmonary capillary wedge pressure 15 mm Hg.
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A left pneumonectomy was performed to permit resumption of anticoagulation. The lung was extremely pale while small hilar vessels were maximally engorged (Figs 3A and 3B). The pulmonary artery had no pulse and the veins were obliterated. The perivascular planes were inflamed and the vessel walls were thickened. With meticulous ligation of all hilar tissues (Fig 3C), the pulmonary vessels were divided and oversewn. The bronchus was divided and closed at the carina, reinforcing the stump with a pericardial fat pad. The specimen was pale with a yellow hue (Fig 3D). The patient was immediately extubated and had an uneventful recovery. She remains anti-coagulated for paroxysmal atrial fibrillation.
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| Comment |
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Management of pulmonary vein stenosis or occlusion is often unsuccessful. Data on the safety and efficacy of angioplasty and stenting is limited to a few small-scale studies. Qureshi and colleagues [6] reported on 17 patients who underwent angioplasty of 30 pulmonary veins with an increase in vessel diameter from 2.6 mm to 6.6 mm (approximately 70% of normal). These procedures were complicated by hemorrhage, venous tear requiring open repair, and stroke in 13% of patients. At a median follow-up of 43 weeks, 47% of patients experienced re-stenosis with all requiring repeat intervention. Overall, repeat intervention was performed on 19 of 30 (63%) veins [6]. In 23 patients with vein stenosis following radiofrequency ablation, Packer and colleagues [7] reported similar results. Twenty veins were dilated and 14 were stented. Re-stenosis occurred in 14 patients (60%). Neither study demonstrated a lasting return to normal perfusion in any dilated vascular territory. The proportion of patients with normal sinus rhythm after these procedures was not reported.
Since the results of angioplasty or stenting for pulmonary vein stenosis are so far unsatisfactory, and because high-grade stenosis or occlusion of a single pulmonary vein leads to loss of 25% of pulmonary function on average, we propose the following guidelines for radiofrequncy ablation:
The functional loss of an entire lung and the operative risk of lung resection, lobectomy, or pneumonectomy mitigate any functional improvement derived from radiofrequency ablation. The usual diagnostic delay associated with pulmonary venous injury precludes early intervention to prevent these strictures. The profound cicatricial response of pulmonary veins to injury suggests that the solution to this problem lies in prevention, rather than treatment.
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This article has been cited by other articles:
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C.-D. Kan and Y.-J. Yang Complete Pulmonary Venous Occlusion After Radiofrequency Ablation Ann. Thorac. Surg., January 1, 2010; 89(1): 340 - 340. [Full Text] [PDF] |
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D. Nehra, I. Inglessis, and H. A. Gaissert Reply. Ann. Thorac. Surg., January 1, 2010; 89(1): 340 - 340. [Full Text] [PDF] |
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L. B. Ware Clinical Year in Review I: Interstitial Lung Disease, Pulmonary Vascular Disease, Pulmonary Infections, and Cardiopulmonary Exercise Testing and Pulmonary Rehabilitation Proceedings of the ATS, September 15, 2009; 6(6): 487 - 493. [Full Text] [PDF] |
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