Pathological Changes in Pulmonary Vasculature after Atrial Fibrillation Ablation

                          http://www.mathewsopenaccess.com/cardiology-Vol-1-Iss-2.html

A well-known complication of radiofrequency ablation is pulmonary vein stenosis. We present a complex case of a patient with pulmonary vein occlusion, which developed within a few months after radiofrequency ablation for atrial fibrillation. The pathologic changes seen on lung biopsy, which developed in the months after the ablation are similar to those seen in pulmonary arterial hypertension. A 67-year-old Caucasian male with a history of rheumatoid arthritis and radiofrequency ablation for atrial fibrillation presented with hypoxic respiratory failure and hemoptysis. In the preceding months he had been treated for recurrent pneumonia and high dose corticosteroids for a histopathologic diagnosis of pulmonary capillaritis. A contrast-enhanced computed tomography of the chest revealed total occlusion of the left inferior, left superior, and right superior pulmonary veins with patent flow only through the right inferior pulmonary vein from the right lower lobe. Surgical specimens revealed vascular remodeling similar to Group 1 pulmonary arterial hypertension. This case is important because of the impressive radiographic imaging and histopathological changes seen in a patient with pulmonary veins stenosis and radiofrequency ablation.

We present the case of a patient with known rheumatoid arthritis (RA) who underwent radiofrequency ablation (RFA) for atrial fibrillation (AF). Less than a year after the ablation the patient developed significant pulmonary vein occlusion involving three out of four pulmonary venous outflow tracts. The surgical lung specimens demonstrated marked vascular remodelling and other pathological changes consistent with an occlusive pulmonary vasculopathy.

This case is a 67 year-old Caucasian male who presented with a chief complaint of “coughing up blood.” He had three-month history of hemoptysis and acute-on-chronic hypoxic respiratory failure. His past medical history consisted of RA and AF, having undergone RFA nine months prior to the onset of symptoms. His RA had been treated with methotrexate, sulfasalazine and hydroxychloroquine. In the three months prior to his admission, he had been treated for recurrent pneumonia. Admission physical exam revealed hypoxia with left sided basilar crackles and respiratory accessory muscle use. Contrastenhanced computed tomography of the chest revealed total occlusion of the left inferior, left superior, and right superior pulmonary veins with patent flow only through the right inferior pulmonary vein from the right lower lobe .