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Pulmonary Edema After Extensive Radiofrequency Ablation for Atrial Fibrillation
Author(s) -
WEBER REINHOLD,
MINNERS JAN,
RESTLE CHRISTIAN,
BUERKLE GERD,
NEUMANN FRANZJOSEF,
KALUSCHE DIETRICH,
KEYL CORNELIUS,
ARENTZ THOMAS
Publication year - 2008
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.2007.01064.x
Subject(s) - medicine , atrial fibrillation , ablation , cardiology , catheter ablation , radiofrequency ablation , pulmonary edema , edema , heart failure , lung
Background: More extensive ablation strategies for the treatment of atrial fibrillation (AF) have increased success rates but are associated with new and sometimes serious complications. We describe a new complication after extensive radiofrequency (RF) ablation in the left atrium (LA) for persistent AF. Methods and Results: Electroanatomic guided circumferential ablation around both ipsilateral pulmonary veins (PV) was performed with the endpoint of complete conduction block. When necessary, supplementary RF applications were added, including ablation of complex fractionated potentials and/or isolation of other thoracic veins and/or linear left atrial lesions. RF energy was delivered via an irrigated tip catheter with a maximum power of 30–35 W. Four out of 120 patients undergoing extensive RF ablation for persistent AF (including two patients with additional LA substrate modification) developed dyspnea, bilateral pulmonary edema, and signs of a systemic inflammatory response syndrome (SIRS) (rise in body temperature, leukocyte count, and C‐reactive protein (CRP levels) 18–48 hours after the procedure. There were no signs of PV stenosis, focal lung injury, left ventricular dysfunction, circulatory failure, or infection. All patients had complete recovery with supportive therapy within 3–4 days after the onset of symptoms. Conclusions: Extensive LA radiofrequency ablation bears the risk of a severe pulmonary edema. Although the precise mechanism is elusive, clinical features point toward a systemic inflammatory response.