Transient left recurrent laryngeal nerve palsy following catheter ablation of atrial fibrillation Rakesh K. Pai, MD, Noel G. Boyle, MD, PhD, John S. Child, MD, Kalyanam Shivkumar, MD, PhD From the UCLA Cardiac Arrhythmia Center, Department of Medicine, Division of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, California. Introduction Catheter ablation procedures for management of atrial fi- brillation continue to evolve. 1,2 The creation of different lesion sets targeting both the “triggers” and “substrate” which predispose the atria to fibrillate. Defining the optimal lesion sets has been hampered by incomplete understanding of the pathogenesis of this arrhythmia and the heterogeneity of the mechanisms responsible for atrial fibrillation. As with any evolving procedure, unexpected complications can oc- cur, some with devastating consequences, such as stroke, 3 pulmonary vein stenosis, 4 pericardial effusion, and the re- cently described atrioesophageal fistula. 5,6 This report de- scribes a potential new complication associated with left atrial ablation: recurrent laryngeal nerve injury leading to transient vocal cord paralysis. Case report A 74-year-old, physically active man with a history of sinus node dysfunction requiring implantation of a dual-chamber pacemaker for symptomatic bradycardia and previous cor- onary artery disease requiring two-vessel coronary artery bypass graft surgery in 1993 was referred to the electro- physiology service. He was evaluated for recurrent symp- tomatic drug-refractory persistent atrial fibrillation with ep- isodes of atrial flutter. He had highly symptomatic spells of atrial fibrillation and required multiple cardioversions. Mul- tiple medications for both rate and rhythm control (includ- ing amiodarone) were prescribed. These therapies were ineffective in maintaining sinus rhythm or controlling ven- tricular response. He was referred for catheter ablation of atrial fibrillation and flutter. Prior to ablation, computed tomographic angiography was performed to define cardiac anatomy. On the day of catheter ablation, transesophageal echocardi- ography confirmed a mildly dilated left atrium (43 mm), with no evidence of left atrial thrombus, and normal left ventricular systolic function. The patient was confirmed to be in isthmus- dependent atrial flutter at the time of study. Intracardiac echo- cardiography was used to facilitate transseptal catheterization. An 8-mm Navi-Star (Biosense Webster, Diamond Bar, CA, USA) ablation catheter was placed into the left atrium. Heparin was administered to achieve an activated clotting time 300 seconds. The left atrium was mapped, and linear ablation lines (power 45 W, temperature 55°C) encircling the pulmonary veins were created (Figure 1). Prior to ablation of the right- sided pulmonary veins, high-output pacing was performed to ensure the absence of phrenic nerve capture. After catheter ablation of the right-sided pulmonary veins, cinefluoroscopy of the diaphragm documented normal diaphragmatic function. Subsequently, a right atrial isthmus line was created, and bi- directional block was confirmed after application of radiofre- quency (RF) energy. The total procedure time was 5 hours 43 minutes. The patient was transferred to the telemetry floor, where he did well overnight and was discharged the following morning without event. The patient was readmitted to the hospital 24 hours after his ablation procedure for hoarseness and dysphagia char- acterized by a choking sensation when he was drinking. Flexible fiberoptic laryngoscopy performed in the emer- gency room revealed left-sided vocal cord paresis with paramedian positioning of the vocal cord. Upper gastroin- testinal barium and Gastrografin swallow study showed no evidence of esophageal perforation or stricture. The patient was treated in the hospital with intravenous steroid therapy (dexamethasone 10 mg IV every 8 hours) and discharged on postprocedure day 3 feeling well and with complete reso- lution of his symptoms. KEYWORDS Catheter ablation; Atrial fibrillation; Recurrent laryngeal nerve injury; Vocal cord paralysis; Ortner syndrome (Heart Rhythm 2005;2: 182–184) Dr. Shivkumar is supported by a Clinical Scientist Development Award from the Doris Duke Charitable Foundation, New York, and a National American Heart Association Scientist Development Grant. Address reprint requests and correspondence: Dr. Kalyanam Shivkumar, Division of Cardiology, Department of Medicine, David Geffen School of Medicine at UCLA, 47-123 CHS, 10833 Le Conte Avenue, Los Angeles, California 90095. E-mail address: kshivkumar@mednet.ucla.edu. (Received August 4, 2004; accepted October 12, 2004.) 1547-5271/$ -see front matter © 2005 Heart Rhythm Society. All rights reserved. doi:10.1016/j.hrthm.2004.10.030