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Ectopic atrial arrhythmias arising from canine thoracic veins during in vivo stellate ganglia stimulation

¹Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California; ²Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana; ³Division of Neurology, Department of Pediatrics, Childrens Hospital and University of Southern California Keck School of Medicine, Los Angeles, California; and ⁴Division of Anatomical Pathology and Laboratory Medicine, Department of Pathology, David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, California

Submitted 11 November 2007 ; accepted in final form 2 June 2008

The purpose of the present study was to determine whether thoracic veins may act as ectopic pacemakers and whether nodelike cells and rich sympathetic innervation are present at the ectopic sites. We used a 1,792-electrode mapping system with 1-mm resolution to map ectopic atrial arrhythmias in eight normal dogs during in vivo right and left stellate ganglia (SG) stimulation before and after sinus node crushing. SG stimulation triggered significant elevations of transcardiac norepinephrine levels, sinus tachycardia in all dogs, and atrial tachycardia in two of eight dogs. Sinus node crushing resulted in a slow junctional rhythm (51 ± 6 beats/min). Subsequent SG stimulation induced 20 episodes of ectopic beats in seven dogs and seven episodes of pulmonary vein tachycardia in three dogs (cycle length 273 ± 35 ms, duration 16 ± 4 s). The ectopic beats arose from the pulmonary vein (n = 11), right atrium (n = 5), left atrium (n = 2), and the vein of Marshall (n = 2). There was no difference in arrhythmogenic effects of left vs. right SG stimulation (13/29 vs. 16/29 episodes, P = nonsignificant). There was a greater density of periodic acid Schiff-positive cells (P < 0.05) and sympathetic nerves (P < 0.05) at the ectopic sites compared with other nonectopic atrial sites. We conclude that, in the absence of a sinus node, thoracic veins may function as subsidiary pacemakers under heightened sympathetic tone, becoming the dominant sites of initiation of focal atrial arrhythmias that arise from sites with abundant sympathetic nerves and periodic acid Schiff-positive cells.

atrial tachycardia; electrophysiology; autonomic nervous system; sympathetic nerves; computerized mapping

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