The purpose of the present study is to determine whether thoracic veins may act as ectopic pacemakers and whether node-like cells and rich sympathetic innervation are present at the ectopic sites. We used a 1792-electrode mapping system with 1-mm resolution to map ectopic atrial arrhythmias in 8 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 (NE) levels, sinus tachycardia in all dogs and atrial tachycardia in 2/8 dogs. Sinus node crushing resulted in a slow junctional rhythm (51 ± 6 bpm). Subsequent SG stimulation induced 20 episodes of ectopic beats in 7 dogs and 7 episodes of pulmonary vein (PV) tachycardia in 3 dogs (cycle length 273 ± 35 ms, duration 16 ± 4 s). The ectopic beats arose from the PV (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=NS). There was a greater density of Periodic Acid Schiff (PAS) positive cells (p<0.05) and sympathetic nerves (p<0.05) at the ectopic sites compared with other non-ectopic 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 PAS-positive cells.