Antiarrhythmic effects of stimulating the left dorsal branch of the thoracic nerve in a canine model of paroxysmal atrial tachyarrhythmias

Background Stellate ganglion nerve activity (SGNA) precedes paroxysmal atrial tachyarrhythmias (PAT) episodes in dogs with intermittent high rate left atrium (LA) pacing. The left dorsal branch of thoracic nerve (LDTN) contains sympathetic nerves originating from the stellate ganglia. Objective To test the hypothesis that high frequency electrical stimulation of the LDTN can cause stellate ganglia damage and suppress PAT. Methods We performed chronic LDTN stimulation in 6 dogs with and 2 dogs without intermittent rapid LA pacing while monitoring the SGNA. Results LDTN stimulation reduced the average SGNA (aSGNA) from 4.36 μV [95% confidence interval, CI, 4.10 to 4.62] at baseline to 3.22 μV [95% CI, 3.04 to 3.40] after 2 weeks (P = 0.028) and completely suppressed all PAT episodes in all dogs studied. Tyrosine hydroxylase (TH) staining showed large damaged regions in both stellate ganglia, with increased percentages of TH-negative cells. Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL) assay showed 23.36% [95% CI 18.74 to 27.98] of ganglion cells in the left and 11.15% [95% CI 9.34 to 12.96] ganglion cells in the right stellate ganglia were positive, indicating extensive cell death. A reduction of SGNA and heart rate were also observed in dogs with LDTN stimulation but without high rate LA pacing. Histological studies of the latter two dogs confirmed the presence of extensive stellate ganglia damage, along with high percentage of TUNEL-positive cells. Conclusions LDTN stimulation damages both LSG and RSG, reduces left SGNA and is antiarrhythmic in this canine model of PAT.