Moss et al Ganglionitis 191 patients with LQTS who had syncopal spells and died from their disease. It may well be that intracardiac and extracardiac neurogenic ganglionic cells are particularly susceptible to hypoperfusion or defibrillator shock injury with resultant intracellular protein damage and secondary inflammatory ganglionitis. We would suggest this as a possible explanation for the ganglionitis findings because they pertain to the descriptions of similar finding in patients with LQTS in 2 publications separated by> 35 years. Could the observed stellate and thoracic ganglionitis, whether a primary or secondary phenomenon, play a triggering role in the precipitation of life-threatening ventricular tachyarrhythmias in these 2 different genetic disease states? Although anything is possible, we think it is unlikely that the minor degree of ganglionitis as described is stimulating the vulnerable myocardium in these patients with high-risk genetic disorders. One would think it is at least as likely that the minor inflammatory damage to the ganglia would reduce transmission of nerve traffic through the ganglia from higher centers rather than exacerbate the sympathetic stimulation to the myocardium. Of course, our comments are speculative, but we suspect the ganglionic findings are minor and are not playing a causal role in the disease process. However, cervical thoracic ganglionectomy should dramatically reduce normal sympathetic traffic to the heart with resultant rhythm stabilization, and this is what was observed in almost all the patients reported in the article by Rizzo et al. 6 The type of gangliocytic injury described by the authors as vacuolation may be subtle and is difficult to discern from figures provided. 6 Vacuolation of ganglion cells has been described in several instances from toxic exposure, to trauma, to aging and is considered nonspecific. 10, 11 It should be noted that stellate and thoracic ganglia are not routinely examined in postmortem examination by pathologists, so there is a paucity of available data on the histological findings in these tissues among patients who die suddenly from cardiac arrhythmias. It might be useful to examine ganglia from patients who die in clinical settings involving multiple electric shocks or syncopal episodes unrelated to congenital arrhythmia to sort out the secondary versus primary nature of the histopathologic findings observed in these ganglia. The authors are to be congratulated for providing a new orientation to the inflammatory activity of the cardiac ganglia in patients with LQTS and CPVT and recurrent cardiac events. The authors have raised more questions than can be answered at this time, and their approach opens the door for further investigations into the role of altered ganglionic structure and function involved in the mechanistic complexities of inherited and acquired cardiac rhythm disorders.