The Irate Stellate Ganglion: IL-6 in Neuroinflammation-induced Ventricular Arrhythmias

Sympathetic nervous system hyperactivity plays a major role in the pathogenesis of ventricular arrhythmias following myocardial infarction (MI).1,2 The stellate ganglia are an important nexus point for sympathetic innervation to the heart.3 Neuroinflammation has been implicated as a mechanism for sympathetic activation in cardiovascular disease. Inflammation within the stellate ganglia has been observed in patients with sudden cardiac death after MI,4,5 long QT syndrome and catecholaminergic polymorphic ventricular tachycardia,6 and electrical storm,7 suggesting a link between inflammation within these ganglia and ventricular arrhythmogenesis.