Increased inflammation promotes ventricular arrhythmia through aggravating left stellate ganglion remodeling in a canine ischemia model

Schematic diagram illustrating how IL-1β injection into LSG aggravates ischemia induced VA. Normally, cardiac ischemia activates afferent signals to the LSG and results in mild inflammation and increased expression of excitatory neurotransmitters (NGF and NPY), as well as increased inhibitory neurotransmitters (nNOS). The inconsistent up-regulation between excitatory and inhibitory neurotransmitters contributes to the increased LSG activity and subsequent incidence of VA. However, IL-1β injection into the LSG results in more prominent inflammatory response. The increased inflammation in the LSG promotes the expression of excitatory neurotransmitters, but suppresses the inhibitory neurotransmitters, which aggravates the imbalance between excitatory and inhibitory neurotransmitters in the LSG and results in significantly increased LSG activity and more incidence of VA. While, IL-1Ra pre-injection could attenuate the pro-arrhythmic effects of IL-1β through regulating the neural remodeling processes.203