Cardiac arrhythmias are traditionally attributed to structural and electrophysiological abnormalities; however, increasing evidence highlights the critical role of systemic inflammation and autonomic dysregulation in arrhythmogenesis. The neuroimmune-cardiac axis represents a bidirectional communication network between the autonomic nervous system and immune signaling pathways that collectively modulate cardiac electrical stability. Pro-inflammatory cytokines and immune mediators influence central autonomic regulatory centers, leading to sympathetic overactivation and parasympathetic withdrawal, reflected by reduced heart rate variability and increased arrhythmic susceptibility. Conversely, autonomic dysfunction further amplifies inflammatory signaling, establishing a self-perpetuating feed-forward loop that promotes electrical instability and adverse cardiac remodeling. Key neuroanatomical structures, including circumventricular organs and the stellate ganglion, serve as critical interfaces linking systemic inflammation to autonomic cardiac control. Inflammatory mediators such as interleukin (IL)-17A and metabolic adipokines like leptin contribute to stellate ganglion remodeling, enhanced sympathetic discharge, and increased vulnerability to ventricular arrhythmias. At the molecular level, activation of the NLRP3 inflammasome plays a central role in integrating inflammatory and electrical signaling pathways by promoting IL-1β and IL-18 release, oxidative stress, calcium handling abnormalities, and gap junction disruption, thereby establishing a proarrhythmic substrate. Importantly, sustained arrhythmias may further potentiate inflammasome activation, reinforcing the vicious cycle between inflammation and electrical instability. Anti-inflammatory and immunomodulatory mediators, including adiponectin and IL-1 receptor antagonists, demonstrate protective effects by restoring autonomic balance and reducing arrhythmic risk. Collectively, the neuroimmune-cardiac axis provides a unified mechanistic framework for understanding arrhythmogenesis and highlights novel therapeutic opportunities targeting both inflammatory and autonomic pathways beyond conventional antiarrhythmic strategies.