The cardiac–cerebral reflex (CCR) is a bidirectional neural loop that continuously links cardiac sensory input with central autonomic control, and thereby governs heart rate, conduction, and myocardial excitability. Once thought of mainly as a homeostatic feedback mechanism, the CCR is now recognized as a key actor in the genesis of malignant arrhythmias and some forms of sudden cardiac death. This narrative review synthesizes current understanding of the CCR from cellular mechanisms to clinical syndromes. We highlight the Central Autonomic Network—with emphasis on the nucleus tractus solitarius and the insular cortex—and trace how aberrant autonomic signaling (excess sympathetic discharge, vagal imbalance) creates both the “spark” and the “substrate” for arrhythmogenesis. We review diagnostic approaches (heart rate variability, baroreflex testing, cardiac 123 I-metaiodobenzylguanidine imaging, prolonged ECG/EEG monitoring), summarize therapeutic options with a focus on neuromodulation (cardiac sympathetic denervation, stellate blockade, vagus nerve stimulation), and propose practical steps for clinicians caring for patients in whom brain–heart interactions are central. Moving from a cardiocentric to a neurocardiac perspective can improve risk stratification and open new management avenues for arrhythmias that resist conventional approaches.
Akram et al. (2026) studied this question. Aberrant cardiac–cerebral reflex signaling is key in malignant arrhythmias and sudden cardiac death, linking autonomic dysfunction with arrhythmogenesis.