Fig. 1.

Mechanisms of brain-heart communication after stroke. A stroke event can activate bidirectional interactions through various pathways such as the hypothalamic-pituitary-adrenal (HPA) axis, autonomic nervous system, and gut-heart microbial interactions, leading to cardiac dysfunction. Activation of the HPA axis after stroke promotes glucocorticoid elevation and subsequent inflammatory responses and oxidative stress in cardiomyocytes. Autonomic dysfunction results in abnormal catecholamine levels that further impact cardiac electrophysiology. Additionally, gut microbiota imbalance following stroke may damage heart health via the gut-heart axis. Overall, a stroke elicits multi-level regulatory effects and network coupling to form the brain-heart axis, thereby inducing or exacerbating cardiac injury.