【】This article examines the evolution of the brain–heart axis from acute stress to chronic decompensation from a temporal perspective. In the acute phase, the cardiac consequences of brain-derived events are dominated by sympathetic storm and catecholamine-mediated toxicity, accompanied by vagal inhibition and microcirculatory dysfunction; both cardiac and cerebral injuries are largely reversible. In the chronic phase, persistently elevated sympathetic tone promotes myocardial remodeling, fibrosis, and metabolic reprogramming, driving a vicious cycle of reciprocal brain–heart injury. The impact of cardiac-originated events on the brain also follows a distinct temporal trajectory, in which reperfusion quality and the integrity of autoregulatory mechanisms critically determine clinical outcomes. However, existing studies are predominantly cross-sectional and rely on single time-point associations, with limited integration of multimodal data. Future research should therefore adopt longitudinal designs with repeated measurements across multiple time points and incorporate multimodal data integration to provide temporal, systemic, and causal insights into brain–heart axis interactions.