The paraventricular thalamic nucleus is involved in sleep-fragmentation-associated cardiac dysfunction after acute myocardial infarction.

Abstract

BACKGROUND: Sleep is essential for cardiac recovery after myocardial infarction (MI), but the impact of altered sleep architecture on repair remains unclear. OBJECTIVE: To investigate how sleep fragmentation affects cardiac repair post-MI and identify underlying neural mechanisms. METHODS: In a mouse model of MI, we assessed sleep patterns and cardiac function. An activity-dependent genetic labeling system in TRAP2 mice was used to identify brain regions involved in MI-induced sleep disturbances. Chemogenetic inhibition of glutamatergic neurons in the paraventricular thalamus (PVT) was performed to evaluate its role in sleep and cardiac regulation. RESULTS: Increased non-rapid eye movement (NREM) sleep fragmentation was negatively associated with cardiac recovery. Inhibition of PVT glutamatergic activity reduced sleep fragmentation and significantly improved cardiac repair. CONCLUSION: Our findings highlight the importance of sleep continuity in post-MI healing and identify the PVT as a key neural regulator of sleep-cardiac interaction. Targeting this pathway may offer a novel therapeutic approach to enhance MI recovery.