Obstructive sleep apnea increases heartbeat-evoked potentials and reorganizes Granger-causal coupling between cortical interoception and autonomic variability during wakefulness.

Obstructive Sleep Apnea (OSA) is a systemic disorder with far-reaching neuro-cardiac consequences that extend beyond sleep. While autonomic and cortical dysregulation in OSA have been studied, the temporal interactions between cortical interoceptive processing and autonomic variability during wakefulness remain poorly understood. This study investigates the severity-dependent alterations in cortical response to cardiac activity and the directionality of HEP–HRV temporal interactions in 366 adults stratified by OSA severity. We analyzed Heartbeat-Evoked Potentials (HEPs) derived from wakeful electroencephalography (EEG) as a marker of cortical interoception and examined their coupling dynamics with heart rate variability (HRV) features using Granger Causality (GC). Our results reveal a significant, monotonic increase in HEP amplitude over central (C3/C4, 320–480 ms) and frontal (F3/F4, 540–680 ms) regions with escalating OSA severity (p < 0.001), indicating heightened cortical sensitivity to cardiac afferent signals. Concurrently, HRV analysis shows progressive autonomic dysfunction, marked by reduced RMSSD, SDNN, SD1, and SD2 in severe OSA (p < 0.01). Crucially, GC analysis uncovers a severity-dependent reorganization of temporal predictive influence: while control individuals exhibit relatively balanced bidirectional interactions, severe OSA displays a predominant strength-based HRV → HEP influence, particularly in frontal regions and parasympathetic-related metrics. These GC-derived findings reflect altered temporal dynamics between cortical interoceptive responses and autonomic variability. Overall, the results demonstrate that OSA induces a persistent, severity-dependent disruption of cortical–autonomic integration during wakefulness, positioning HEP amplitude and GC-based temporal coupling measures as promising non-invasive biomarkers for assessing the systemic neurological impact of OSA.