Sleep Instability and Severe Obstructive Sleep Apnea are Associated with Carotid Atherosclerotic Burden but Not Plaque Vulnerability in Acute Ischemic Stroke.

PURPOSE: Sleep disorders, including sleep instability and obstructive sleep apnea-hypopnea syndrome (OSAHS), are closely associated with cardiovascular and cerebrovascular disease. Prior studies have primarily focused on OSAHS, characterized by respiratory events, with limited attention to non-respiratory sleep disturbances. In patients with acute ischemic stroke (AIS), the relationship between sleep instability and carotid atherosclerotic burden, as well as plaque vulnerability, remains unclear. PATIENTS AND METHODS: In this cross-sectional study, 1003 hospitalized patients with AIS were enrolled. All participants underwent portable sleep monitoring (PSM) within 72 hours of admission. Sleep instability derived from cardiopulmonary coupling (CPC) analysis was categorized into low- and high-sleep instability groups according to the median value, while OSAHS severity was classified based on the apnea-hypopnea index (AHI). Carotid ultrasonography was performed to measure common carotid intima-media thickness (CIMT) and to assess the presence of carotid plaques and ultrasound-defined vulnerable plaque features. Multivariable linear and logistic regression analyses were used to examine the associations of sleep instability and OSAHS severity with carotid atherosclerotic phenotypes. RESULTS: In multivariable regression models, CPC-derived sleep instability was associated with increased CIMT (β = 0.042 mm, 95% CI: 0.021-0.062, P < 0.001) and was associated with an increased prevalence of carotid plaque (adjusted OR = 2.68, 95% CI: 1.76-4.08). The severity of OSAHS showed a graded association with CIMT, while only severe OSAHS was significantly associated with carotid plaque (adjusted OR = 2.11, 95% CI: 1.15-3.87), and mild-to-moderate OSAHS showed no significant association across models. Neither CPC-derived sleep instability nor OSAHS severity was significantly associated with vulnerable plaque features. Compared with mild-to-moderate OSAHS, CPC-derived sleep instability showed a stronger and more consistent association with carotid atherosclerotic burden, suggesting that it may provide vascular risk information beyond traditional AHI-based stratification. CONCLUSION: In AIS patients, CPC-derived sleep instability and severe OSAHS each showed associations with carotid atherosclerotic burden in separate adjusted models, whereas no significant association was observed with plaque vulnerability. Although both CPC-derived sleep instability and AHI reflect underlying physiological oscillations related to periodic respiratory activity during sleep, CPC-derived sleep instability additionally captures non-respiratory sleep instability and autonomic dysregulation, thereby providing a complementary perspective for the assessment of sleep-related vascular risk.