ArticleNature and science of sleep2026
Sleep Instability and Severe Obstructive Sleep Apnea are Associated with Carotid Atherosclerotic Burden but Not Plaque Vulnerability in Acute Ischemic Stroke.
Article in Nature and science of sleep, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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13 authors.
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Abstract
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, 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.
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