Association of Polysomnographic Sleep Parameters With Neuroimaging Biomarkers of Cerebrovascular Disease in Older Adults With Sleep Apnea
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Abstract
Background and Objectives Our objective was to determine whether polysomnographic (PSG) sleep parameters are associated with neuroimaging biomarkers of cerebrovascular disease (CVD) related to white matter (WM) integrity in older adults with obstructive sleep apnea (OSA).
Methods From the population-based Mayo Clinic Study of Aging, we identified participants without dementia who underwent at least 1 brain MRI and PSG. We quantified 2 CVD biomarkers: WM hyperintensities (WMHs) from fluid-attenuated inversion recovery (FLAIR)-MRI, and fractional anisotropy of the genu of the corpus callosum (genu FA) from diffusion MRI. For this cross-sectional analysis, we fit linear models to assess associations between PSG parameters (NREM stage 1 percentage, NREM stage 3 percentage [slow-wave sleep], mean oxyhemoglobin saturation, and log of apnea-hypopnea index [AHI]) and CVD biomarkers (log of WMH and log of genu FA), respectively, while adjusting for age (at MRI), sex, APOE ε4 status, composite cardiovascular and metabolic conditions (CMC) score, REM stage percentage, sleep duration, and interval between MRI and PSG.
Results We included 140 participants with FLAIR-MRI (of which 103 had additional diffusion MRI). The mean ± SD age was 72.7 ± 9.6 years at MRI with nearly 60% being men. The absolute median (interquartile range [IQR]) interval between MRI and PSG was 1.74 (0.9–3.2) years. 90.7% were cognitively unimpaired (CU) during both assessments. For every 10-point decrease in N3%, there was a 0.058 (95% CI 0.006–0.111, p = 0.030) increase in the log of WMH and 0.006 decrease (95% CI −0.012 to −0.0002, p = 0.042) in the log of genu FA. After matching for age, sex, and N3%, participants with severe OSA had higher WMH (median [IQR] 0.007 [0.005–0.015] vs 0.006 [0.003–0.009], p = 0.042) and lower genu FA (median [IQR] 0.57 [0.55–0.63] vs 0.63 [0.58–0.65], p = 0.007), when compared with those with mild/moderate OSA.
Discussion We found that reduced slow-wave sleep and severe OSA were associated with higher burden of WM abnormalities in predominantly CU older adults, which may contribute to greater risk of cognitive impairment, dementia, and stroke. Our study supports the association between sleep depth/fragmentation and intermittent hypoxia and CVD biomarkers. Longitudinal studies are required to assess causation.
Glossary
- AD=
- Alzheimer disease;
- AHI=
- apnea-hypopnea index;
- BP=
- blood pressure;
- CPAP=
- continuous positive airway pressure;
- CU=
- cognitively unimpaired;
- CVD=
- cerebrovascular disease;
- DTI=
- diffusion tensor imaging;
- FA=
- fractional anisotropy;
- FLAIR=
- fluid-attenuated inversion recovery;
- genu FA=
- FA in the genu of the corpus callosum;
- IQR=
- interquartile range;
- MCI=
- mild cognitive impairment;
- MCSA=
- Mayo Clinic Study of Aging;
- N1%=
- NREM stage 1 percentage;
- N3%=
- NREM stage 3 percentage;
- OSA=
- obstructive sleep apnea;
- PAP=
- positive airway pressure;
- SpO2=
- oxyhemoglobin saturation;
- SWA=
- slow-wave activity;
- SWS=
- slow-wave sleep;
- TIV=
- total intracranial volume;
- TST=
- total sleep time;
- VCID=
- vascular contributions to cognitive impairment and dementia;
- WM=
- white matter;
- WMH=
- white matter hyperintensity
Footnotes
Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.
Submitted and externally peer reviewed. The handling editor was Associate Editor Barbara Jobst, MD, PhD, FAAN.
- Received December 11, 2022.
- Accepted in final form March 23, 2023.
- © 2023 American Academy of Neurology
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