ArticleSpringerPlus2016
Cerebral hemodynamics is altered in patients with sleep apnea/hypopnea syndrome.
Article in SpringerPlus, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Sleep Disorders and Stroke: Pathophysiological Links, Clinical Implications, and Management Strategies.Medical sciences (Basel, Switzerland) · 2025Review
- Walking the fine line between OSA and aging.Sleep & breathing = Schlaf & Atmung · 2025Review
- Retinal microcirculation characteristics in obstructive sleep apnea/hypopnea syndrome evaluated by OCT-angiography: a literature review.International ophthalmology · 2022Review
- Longitudinal changes in regional cerebral blood flow in late middle-aged and older adults with treated and untreated obstructive sleep apnea.Human brain mapping · 2021Article
- Retinal vascular impairment in patients newly diagnosed with obstructive sleep apnea syndrome.Multidisciplinary respiratory medicine · 2021Article
- Sleep and Stroke: New Updates on Epidemiology, Pathophysiology, Assessment, and Treatment.Current sleep medicine reports · 2019Article
- Evaluation of retinal vasculature before and after treatment of children with obstructive sleep apnea-hypopnea syndrome by optical coherence tomography angiography.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
According to recent epidemiologic studies, patients with sleep apnea/hypopnea syndrome (SAHS) are at increased risk of cardiovascular diseases, including stroke. However, the mechanisms are not well defined. Nocturnal apneas can trigger acute cerebral ischemia in predisposed patients and impaired vasodilatation is present in SAHS, but few studies have explored vascular cerebral dysfunction and often gave inconclusive results. The aims of our study were to assess whether patients with SAHS have impairment of cerebral hemodynamics with respect to controls, and to investigate a possible relationship with clinical data. We studied two groups, one of 76 SAHS patients and another one of 76 non-SAHS subjects matched for age, sex and main cardiovascular risk factors. All participants underwent a daytime transcranial Doppler study of right middle cerebral artery to record cerebral blood flow velocity and cerebrovascular reactivity by means of breath-holding test (BHT). SAHS patients have a reduction in mean cerebral blood flow velocity (MFV) (52 ± 9 vs 60 ± 12 cms/s, p < 0.001) and BHT (31 ± 12 vs 36 ± 11 %, p = 0.005) when compared to non-SAHS controls. Moreover, MFV correlated negatively with the presence of coronary disease, and BHT with female sex and arterial pressure. On the other hand, in the SAHS group, MFV correlated negatively with oxygen desaturation severity. Patients with SAHS have impaired MFV and cerebrovascular reactivity when compared to controls. Interestingly, poorly controlled or unknown hypertension and severe nocturnal hypoxemia caused additional cerebral hemodynamic disturbances to these patients.
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