Abstract

Obstructive sleep apnea hypopnea syndrome (OSAHS) is associated with increased risk of cerebrovascular disease. The aim of the present study was to investigate the association between the presence of the small vessel disease (SVD) of the brain in patients with OSAHS. The study included 24 patients with moderate to severe OSAHS and 34 healthy volunteers. All the subjects underwent magnetic resonance imaging (MRI) of the brain, in order to sought periventricular white matter (PVWM), deep white matter (DWM) and brainstem SVD. Among patients with OSAHS, 79.1% had SVD (grade 1–3, Fazekas score) in DWM and 91.7% in PVWM while 22.4% had brainstem—white matter hyperintensities (B-WMH). Patients with OSAHS had a much higher degree of SVD in the DWM and PVWM compared to the control group (p < 0.001). The multivariate analysis showed an independent significant association of OSAHS with SVD (DWM and PVWM) (p = 0.033, OR 95% CI: 8.66 (1.19–63.08) and: p = 0.002, OR 95% CI: 104.98 (5.15–2141)). The same analysis showed a moderate association of OSAHS with B-WMH (p = 0.050, OR 15.07 (0.97–234.65)). Our study demonstrated an independent significant association of OSAHS with SVD and a moderate association of OSAHS with B-WMH.

Highlights

  • Obstructive sleep apnea hypopnea syndrome (OSAHS) affects 5–10% of the population.The severity of the syndrome in determined by the number of apneas and hypopneas taking place during an hour of sleep as well as by the seriousness of the patient’s symptoms at daytime [1,2]

  • Patients with OSAHS had a much higher degree of small vessel disease (SVD) in the deep white matter (DWM), periventricular white matter (PVWM) compared to the control group with statistically significant difference (p < 0.001) (Figures 2 and 3)

  • The duration of the disorder (OSAHS) is an important factor that affects the presence of SVD (p < 0.001) (Figure S1a–d))

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Summary

Introduction

Obstructive sleep apnea hypopnea syndrome (OSAHS) affects 5–10% of the population. The severity of the syndrome in determined by the number of apneas and hypopneas taking place during an hour of sleep (apnea-hypopnea index—AHI) as well as by the seriousness of the patient’s symptoms at daytime [1,2]. The pathophysiology of OSAHS is multifactorial and possibly lies on a genetic background, as well as on various factors, such as obesity that may contribute significantly [1]. OSAHS impact on patients with ischemic stroke (IS) or transient ischemic attack is quite higher when compared to the general public. It seems that OSAHS constitutes a factor that influences the course of an IS and the patient’s functionality, after the stroke [3,4]. A recent study observed a high prevalence and variability of

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