scholarly journals Nocturnal cerebral hypoxia in obstructive sleep apnoea: a randomised controlled trial

2018 ◽  
Vol 51 (5) ◽  
pp. 1800032 ◽  
Author(s):  
Esther I. Schwarz ◽  
Michael Furian ◽  
Christian Schlatzer ◽  
John R. Stradling ◽  
Malcolm Kohler ◽  
...  

Cerebral hypoxia may promote cerebral damage in patients with obstructive sleep apnoea (OSA). We investigated whether OSA patients experience nocturnal cerebral hypoxia that is prevented by continuous positive airway pressure (CPAP).OSA patients using CPAP underwent sleep studies including pulse oximetry (arterial oxygen saturation (SpO2)) and near-infrared spectroscopy to monitor cerebral tissue oxygenation (CTO) at baseline and after 2 weeks on either subtherapeutic or therapeutic CPAP according to randomised allocation. Changes in oxygenation at end of the 2-week intervention were compared between groups.Among 21 patients (mean apnoea/hypopnoea index 50.3 events·h−1), OSA recurred in all nine patients using subtherapeutic CPAP and in none of the patients using therapeutic CPAP: mean (95% CI) between-group differences in changes of oxygen desaturation index from baseline to 2 weeks +40.7 (31.1–50.4) events·h−1 for SpO2 and +37.0 (25.3–48.7) events·h−1 for CTO (both p<0.001). Mean nocturnal SpO2 and CTO decreased more in patients using subtherapeutic versus therapeutic CPAP: −2.4 (−3.4–−1.1)% and −3.8 (−7.4–−0.1)%, respectively; both p<0.03. Severe CTO drops ≥13% associated with cerebral dysfunction in previous studies occurred in four out of nine patients using subtherapeutic CPAP, but in none out of 12 patients using therapeutic CPAP (p=0.01).In patients with OSA, CPAP withdrawal resulted in nocturnal cerebral deoxygenation, suggesting a role of cerebral hypoxia in predisposing untreated OSA patients to cerebral damage.

2020 ◽  
Vol 55 (5) ◽  
pp. 1901945 ◽  
Author(s):  
Martino F. Pengo ◽  
Davide Soranna ◽  
Alice Giontella ◽  
Elisa Perger ◽  
Paola Mattaliano ◽  
...  

The treatment for obstructive sleep apnoea (OSA) with continuous positive airway pressure (CPAP) or mandibular advancement devices (MADs) is associated with blood pressure (BP) reduction; however, the overall effect is modest. The aim of this systematic review and meta-analysis of randomised controlled trials (RCTs) comparing the effect of such treatments on BP was to identify subgroups of patients who respond best to treatment.The article search was performed in three different databases with specific search terms and selection criteria. From 2289 articles, we included 68 RCTs that compared CPAP or MADs with either passive or active treatment. When all the studies were pooled together, CPAP and MADs were associated with a mean BP reduction of −2.09 (95% CI −2.78– −1.40) mmHg for systolic BP and −1.92 (95% CI −2.40– −1.43) mmHg for diastolic BP and −1.27 (95% CI −2.34– −0.20) mmHg for systolic BP and −1.11 (95% CI −1.82– −0.41) mmHg for diastolic BP, respectively. The subgroups of patients who showed a greater response were those aged <60 years (systolic BP −2.93 mmHg), with uncontrolled BP at baseline (systolic BP −4.14 mmHg) and with severe oxygen desaturations (minimum arterial oxygen saturation measured by pulse oximetry <77%) at baseline (24-h systolic BP −7.57 mmHg).Although this meta-analysis shows that the expected reduction of BP by CPAP/MADs is modest, it identifies specific characteristics that may predict a pronounced benefit from CPAP in terms of BP control. These findings should be interpreted with caution; however, they are particularly important in identifying potential phenotypes associated with BP reduction in patients treated for OSA.


Thorax ◽  
2018 ◽  
Vol 74 (5) ◽  
pp. 496-499 ◽  
Author(s):  
Sylvain Recoquillon ◽  
Jean-Louis Pépin ◽  
Bruno Vielle ◽  
Ramaroson Andriantsitohaina ◽  
Vanessa Bironneau ◽  
...  

Systemic inflammation and metabolic disorders are among the mechanisms linking obstructive sleep apnoea (OSA) and cardiovascular disease (CVD). In 109 patients with severe OSA and no overt CVD, biomarkers of inflammation (C reactive protein, interleukin-6, tumour necrosis factor-α and its receptors, adiponectin, leptin and P-selectin), glucose and lipid metabolism, and N-terminal pro-brain natriuretic peptide, were measured before and after 2 months of treatment with a mandibular advancement device (MAD) (n=55) or a sham device (n=54). MAD reduced the Apnoea–Hypopnoea Index (p<0.001) but had no effect on circulating biomarkers compared with the sham device, despite high treatment adherence (6.6 hour/night).Trial registration numberNCT01426607.


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