IntroductionContinuous positive airway pressure (CPAP) is currently the treatment of choice for sleepiness in patients with obstructive sleep apnoea (OSA); however, adherence is often thought to be suboptimal. We investigated the effects of suboptimal CPAP usage on objective and subjective sleepiness parameters in patients with OSA.Material and methodsIn this 2-week, parallel, double-blind, randomised controlled trial we enrolled moderate-to-severe OSA patients with excessive pre-treatment daytime sleepiness (Epworth sleepiness scale (ESS) score >10 points) who had suboptimal CPAP adherence over ≥12 months (mean nightly usage time 3–4 h). Patients were allocated through minimisation to either subtherapeutic CPAP (“sham CPAP”) or continuation of CPAP (“therapeutic CPAP”). A Bayesian analysis with historical priors calculated the posterior probability of superiority.ResultsBetween May, 2016 and November, 2018, 57 patients (aged 60±8 years, 79% male, 93% Caucasian) were allocated in total, and 52 who completed the study (50% in each arm) were included in the final analysis. The unadjusted ESS score increase was 2.4 points (95% CI 0.6–4.2, p=0.01) in the sham-CPAP group when compared to continuing therapeutic CPAP. The probability of superiority of therapeutic CPAP over sham CPAP was 90.4% for ESS, 90.1% for systolic blood pressure and 80.3% for diastolic blood pressure.ConclusionsPatients with moderate-to-severe OSA and daytime sleepiness are still getting a substantial benefit from suboptimal CPAP adherence, albeit not as much as they might get if they adhered more. Whether a similar statement can be made for even lower adherence levels remains to be established in future trials.

Background: The pathogenesis and etiology of thoracic aortic aneurysms (TAA) are largely unknown. Preliminary data from patients with aortic dissection and abdominal aneurysms suggest a causal link of obstructive sleep apnea (OSA) on aortic disease. Objectives: The aim of the study was to assess the prevalence of OSA in patients with TAA compared to a matched control group. Method: In this prospective parallel-cohort study, we 2-to-1 matched 208 patients with verified TAA (at the aortic sinus and/or ascending aorta) to 104 controls without TAA according to sex, age, height, weight, and left ventricular ejection fraction. All participants underwent an ultrasound of the thoracic aorta and a level III respiratory polygraphy. OSA was defined as apnea-hypopnea index 5/h. The prevalence of OSA was compared with conditional logistic regression and controlling for the matching variables. Results: A total of 312 patients (mean age 65 ± 11 years, 82% male, mean body mass index 27 ± 4 kg/m2) were successfully 2-to-1 matched in the final model. Prevalence of OSA was significantly higher in the TAAgroup when compared to the matched control group (63 vs. 47%; odds ratio 1.87 [95% CI 1.05-3.34]; p = 0.03). When applying a higher apnea-hypopnea index threshold (15/h), the odds ratio increased to 3.25 (95% CI 1.65-6.42; p < 0.001). The median apnea-hypopnea index was higher in patients with TAA (9.2/h [3.3-20.0] vs. 4.5/h [2.2-11.1], p < 0.001). Conclusions: Patients with TAA have a higher prevalence of OSA when compared to the general population. Since OSA is effectively treatable and might contribute to the pathogenesis of TAA, further longitudinal trials are needed to assess the association between OSA and TAA.

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BackgroundObstructive sleep apnea (OSA) is associated with an increased prevalence of aortic aneurysms, and it has also been suggested that severe OSA furthers aneurysm expansion in the abdomen. We evaluated whether OSA is a risk factor for the progression of ascending thoracic aortic aneurysms (TAA).MethodsPatients with TAA underwent yearly standardised echocardiographic measurements of the ascending aorta over 3 years, and two level-III sleep studies. The primary outcome was the expansion rate of TAA in relation to the apnea-hypopnea-index (AHI). Secondary outcomes included surveillance for aortic events (composite endpoints of rupture, dissection, elective surgery, and death).ResultsBetween July 2014 and March 2020, 230 patients (median age 70 years, 78% male) participated in the cohort. At baseline, 34.8% of patients had an AHI of ≥15 events·h−1. There was no association between TAA diameters and the AHI at baseline. After 3 years mean expansion rates were 0.55±1.25 mm at the aortic sinus and 0.60±1.12 mm at the ascending aorta. In the regression analysis, after controlling for baseline diameter and cardiovascular risk factors, there was strong evidence for a positive association of TAA expansion with AHI (aortic sinus estimate 0.025 mm [95%CI 0.009 to 0.040], p<0.001; ascending aorta estimate 0.026 mm [95%CI 0.011 to 0.041], p=0.001). Twenty participants (8%) experienced an aortic event, however, there was no association with OSA severity.ConclusionOSA may be a modest but independent risk factor for faster TAA expansion and thus potentially contributes to life-threatening complications in aortic disease.

Impaired cerebral vascular reactivity (CVR) increases long-term stroke risk. Obstructive sleep apnoea (OSA) is associated with peripheral vascular dysfunction and vascular events. The aim of this trial was to evaluate the effect of continuous positive airway pressure (CPAP) withdrawal on CVR.41 OSA patients (88% male, mean age 57±10 years) were randomised to either subtherapeutic or continuation of therapeutic CPAP. At baseline and after 2 weeks, patients underwent a sleep study and magnetic resonance imaging (MRI). CVR was estimated by quantifying the blood oxygen level-dependent (BOLD) MRI response to breathing stimuli.OSA did recur in the subtherapeutic CPAP group (mean treatment effect apnoea–hypopnoea index +38.0 events·h−1, 95% CI 24.2–52.0; p<0.001) but remained controlled in the therapeutic group. Although there was a significant increase in blood pressure upon CPAP withdrawal (mean treatment effect +9.37 mmHg, 95% CI 1.36–17.39; p=0.023), there was no significant effect of CPAP withdrawal on CVR assessedviaBOLD MRI under either hyperoxic or hypercapnic conditions.Short-term CPAP withdrawal did not result in statistically significant changes in CVR as assessed by functional MRI, despite the recurrence of OSA. We thus conclude that, unlike peripheral endothelial function, CVR is not affected by short-term CPAP withdrawal.