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The classification of obstructive sleep apnea is on the basis of sleep study criteria that may not adequately capture disease heterogeneity. Improved phenotyping may improve prognosis prediction and help select therapeutic strategies. This study used cluster analysis to investigate the clinical clusters of obstructive sleep apnea. An ascending hierarchical cluster analysis was performed on baseline symptoms, physical examination, risk factor exposure and co-morbidities from 18,263 participants in the OSFP (French national registry of sleep apnea). The probability for criteria to be associated with a given cluster was assessed using odds ratios, determined by univariate logistic regression. Six clusters were identified, in which patients varied considerably in age, sex, symptoms, obesity, co-morbidities and environmental risk factors. The main significant differences between clusters were minimally symptomatic versus sleepy obstructive sleep apnea patients, lean versus obese, and among obese patients different combinations of co-morbidities and environmental risk factors. Our cluster analysis identified six distinct clusters of obstructive sleep apnea. Our findings underscore the high degree of heterogeneity that exists within obstructive sleep apnea patients regarding clinical presentation, risk factors and consequences. This may help in both research and clinical practice for validating new prevention programs, in diagnosis and in decisions regarding therapeutic strategies.

The association between obstructive sleep apnea (OSA) and cardiovascular morbidity and mortality is largely the result of myocardial anomalies. In this Review, the authors discuss the mechanisms that lead to myocardial damage and cardiac dysfunction in patients with OSA, and the potential beneficial effects of nasal continuous positive airway pressure on cardiac symptoms and hemodynamic parameters in these patients. Obstructive sleep apnea (OSA) is associated with cardiovascular morbidity and mortality, largely as a result of myocardial anomalies. Numerous mechanisms cause OSA-related myocardial damage. The majority are initiated as a result of OSA-induced, chronic, intermittent hypoxia. The most-important mechanisms that lead to myocardial damage are increased sympathetic activity, endothelial dysfunction, systemic inflammation, oxidative stress, and metabolic anomalies. All these mechanisms promote the development of hypertension, which is common in patients with OSA. Hypertensive cardiomyopathy and coronary heart disease, as well as obesity-related, diabetic, and tachycardia-induced cardiomyopathies, are also associated with OSA. Left ventricular hypertrophy, myocardial fibrosis, atrial dilatation, and left ventricular systolic and diastolic dysfunction in patients with OSA explain the association of the disease with these clinical outcomes. The gold-standard treatment for OSA, nasal continuous positive airway pressure (CPAP), might improve cardiac symptoms and hemodynamic parameters in patients with the disease. However, large clinical trials are required to improve our understanding of the cardiac consequences of OSA, and determine the effect of treatment, particularly CPAP, on myocardial damage in symptomatic patients and primary prevention of cardiovascular disorders. Key Points Obstructive sleep apnea (OSA) causes chronic, intermittent hypoxia, which leads to an increase in sympathetic activity, endothelial dysfunction, systemic inflammation, oxidative stress, metabolic anomalies, and myocardial damage Hypertension is common in patients with OSA Hypertensive cardiomyopathy, coronary heart disease, and obesity-related, diabetic, and tachycardia-induced cardiomyopathies are associated with OSA The main myocardial anomalies observed during OSA are left ventricular hypertrophy, myocardial fibrosis, and atrial dilatation Nasal continuous positive airway pressure (CPAP) could improve cardiac symptoms and hemodynamic parameters in patients with OSA Large clinical trials are needed to determine the impact of CPAP treatment on myocardial damage in patients with OSA

More advanced knowledge is needed on how COPD alters the clinical presentation of obstructive sleep apnea (OSA) and how the association of both diseases, known as 'overlap syndrome' (OVS), impacts on cardiovascular health. To investigate differences between patients with OVS and those with moderate-to-severe OSA alone. A cross-sectional study conducted in the French National Sleep Apnea Registry between January 1997 and January 2017. Univariable and multivariable logistic regression models were used to compare OVS versus OSA alone on symptoms and cardiovascular health. 46,786 patients had moderate-to-severe OSA. Valid spirometry was available for 16,466 patients: 14,368 (87%) had moderate-to-severe OSA alone and 2098 (13%) had OVS. A lower proportion of OVS patients complained of snoring, morning headaches and excessive daytime sleepiness compared to OSA alone (median Epworth Sleepiness Scale score: 9 [interquartile range (IQR) 6-13] versus 10 (IQR 6-13), respectively; P <0.02). Similarly, a lower proportion of OVS patients (35.6% versus 39.4%, respectively; P <0.01) experienced sleepiness while driving. In contrast, 63.5% of the OVS population experienced nocturia compared to 58.0% of the OSA population (P<0.01). Apnea hypopnea index (36 [25; 52] vs 33.1 [23.3; 50]), oxygen desaturation index (28 [15; 48] vs 25.2 [14; 45]) and mean nocturnal SaO2 (92 [90; 93.8] vs 93 [91.3; 94]) were significantly more altered in the OVS group. Associated COPD had no effect on the prevalence of hypertension and stroke. After controlling for main confounders, COPD severity was associated in a dose-response relationship with a higher prevalence of coronary heart disease, heart failure and peripheral arteriopathy. In adults with moderate-to-severe OSA, OVS was minimally symptomatic, but exhibited higher odds for prevalent coronary heart disease, heart failure and peripheral arteriopathy.

Data from women (n = 305, aged 43 [34; 53] years-old, BMI 44.2 [40.8; 48.2] kg/m2) included in the Severe Obesity Outcome Network (SOON) cohort were analyzed (i) to evaluate collinearity between the different anthropometric markers, (ii) to compare the association of markers with hypertension, type 2 diabetes, obstructive sleep apnea syndrome (OSAS) and other cardiometabolic risks. Hip, waist and neck circumferences correlated with BMI with respectively less collinearity (r = 0.70, r = 0.59 and r = 0.37, respectively, p<0.001) whereas waist-to-hip ratio was not correlated (r = 0.11, p = 0.072). Waist and neck circumferences were significantly associated with hypertension, type 2 diabetes and OSAS in univariate logistic regressions, waist-to-hip ratio with hypertension and type 2 diabetes. Hip circumference was inversely correlated with type 2 diabetes (OR 0.970 (95CI: 0.948; 0.991) p = 0.006). BMI was only linked to OSAS (OR 1.092 (95CI: 1.043; 1.143) p<0.001). Neck circumference was the only marker significantly associated with all cardiometabolic risk markers (HOMA-IR, apnea-hypopnea index, Log Triglycerides/HDL-c, alanin-aminotransferase, aspartate-aminotransferase, gammaglutamyl transpeptidase). Neck circumference appears the most appropriate anthropometric marker to identify the fat distribution associated with high cardiometabolic risk in women with severe obesity.

To determine the effect of continuous positive airway pressure (CPAP), the gold standard treatment for obstructive sleep apnea syndrome (OSAS), on gait control in severe OSAS patients. We conducted a randomized, double-blind, parallel-group, sham-controlled monocentric study in Grenoble Alpes University Hospital, France. Gait parameters were recorded under single and dual-task conditions using a visuo-verbal cognitive task (Stroop test), before and after the 8-week intervention period. Stride-time variability, a marker of gait control, was the primary study endpoint. Changes in the determinants of gait control were the main secondary outcomes. ClinicalTrials.gov Identifier: (NCT02345694). 24 patients [median (Q1; Q3)]: age: 59.5 (46.3; 66.8) years, 87.5% male, body mass index: 28.2 (24.7; 29.8) kg. m −2 , apnea–hypopnea index: 51.6 (35.0; 61.4) events/h were randomized to be treated by effective CPAP (n = 12) or by sham-CPAP (n = 12). A complete case analysis was performed, using a mixed linear regression model. CPAP elicited no significant improvement in stride-time variability compared to sham-CPAP. No difference was found regarding the determinants of gait control. This study is the first RCT to investigate the effects of CPAP on gait control. Eight weeks of CPAP treatment did not improve gait control in severe non-obese OSAS patients. These results substantiate the complex OSAS-neurocognitive function relationship.

Sleep apnea (SA) is common in Down syndrome (DS), but its impact on daytime autonomic control is poorly described. The aim of this study was to assess the impact of SA on autonomic control of heart rate (HR) and blood pressure (BP) during a Head-Up Tilt test (HUTT) in adults with DS. Ancillary cross-sectional analysis of an observational study conducted on 28 adults with DS (31.7 ± 7.4 years; 32% female) free from congenital cardiopathy, thyroid disorders, or medication that impact autonomic control were included. Full-night polysomnography and HUTT were performed. Temporal and spectral analyses were performed on the signals of RR intervals, systolic and diastolic blood pressures (SBP and DBP). SBP and DBP min-max variations were specifically analyzed during the initial 3 min post-tilting (3minUp). 21 (75%) subjects presented moderate-severe SA (Apnea-Hypopnea Index ≥ 15/h). During the 3minUp, moderate-severe SA group showed reduced min-max variations in systolic and diastolic blood pressures (40.0 ± 10.2 vs. 51.7 ± 18.7 mmHg and 27.0 ± 7.2 vs. 39.9 ± 17.4 mmHg, all p  < 0.05) with blunted vascular sympathetic activity during the entire orthostatic phase (LF SBP ; 24.3 ± 11.7 vs. 28.6 ± 9.8 nu; p  < 0.05). SA-related intermittent hypoxia, rather than sleep fragmentation was associated with changes in SBP during the 3minUp. The baroreflex sensitivity and heart rate variability parameters were similar in both groups. SA was associated with a blunted autonomic control of BP during HUTT, without changes in HR variability parameters. SA-related intermittent hypoxia, rather than sleep fragmentation seems to play a key role in these alterations.

The purpose of this study is to objectively assess by polysomnography total sleep time and sleep macrostructure in glaucomatous versus non-glaucomatous individuals after adjusting for possible confounding factors affecting the quality of sleep. This is an observational, prospective, single-center, case-controlled study using a sleep research database (MARS e-Cohort) collecting clinical data, comorbidities, medications, and sleep studies of glaucomatous and non-glaucomatous individuals. The diagnosis of glaucoma was confirmed with a full comprehensive ophthalmological examination including a visual field test. Total sleep time and the main sleep parameters (time spent in stages 1, 2, 3 and 4, microarousals, apnea–hypopnea index, and indices of hypoxic burden) were compared in glaucomatous and non-glaucomatous individuals after adjusting for age, anthropometric data, and comorbidities. The study included 33 glaucomatous and 66 non-glaucomatous individuals. The median total sleep time was 325 min [273; 398] for the control group and 311 min [244; 349] for the glaucoma group. After adjusting for the potential confounding factors, there was no significant difference in total sleep time ( p  = 0.3) and other sleep parameters between the control group and the glaucoma group. The sleep macrostructure was comparable in the glaucomatous and non-glaucomatous individuals after careful adjustment for confounders.

The symptomatic response to continuous positive airway pressure (CPAP) therapy in COPD-obstructive sleep apnea overlap syndrome (OVS) compared to OSA syndrome (OSA) alone has not been well studied so far. The aim of this study is to explore main differences in the clinical response to CPAP treatment in OVS compared to OSA alone. Using prospective data from the French National Sleep Apnea Registry, we conducted an observational study among 6320 patients with moderate-to-severe OSA, available spirometry, and at least one follow-up visit under CPAP therapy. CPAP efficacy measured on the residual apnea-hypopnea index and median adherence were similar between OVS and OSA patients. In both groups, the overall burden of symptoms related to sleep apnea improved with CPAP treatment. In a multivariable model adjusted for age, gender, body mass index, adherence to treatment and residual apnea-hypopnea index, OVS was associated with higher odds for persistent morning headaches (OR: 1.37 [95% CI; 1.04; 1.79]; P = 0.02), morning tiredness (OR: 1.33 [95% CI: 1.12; 1.59]; P<0.01), daytime sleepiness (OR; 1.24 [95% CI: 1.4; 1.46]: P<0.01) and exertional dyspnea (OR: 1.26 [95% CI: 1.00;1.58]; P = 0.04) when compared with OSA alone. CPAP therapy was effective in normalizing the apnea-hypopnea index and significantly improved OSA-related symptoms, regardless of COPD status. CPAP should be offered to patients with OVS on a trial basis as a significant improvement in OSA-related symptoms can be expected, although the range of response may be less dramatic than in OSA alone.

BackgroundArterial stiffness, measured by pulse wave velocity (PWV), is a strong independent predictor of late cardiovascular events and mortality. It is recognised that obstructive sleep apnoea (OSA) is associated with cardiovascular comorbidities and mortality. Although previous meta-analyses concluded that PWV is elevated in OSA, we feel that an individual patient data analysis from nine relatively homogeneous studies could help answer: to what extent does OSA drive arterial stiffness?MethodsIndividual data from well-characterised patients referred for suspicion of OSA, included in nine studies in which carotid–femoral PWV was measured using a Complior device, were merged for an individual patient data meta-analysis.Results893 subjects were included (age: 56±11 (mean±SD), 72% men, 84% with confirmed OSA). Body Mass Index varied from 15 to 81 kg/m2 (30±7 kg/m2). PWV ranged from 5.3 to 20.5 m/s (10.4±2.3 m/s). In univariate analysis, log(PWV) was strongly related to age, gender, systolic blood pressure, presence of type 2 diabetes (all p<0.01) as well as to dyslipidaemia (p=0.03) and an Epworth Sleepiness Scale score ≥9 (p=0.04), whereas it was not related to obesity (p=0.54), a severe Apnoea–Hypopnoea Index (p=0.14), mean nocturnal saturation (p=0.33) or sleep time with oxygen saturation below 90% (p=0.47). In multivariable analysis, PWV was independently associated with age, systolic blood pressure and diabetes (all p<0.01), whereas severe OSA was not significantly associated with PWV.ConclusionOur individual patient meta-analysis showed that elevated arterial stiffness in patients with OSA is driven by conventional cardiovascular risk factors rather than apnoea parameters.

Background: The capacity to diagnose obstructive sleep apnoea (OSA) must be expanded to meet an estimated disease burden of nearly one billion people worldwide. Validated alternatives to the gold standard polysomnography (PSG) will improve access to testing and treatment. This study aimed to evaluate the diagnosis of OSA, using measurements of mandibular movement (MM) combined with automated machine learning analysis, compared to in-home PSG. Methods: 40 suspected OSA underwent single overnight in-home sleep testing with PSG (Nox A1, ResMed, Australia) and simultaneous MM monitoring (Sunrise, Sunrise SA, Belgium). PSG recordings were manually analysed by two expert sleep centres (Grenoble and London); MM analysis was automated. The Obstructive Respiratory Disturbance Index calculated from the MM monitoring (MM-ORDI) was compared to the PSG (PSG-ORDI) using intraclass correlation coefficient and Bland-Altman analysis. Receiver operating characteristic curves (ROC) were constructed to optimise the diagnostic performance of the MM monitor at different PSG-ORDI thresholds (5, 15 and 30 events/hour). Results: 31 patients were included in the analysis (58% men; mean (SD) age: 48 (15) years; BMI: 30.4 (7.6) kg/m2). Good agreement was observed between MM-ORDI and PSG-ORDI (median bias 0.00; 95% CI -23.25 to +9.73 events/hour). However, for patients with no or mild OSA, MM monitoring overestimated disease severity (PSG-ORDI 5-15: MM-ORDI overestimation +3.70 (95% CI -0.53 to +18.32) events/hour). In patients with moderate-severe OSA, there was an underestimation (PSG-ORDI >15: MM-ORDI underestimation -8.70 (95% CI -28.46 to +4.01) events/hour). ROC optimal cut-off values for PSG-ORDI thresholds of 5, 15, 30 events/hour were: 9.53, 12.65 and 24.81 events/hour, respectively. These cut-off values yielded a sensitivity of 88, 100 and 79%, and a specificity of 100, 75, 96%. The positive predictive values were: 100, 80, 95% and the negative predictive values 89, 100, 82%, respectively. Conclusion: The diagnosis of OSA, using MM with machine learning analysis, is comparable to manually scored in-home PSG. Therefore, this novel monitor could be a convenient diagnostic tool that can easily be used in the patients’ own home.