Continuous Positive Airway Pressure but Not GLP1-mediated Weight Loss Improves Early Cardiovascular Disease in Obstructive Sleep Apnea: A Randomized Proof-of-Concept Study.

Rationale: Obstructive sleep apnea (OSA) is an independent risk factor for cardiovascular (CV) morbidity and mortality, but the benefit of continuous positive airway pressure (CPAP) is uncertain. However, most randomized controlled trials have focused on the role of CPAP in secondary prevention, although there is growing evidence of a potential benefit on early CV disease. Weight loss in combination with CPAP may be superior but is difficult to achieve and maintain with conventional measures alone. Objectives: The aim of this study was to gain insights into the effect of CPAP on early atherosclerotic processes and to compare it with a glucagon-like peptide (GLP)-1-mediated weight loss regimen in patients with OSA. Methods: We performed a randomized proof-of-concept study comparing CPAP, a GLP1-mediated weight-loss regimen (liraglutide [Lir]), and both in combination for 24 weeks in 30 consecutive patients with OSA (apnea-hypopnea index >15 events/h; body mass index 30-40 kg/m2; and no history of diabetes, heart failure, or unstable CV disease). In addition to extensive evaluation for CV risk factors and endothelial function at baseline and end of study, subjects underwent 18F-fluoro-2-deoxy-D-glucose positron emission tomography-computed tomography (18F-FDG PET-CT) for the measurement of aortic wall inflammation (target-to-background ratio) and coronary computed tomography angiography for semiautomated coronary plaque analysis. Results: Baseline characteristics were similar between groups. CPAP alone and in combination resulted in greater reduction in apnea-hypopnea index than Lir alone (mean difference, -45 and -43 events/h, respectively, vs. -12 events/h; P < 0.05). Both Lir and combination treatment led to significant weight loss, but only CPAP alone resulted in significant decrease in vascular inflammation (aortic wall target-to-background ratio from 2.03 ± 0.34 to 1.84 ± 0.43; P = 0.010), associated with an improvement in endothelial function and a decrease in C-reactive protein. Low-attenuation coronary artery plaque volume as a marker of unstable plaque also decreased with CPAP (from 571 ± 490 to 334 ± 185 mm3) and with combination therapy (from 401 ± 145 to 278 ± 126 mm3) but not with Lir. Conclusions: These data suggest that CPAP therapy, but not GLP1-mediated weight loss, improves vascular inflammation and reduces unstable plaque volume in patients with OSA. Further large randomized controlled studies are warranted to assess the benefit of CPAP therapy in modifying early CV disease. Clinical trial registered with www.clinicaltrials.gov (NCT04186494).

Prediction of low pulse oxygen saturation in COVID-19 using remote monitoring post hospital discharge.

BACKGROUND: Monitoring systems have been developed during the COVID-19 pandemic enabling clinicians to remotely monitor physiological measures including pulse oxygen saturation (SpO2), heart rate (HR), and breathlessness in patients after discharge from hospital. These data may be leveraged to understand how symptoms vary over time in COVID-19 patients. There is also potential to use remote monitoring systems to predict clinical deterioration allowing early identification of patients in need of intervention. METHODS: A remote monitoring system was used to monitor 209 patients diagnosed with COVID-19 in the period following hospital discharge. This system consisted of a patient-facing app paired with a Bluetooth-enabled pulse oximeter (measuring SpO2 and HR) linked to a secure portal where data were available for clinical review. Breathlessness score was entered manually to the app. Clinical teams were alerted automatically when SpO2 < 94 %. In this study, data recorded during the initial ten days of monitoring were retrospectively examined, and a random forest model was developed to predict SpO2 < 94 % on a given day using SpO2 and HR data from the two previous days and day of discharge. RESULTS: Over the 10-day monitoring period, mean SpO2 and HR increased significantly, while breathlessness decreased. The coefficient of variation in SpO2, HR and breathlessness also decreased over the monitoring period. The model predicted SpO2 alerts (SpO2 < 94 %) with a mean cross-validated. sensitivity of 66 ± 18.57 %, specificity of 88.31 ± 10.97 % and area under the receiver operating characteristic of 0.80 ± 0.11. Patient age and sex were not significantly associated with the occurrence of asymptomatic SpO2 alerts. CONCLUSION: Results indicate that SpO2 alerts (SpO2 < 94 %) on a given day can be predicted using SpO2 and heart rate data captured on the two preceding days via remote monitoring. The methods presented may help early identification of patients with COVID-19 at risk of clinical deterioration using remote monitoring.

Chronic obstructive pulmonary disease and obstructive sleep apnoea overlap: co-existence, co-morbidity, or causality?

PURPOSE OF REVIEW: The chronic obstructive pulmonary disease and obstructive sleep apnoea overlap syndrome is associated with higher morbidity and mortality rates than either disease alone. There is evidence of a bidirectional relationship between the two conditions, with the overlap syndrome encompassing a spectrum of clinical phenotypes. RECENT FINDINGS: This review examines the evidence for the various factors that determine the overlap syndrome, the impact overlap syndrome has on co-morbidities, and implications for diagnosis and treatment. SUMMARY: The accurate diagnosis of the overlap syndrome is critical given its implications for treatment optimisation and reduction in healthcare utilisation and costs.

Non-dipping nocturnal blood pressure correlates with obstructive sleep apnoea severity in normotensive subjects and may reverse with therapy.

BACKGROUND: Obstructive sleep apnoea (OSA) is strongly associated with systemic hypertension, but there are limited data on the relationship with blood pressure (BP) in normotensive subjects. Here, we examined the relationship of OSA with nocturnal BP in a documented diurnal normotensive cohort, explored potential intermediate pathways and assessed the effects on BP of continuous positive airways pressure (CPAP) therapy. METHODS: 65 males referred for assessment of possible OSA and normotensive on 24-hour BP monitoring underwent overnight inpatient polysomnography (age 41±7 years, body mass index (BMI) 34±6 kg·m-2, apnoea-hypopnoea index (AHI) 14 (interquartile range 5-26)). Urine and serum were assessed for markers of sympathetic activation, renin-angiotensin-aldosterone system activity, oxidative stress, endothelial function and systemic inflammation. In a subset of patients, 24-hour BP monitoring was repeated after CPAP therapy. RESULTS: Within this normotensive cohort, night-time systolic and diastolic BP and nocturnal BP dip were highest in the fourth OSA severity quartile (p<0.05). Nocturnal BP dip correlated with AHI (r=-0.327, p<0.05) and oxygen desaturation index (ODI) (r=-0.371, p<0.05), but only ODI was an independent predictor of BP dip (B=-0.351, p<0.01) and non-dipping status (B=0.046, p<0.05). Overnight urinary norepinephrine correlated with nocturnal systolic BP (r=0.387, p<0.01) with a trend towards correlation with systolic dipping (p=0.087). In 20 CPAP-treated patients, night-time systolic BP decreased (p<0.05) and mean nocturnal BP dip increased (p≤0.05). CONCLUSION: In this normotensive cohort, OSA severity was associated with higher nocturnal BP, which improved following CPAP therapy, and intermittent hypoxia was the most important OSA-related variable in this relationship.

Cardiovascular manifestations in obstructive sleep apnea: current evidence and potential mechanisms.

Obstructive sleep apnea (OSA) is an increasingly prevalent health concern characterized by repeated episodes of pharyngeal collapse during sleep. It is frequently associated with daytime sleepiness and impaired functional capacity, but it is also linked to cardiovascular disease by a growing body of epidemiological, clinical, and translational research. The severity of OSA is traditionally evaluated by the apnea­hypopnea index (AHI), but the value of this marker as a predictor of cardiovascular outcomes is limited. Thus, there is an increasing focus on alternative classification methods such as the hypoxic burden, other polysomnographic traits, and phenotypic subgroups based on clinical symptoms. There is a need to identify subgroups of patients with OSA who will benefit most from treatment, as recent large randomized controlled trials in selected populations have failed to show benefit in reducing overall cardiovascular mortality. Obstructive sleep apnea adversely affects cardiovascular structure and function by several distinct mechanisms such as intermittent hypoxia, sleep fragmentation, and intrathoracic pressure swings. These mechanisms lead to sympathetic activation, inflammation, and oxidative stress, which may result in the clinical consequences of OSA such as hypertension, coronary artery disease, heart failure, and cerebrovascular disease. This review focuses on the epidemiology and potential mechanisms of cardiovascular diseases in OSA. Furthermore, we will briefly discuss the role of personalized medicine, alternative treatment options, and precise phenotyping to optimize treatment of this complex condition and its associated cardiovascular risk.

Impact of temperature on obstructive sleep apnoea in three different climate zones of Europe: Data from the European Sleep Apnoea Database (ESADA).

Recent studies indicate that ambient temperature may modulate obstructive sleep apnoea (OSA) severity. However, study results are contradictory warranting more investigation in this field. We analysed 19,293 patients of the European Sleep Apnoea Database (ESADA) cohort with restriction to the three predominant climate zones according to the Köppen-Geiger climate classification: Cfb (warm temperature, fully humid, warm summer), Csa (warm temperature, summer dry, hot summer), and Dfb (snow, fully humid, warm summer). Average outside temperature values were obtained and several hierarchical regression analyses were performed to investigate the impact of temperature on the apnea-hypopnea index (AHI), oxygen desaturation index (ODI), time of oxygen saturation <90% (T90) and minimum oxygen saturation (MinSpO2 ) after controlling for confounders including age, body mass index, gender, and air conditioning (A/C) use. AHI and ODI increased with higher temperatures with a standardised coefficient beta (ß) of 0.28 for AHI and 0.25 for ODI, while MinSpO2 decreased with a ß of -0.13 (all results p < .001). When adjusting for climate zones, the temperature effect was only significant in Cfb (AHI: ß = 0.11) and Dfb (AHI: ß = 0.08) (Model 1: p < .001). The presence of A/C (3.9% and 69.3% in Cfab and Csa, respectively) demonstrated only a minor increase in the prediction of the variation (Cfb: AHI, R2 +0.003; and Csa: AHI, R2 +0.007; both p < .001). Our present study indicates a limited but consistent influence of environmental temperature on OSA severity and this effect is modulated by climate zones.

Evaluation of a multicomponent grading system for obstructive sleep apnoea: the Baveno classification.

New findings on pathophysiology, epidemiology, and outcome have raised concerns on the relevance of the apnoea-hypopnoea index (AHI) in the classification of obstructive sleep apnoea (OSA) severity. Recently, a multicomponent grading system decision integrating symptomatology and comorbidities (Baveno classification), was proposed to characterise OSA and to guide therapeutic decisions. We evaluated whether this system reflects the OSA population, whether it translates into differences in outcomes, and whether the addition of AHI improves the scheme. A total of 14 499 OSA patients from the European Sleep Apnoea Database cohort were analysed. The groups were homogeneously distributed and were found to clearly stratify the population with respect to baseline parameters. Differences in sleepiness and blood pressure between the groups were analysed in a subgroup of patients after 24-36 months of treatment. Group A (minor symptoms and comorbidities) did not demonstrate any effect of treatment on outcome. However, groups B (severe symptoms, minor comorbidities), C (minor symptoms, severe comorbidities) and D (severe symptoms and comorbidities) were associated with improvement in either or both parameters with treatment. The AHI is an essential prerequisite of the diagnosis; however, adding the AHI did not improve the classification. Rather, it was inferior with respect to guiding the treatment decision. Thus, the Baveno classification allows a better stratification of the OSA population and may provide a better guidance for therapeutic decisions in OSA.

Impact of Sleep Apnea on Cardioembolic Risk in Patients With Atrial Fibrillation: Data From the ESADA Cohort.

BACKGROUND AND PURPOSE: An accurate determination of the cardioembolic risk in patients with atrial fibrillation (AF) is crucial to prevent consequences like stroke. Obstructive sleep apnea (OSA) is a known risk factor for both AF and stroke. We aim to explore a possible association between OSA and an increased cardioembolic risk in patients with AF. METHODS: We assessed data from the ESADA (European Sleep Apnea Database) cohort where patients with known AF and OSA were included. Parameters of OSA severity and related hypoxia like lowest Spo2 and 4% oxygen desaturation index were analyzed. Patients were stratified according to their cardioembolic risk estimated with the CHA2DS2-VASc score. RESULTS: From the initial cohort of 14 646 patients, a final set of 363 patients were included in the analysis. Indices of hypoxia during sleep were associated with increased CHA2DS2-VASc score (4% oxygen desaturation index 17.9 versus 29.6 versus 30.5 events/hour and the lowest Spo2 81.2 versus 77.8 versus 77.5% for low, moderate, and high cardioembolic risk, respectively, P<0.05). CONCLUSIONS: These results support the potential role of OSA-related hypoxia in the risk for cardioembolic complications such as stroke in patients with AF.

European Respiratory Society statement on sleep apnoea, sleepiness and driving risk.

Obstructive sleep apnoea (OSA) is highly prevalent and is a recognised risk factor for motor vehicle accidents (MVA). Effective treatment with continuous positive airway pressure has been associated with a normalisation of this increased accident risk. Thus, many jurisdictions have introduced regulations restricting the ability of OSA patients from driving until effectively treated. However, uncertainty prevails regarding the relative importance of OSA severity determined by the apnoea-hypopnoea frequency per hour and the degree of sleepiness in determining accident risk. Furthermore, the identification of subjects at risk of OSA and/or accident risk remains elusive. The introduction of official European regulations regarding fitness to drive prompted the European Respiratory Society to establish a task force to address the topic of sleep apnoea, sleepiness and driving with a view to providing an overview to clinicians involved in treating patients with the disorder. The present report evaluates the epidemiology of MVA in patients with OSA; the mechanisms involved in this association; the role of screening questionnaires, driving simulators and other techniques to evaluate sleepiness and/or impaired vigilance; the impact of treatment on MVA risk in affected drivers; and highlights the evidence gaps regarding the identification of OSA patients at risk of MVA.

Superior hypertension control with betablockade in the European Sleep Apnea Database.

AIMS: Arterial hypertension is highly prevalent and difficult to control in patients with obstructive sleep apnea (OSA). High sympathoadrenergic activity is a hallmark physiological phenomenon in OSA. We hypothesized that an antihypertensive drug with inhibitory properties on this activity, such as beta blockers (BBs), may be particularly efficacious in OSA patients. METHODS: Hypertensive OSA patients receiving blood pressure-lowing treatment in the European Sleep Apnea Database (ESADA) (n = 5818, 69% men, age 58 ±â€Š11 years, body mass index 33 ±â€Š7 kg/m2, apnea hypopnea index 34 ±â€Š26 events/h) were analyzed. Reported medications [BB, diuretic, renin-angiotensin blocker (RAB), calcium channel blocker (CCB), and centrally acting antihypertensive (CAH)] were classified according to ATC code. Office blood pressure was compared in patients with monotherapy or combination therapy controlling for confounders. RESULTS: Poorly controlled SBP according to the ESC/ESH guidelines was found in 66% of patients. Patients receiving monotherapy with RAB, CCB or CAH had 2.2 (95% CI 1.4-3.0), 3.0 (1.9-4.1) and 3.0 (1.7-4.7) mmHg higher SBP compared with those on BB (adjusted model, P = 0.007, 0.008 and 0.017, respectively). In those with a combination of two antihypertensive drugs, SBP was 5.5 (4.0-7.1), 5.1 (3.7-6.6), 4.3 (2.5-6.1) and 3.1 (1.6-4.6) mmHg higher in those on CCB/RAB, BB/RAB, BB/CCB or diuretic/RAB compared with those on BB/diuretic (adjusted model, P < 0.001, <0.001, 0.018 and 0.036, respectively). CONCLUSION: Poorly controlled blood pressure was common in OSA patients with antihypertensive medication. Treatment with BB alone or BB in combination with a diuretic was associated with the lowest systolic pressure in this large clinical cohort.

Mechanisms of intermittent hypoxia-mediated macrophage activation - potential therapeutic targets for obstructive sleep apnoea.

Intermittent hypoxia (IH) plays a key role in the pathogenesis of insulin resistance (IR) in obstructive sleep apnoea (OSA). IH induces a pro-inflammatory phenotype of the adipose tissue with M1 macrophage polarisation, subsequently impeding adipocyte insulin signalling, and these changes are in striking similarity to those seen in obesity. However, the detailed molecular mechanisms of IH-induced macrophage polarisation are unknown and identification of same should lead to the identification of novel therapeutic targets. In the present study, we tested the hypothesis that IH acts through similar mechanisms as obesity, activating Toll-like-receptor (TLR)4/nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) and nucleotide-binding domain (NOD)-like receptor protein 3 (NLRP3) signalling pathways leading to the upregulation and secretion of the key cytokines interleukin (IL)-1ß and IL-6. Bone-marrow derived macrophages (BMDMs) from lean and obese C57BL/6 male mice were exposed to a state-of-the-art in vitro model of IH. Independent of obesity, IH led to a pro-inflammatory M1 phenotype characterised by increased inducible nitric oxide synthase and IL-6 mRNA expression, robust increase in NF-κB DNA-binding activity and IL-6 secretion. Furthermore, IH significantly increased pro-IL-1ß mRNA and protein expression and mature IL-1ß secretion compared to control treatment. Providing mechanistic insight, pre-treatment with the TLR4 specific inhibitor, TAK-242, prevented IH-induced M1 polarisation and upregulation of IL-1ß mRNA and pro-IL-1ß protein expression. Moreover, IH-induced increase in IL-1ß secretion was prevented in BMDMs isolated from NLRP3 knockout mice. Thus, targeting TLR4/NF-κB and NLRP3 signalling pathways may provide novel therapeutic options for metabolic complications in OSA.

Estimation of respiration rate and sleeping position using a wearable accelerometer.

Wearable inertial sensors offer the possibility to monitor sleeping position and respiration rate during sleep, enabling a comfortable and low-cost method to remotely monitor patients. Novel methods to estimate respiration rate and position during sleep using accelerometer data are presented, with algorithm performance examined for two sensor locations, and accelerometer-derived respiration rate compared across sleeping positions. Eleven participants (9 male; aged: 47.82±14.14 years; BMI 30.9±5.27 kg/m2; AHI 5.77±4.18) undergoing a scheduled clinical polysomnography (PSG) wore a tri-axial accelerometer on their chest and upper abdomen. PSG cannula flow and position data were used as benchmark data for respiration rate (breaths per minute, bpm) and position. Sleeping position was classified using logistic regression, with features derived from filtered acceleration and orientation. Accelerometer-derived respiration rate was estimated for 30 s epochs using an adaptive peak detection algorithm which combined filtered acceleration and orientation data to identify individual breaths. Sensor-derived and PSG respiration rates were then compared. Mean absolute error (MAE) in respiration rate did not vary between sensor locations (abdomen: 1.67±0.37 bpm; chest: 1.89±0.53 bpm; p=0.52), while reduced MAE was observed when participants lay on their side (1.58±0.54 bpm) compared to supine (2.43±0.95 bpm), p<0.01. MAE was less than 2 bpm for 83.6% of all 30 s windows across all subjects. The position classifier distinguished supine and left/right with a ROC AUC of 0.87, and between left and right with a ROC AUC of 0.94. The proposed methods may enable a low-cost solution for in-home, long term sleeping posture and respiration monitoring.

The Impact of Telehealth on the Organization of the Health System and Integrated Care.

Sleep medicine is a rapidly developing field of medicine that is well-suited to initiatives such as Telehealth to provide safe, effective clinical care to an expanding group of patients. The increasing prevalence of sleep disorders has resulted in long waiting lists and lack of specialist availability. Telemedicine has potential to facilitate a move toward an integrated care model, which involves professionals from different disciplines and different organizations working together in a team-oriented way toward a shared goal of delivering all of a person's care requirements. Issues around consumer health technology and nonphysician sleep providers are discussed further in the article.

Understanding the pathophysiological mechanisms of cardiometabolic complications in obstructive sleep apnoea: towards personalised treatment approaches.

In January 2019, a European Respiratory Society research seminar entitled "Targeting the detrimental effects of sleep disturbances and disorders" was held in Dublin, Ireland. It provided the opportunity to critically review the current evidence of pathophysiological responses of sleep disturbances, such as sleep deprivation, sleep fragmentation or circadian misalignment and of abnormalities in physiological gases such as oxygen and carbon dioxide, which occur frequently in respiratory conditions during sleep. A specific emphasis of the seminar was placed on the evaluation of the current state of knowledge of the pathophysiology of cardiovascular and metabolic diseases in obstructive sleep apnoea (OSA). Identification of the detailed mechanisms of these processes is of major importance to the field and this seminar offered an ideal platform to exchange knowledge, and to discuss pitfalls of current models and the design of future collaborative studies. In addition, we debated the limitations of current treatment strategies for cardiometabolic complications in OSA and discussed potentially valuable alternative approaches.

Ambulatory detection of sleep apnea using a non-contact biomotion sensor.

The high prevalence of obstructive sleep apnea has led to increasing interest in ambulatory diagnosis. The SleepMinder™ (SM) is a novel non-contact device that employs radiofrequency wave technology to assess the breathing pattern, and thereby estimate obstructive sleep apnea severity. We assessed the performance of SleepMinder™ in the home diagnosis of obstructive sleep apnea. One-hundred and twenty-two subjects were prospectively recruited in two protocols, one from an unselected sleep clinic cohort (n = 67, mean age 51 years) and a second from a hypertension clinic cohort (n = 55, mean age 58 years). All underwent 7 consecutive nights of home monitoring (SMHOME ) with the SleepMinder™ as well as inpatient-attended polysomnography in the sleep clinic cohort or cardiorespiratory polygraphy in the hypertension clinic cohort with simultaneous SleepMinder™ recordings (SMLAB ). In the sleep clinic cohort, median SMHOME apnea-hypopnea index correlated significantly with polysomnography apnea-hypopnea index (r = .68; p < .001), and in the hypertension clinic cohort with polygraphy apnea-hypopnea index (r = .7; p < .001). The median SMHOME performance against polysomnography in the sleep clinic cohort showed a sensitivity and specificity of 72% and 94% for apnea-hypopnea index ≥ 15. Device performance was inferior in females. In the hypertension clinic cohort, SMHOME showed a 50% sensitivity and 72% specificity for apnea-hypopnea index ≥ 15. SleepMinder™ classified 92% of cases correctly or within one severity class of the polygraphy classification. Night-to-night variability in home testing was relatively high, especially at lower apnea-hypopnea index levels. We conclude that the SleepMinder™ device provides a useful ambulatory screening tool, especially in a population suspected of obstructive sleep apnea, and is most accurate in moderate-severe obstructive sleep apnea.

Unique sleep-stage transitions determined by obstructive sleep apnea severity, age and gender.

In obstructive sleep apnea, patients' sleep is fragmented leading to excessive daytime sleepiness and co-morbidities like arterial hypertension. However, traditional metrics are not always directly correlated with daytime sleepiness, and the association between traditional sleep quality metrics like sleep duration and arterial hypertension is still ambiguous. In a development cohort, we analysed hypnograms from mild (n = 209), moderate (n = 222) and severe (n = 272) obstructive sleep apnea patients as well as healthy controls (n = 105) from the European Sleep Apnea Database. We assessed sleep by the analysis of two-step transitions depending on obstructive sleep apnea severity and anthropometric factors. Two-step transition patterns were examined for an association to arterial hypertension or daytime sleepiness. We also tested cumulative distributions of wake as well as sleep-states for power-laws (exponent α) and exponential distributions (decay time τ) in dependency on obstructive sleep apnea severity and potential confounders. Independent of obstructive sleep apnea severity and potential confounders, wake-state durations followed a power-law distribution, while sleep-state durations were characterized by an exponential distribution. Sleep-stage transitions are influenced by obstructive sleep apnea severity, age and gender. N2 → N3 → wake transitions were associated with high diastolic blood pressure. We observed higher frequencies of alternating (symmetric) patterns (e.g. N2 → N1 → N2, N2 → wake → N2) in sleepy patients both in the development cohort and in a validation cohort (n = 425). In conclusion, effects of obstructive sleep apnea severity and potential confounders on sleep architecture are small, but transition patterns still link sleep fragmentation directly to obstructive sleep apnea-related clinical outcomes like arterial hypertension and daytime sleepiness.

Nondipping Nocturnal Blood Pressure Predicts Sleep Apnea in Patients With Hypertension.

STUDY OBJECTIVES: Systemic hypertension is highly prevalent in obstructive sleep apnea (OSA) but there are limited data on OSA prevalence in cohorts with hypertension comparing dippers and nondippers. We investigated this relationship in a clinic-based cohort of patients with hypertension who were not screened for any pretest possibility of OSA. METHODS: A total of 100 patients with hypertension aged (mean ± SD) 58 ± 10 years, body mass index 30.5 ± 6.1 kg/m2, and Epworth Sleepiness Scale score 6 ± 4 were included. All underwent overnight attended sleep studies and 24-hour ambulatory blood pressure monitoring. The primary study end-point was OSA prevalence based on the standard criteria of apnea-hypopnea index (AHI) ≥ 15 events/h in patients with dipping and nondipping nocturnal blood pressure. RESULTS: Results showed 10.5% of dippers and 43.5% of nondippers had an AHI ≥ 15 (chi-square P = .001). In univariate analysis, AHI correlated significantly with blood pressure dip (r = -.26, P < .05), as did ESS (r = -.28, P < .05). In linear regression, AHI predicted the magnitude of blood pressure dip (standardised ß = -.288, P = .03), whereas age, body mass index, systolic blood pressure and diastolic blood pressure did not. CONCLUSIONS: Patients with nondipping nocturnal blood pressure are at high risk of OSA, regardless of symptom profile, which supports the recommendation that such patients should be assessed for co-existing OSA.

Adipose tissue as a key player in obstructive sleep apnoea.

Obstructive sleep apnoea (OSA) is a major health concern worldwide and adversely affects multiple organs and systems. OSA is associated with obesity in >60% of cases and is independently linked with the development of numerous comorbidities including hypertension, arrhythmia, stroke, coronary heart disease and metabolic dysfunction. The complex interaction between these conditions has a significant impact on patient care and mortality. The pathophysiology of cardiometabolic complications in OSA is still incompletely understood; however, the particular form of intermittent hypoxia (IH) observed in OSA, with repetitive short cycles of desaturation and re-oxygenation, probably plays a pivotal role. There is fast growing evidence that IH mediates some of its detrimental effects through adipose tissue inflammation and dysfunction. This article aims to summarise the effects of IH on adipose tissue in experimental models in a comprehensive way. Data from well-designed controlled trials are also reported with the final goal of proposing new avenues for improving phenotyping and personalised care in OSA.