Symptomatic OSA Research Articles

Same sleep disorder but different sleep patterns: individual differences in sleep health and depressive symptomatology in veterans with obstructive sleep apnea.

Poor sleep health, a composite measure of key sleep characteristics, may relate to increased depressive symptoms among individuals treated for obstructive sleep apnea. The current investigation examined the association between sleep health and depressive symptomatology. In a pilot sample of 13 symptomatic OSA military Veterans with adequate CPAP adherence (mean age = 54.8, 76.9% male, 100% White), empirically validated cutoffs were applied to actigraphy-derived sleep variables: duration, efficiency, timing, and regularity. Participants with zero optimal sleep scores had significantly higher depressive scores (M = 19.0, SD = 3.0) than participants with 1 or 2 (M = 9.8. SD = 4.3, p = .016) and 3 or more optimal sleep scores (M = 11.3, SD = 4.9, p = .038). These preliminary findings suggest that better sleep health was associated with lower depressive symptomatology. Future work should replicate these preliminary findings in a larger sample.

Sleep health disparities and its impact on Alzheimer’s disease risk: Examining race specific physiologic mechanisms

AbstractBlacks/African‐Americans (blacks) take longer to fall asleep, have lower sleep efficiency and spend a smaller proportion of time in deep stages of non‐rapid eye movement (NREM) slow wave sleep/activity [SWS]), relative to non‐Hispanic whites (whites). Notably, blacks have a higher burden of severe obstructive sleep apnea [OSA] with excessive daytime sleepiness (EDS). These sleep metrics have been linked to increased vascular risks, inflammation, brain injury, and cognitive impairment, all known risk factors for Alzheimer’s disease (AD). This presentation will provide an update on putative mechanisms that underlie the association between sleep and risk of developing AD, both from a mechanistic (primarily preclinical) as well as a clinical/epidemiological perspective, with a focus on how disturbed sleep might be a race‐dependent physiologic risk conferring increased AD‐risk in blacks. It is vital to examine how sociocultural factors, often through behavioral processes, become physiologically expressed as increased AD‐risk in blacks. Data presented will include cross‐sectional and longitudinal studies. Utilizing data from various cohorts including NYU cohort of older‐adults participating in studies of sleep, aging and memory, and the National Alzheimer’s Coordinating Center, we will describe novel evidence implicating sleep health disparities [SHD] (i.e., shorter sleep duration [SD], smaller proportion of time in deep stages of NREM SWS/SWA and disproportionate burden of symptomatic OSA, that are more prevalent among racial/ethnic minorities, as a risk factor for AD; as a physiologic marker associated with AD pathology/biomarkers (i.e. amyloid and tau), and as a modifier of AD‐risk. We will describe race and sex specific mechanisms underlying SHD‐AD risk, including independent and synergistic effects with Aβ and/or tau, as well as vascular risk. Race‐specific associations of micro and macro‐architectural sleep parameters with novel plasma AD biomarkers will also be presented. Findings will show that social determinants of health factors mediate heterogeneity in sleep and AD outcomes, with Black subjects having worse SHD metrics i.e., shorter SD, reduced NREM SWS/SWA and greater OSA severity, and exhibiting worse race‐specific AD pathology and CVD risk markers (i.e., worse office‐based Framingham Heart Study general CVD [FHS‐CVD] risk scores, & greater WML and abnormal DKI indices) potentially leading to AD disparities.

0698 Genetic susceptibility to elevated C-reactive protein and risk of obstructive sleep apnea in US men and women

Abstract Introduction Obstructive sleep apnea (OSA) may trigger inflammation. However, growing evidence suggests a role for inflammation in predisposing OSA through increased upper airway size/collapsibility and altered ventilatory control. Inflammation also promotes sleep disturbance and excessive daytime sleepiness (EDS). Genetic analysis may provide further insights into the causal relationship between chronic inflammation and OSA incidence. Methods In 33,171 participants of European ancestry from the Nurses’ Health Study (NHS), NHS2 and the Health Professionals Follow-up Study, we quantified genetic predisposition to inflammation using a weighted polygenic risk score (PRS) based on 51 loci identified for C-reactive protein (CRP) in a recent genome-wide association meta-analysis. OSA was determined using self-reported diagnoses, which were demonstrated to reliably indicate moderate-to-severe OSA in these cohorts. EDS was defined based on self-reports of disrupted daily activities due to sleepiness ≥4 days/week. Multivariable logistic regression was used to estimate the odds ratio (OR) for OSA risk according to the number of risk alleles, adjusted for age, sex, BMI, genotyping platforms and 10 genetic principal components. Mendelian randomization using individual-level participant data was performed to evaluate the association between genetically determined CRP levels and OSA risk. Results A total of 3,163 participants (9.5%) had clinically diagnosed OSA (575 with EDS). While the CRP PRS (explained 5.0% variance in circulating levels) was not associated with OSA risk overall (OR per increment of 5 risk alleles: 1.00; 95% CI: 0.96, 1.04; p=0.96), a significant positive association was observed for OSA with concurrent EDS (Comparable OR: 1.13; 95% CI: 1.04, 1.23; p=0.003). In contrast, among participants without clinically diagnosed OSA, there was no association between the PRS and EDS (Comparable OR for EDS: 1.02; 95% CI: 0.98, 1.06; p=0.28). In Mendelian randomization, each doubling of genetically elevated CRP was associated with 44% higher odds of OSA with EDS (95% CI: 1.13, 1.82). Conclusion Chronic inflammation (characterized by elevated CRP levels) may be casually associated with risk of developing symptomatic OSA with EDS, but not OSA or EDS alone. To confirm our findings, future investigations are needed to evaluate the genetic associations with objective measures of OSA severity across diverse populations and elucidate mechanisms driven by specific inflammatory mediators. Support (If Any) NIH grants UM1CA186107, U01CA176726, U01CA167552, K01HL143034, R35HL135818

Impact of a Multimodal Telemonitoring Intervention on CPAP Adherence in Symptomatic OSA and Low Cardiovascular Risk: A Randomized Controlled Trial

One of the major challenges in treating OSA is to achieve adequate CPAP adherence. Telemonitoring has the potential to provide individualized management and early recognition of problems during treatment. What is the effect of a multimodal telemonitoring intervention on treatment adherence, quality of life, and functional status in symptomatic patients with OSA and low cardiovascular risk? In a multicenter, randomized controlled trial, patients newly diagnosed with OSA were randomly assigned to multimodal telemonitoring for 6months vsusual care (UC). Telemonitoring consisted of built-in electronic alert algorithms for early adjustment of CPAP treatment in case of side effects, leaks, or persistent residual events. The primary outcome was CPAP adherence (in hours per night). Secondary outcomes included daily symptoms such as fatigue and sleepiness, and quality of life measured by using self-reported questionnaires. A total of 206 patients with OSA and a median age of 50.6 years (interquartile range [IQR], 42.1; 58.1 years) were included in the study; they were predominantly male (63%) with a median BMI of 30.6kg/m2 (IQR, 26.8; 35.1kg/m2) and a median apnea-hypopnea index of 45.2 events/h (IQR, 34.0; 60.0 events/h). Of these, 102 received UC and 104 received telemonitoring. After 6months of treatment, CPAP adherence was similar in the two groups when assessed either by mean duration of usage (4.73 ± 2.48h per night in the telemonitoring group and 5.08 ± 2.44h per night in the UC group; P= .30) or in percentage of patients adherent to treatment (> 4h usage per night, > 70%nights; 64%in the telemonitoring group vs72%in the UC group; P= .24). There was no significant difference between the groups in effect size of improvement in fatigue and sleepiness. In patients with severe OSA and low cardiovascular risk, multimodal telemonitoring did not increase CPAP adherence. For both the telemonitoring and UC groups, similar improvements in daytime symptoms were achieved. ClinicalTrials.gov; No.: 01796769; URL: www.clinicaltrials.gov.

Sleep disorders in pregnancy and their association with pregnancy outcomes: a prospective observational study.

Sleep disturbances such as insomnia, nocturnal awakenings, restless legs syndrome, habitual snoring, and excessive daytime sleepiness are frequent during pregnancy, and these have been linked to adverse maternal and fetal outcomes. A prospective observational study was performed in high-risk Indian pregnant women. We used modified Berlin questionnaire (MBQ), Pittsburgh sleep quality index (PSQI), International Restless Legs Syndrome Study Group 2011 criteria, and Epworth sleepiness scale to diagnose various sleep disorders, such as symptomatic OSA, poor sleep quality and insomnia, RLS, and excessive daytime sleepiness, respectively, in successive trimesters of pregnancy. Outcome variables of interest were development of gestational hypertension (GH), gestational diabetes mellitus (GDM), and cesarean delivery (CS); the Apgar scores; and low birth weight (LBW). The relationship between sleep disorders and outcomes was explored using logistic regression analysis. Outcome data were obtained in 209 deliveries. As compared to nonsnorers, women who reported snoring once, twice, and thrice or more had odds ratios for developing GH-4.0 (95 % CI 1.3-11.9), 1.5 (95 % CI 0.5-4.5), and 2.9 (95 % CI 1.0-8.2) and for undergoing CS-5.3 (95 % CI 1.7-16.3), 4.9 (95 % CI 1.8-13.1), and 5.1 (95 % CI 1.9-14.9), respectively. Pregnant women who were persistently positive on MBQ had increased odds for GH and CS. Snoring and high-risk MBQ in pregnant women are strong risk factors for GH and CS. In view of the significant morbidity and health care costs, simple screening of pregnant women with questionnaires such as MBQ may have clinical utility.

CPAP Improves Endothelial Function in Patients With Minimally Symptomatic OSA: Results From a Subset Study of the MOSAIC Trial

Minimally symptomatic OSA is a highly prevalent disorder, and the effects of CPAP on vascular function in these patients are unknown. This trial aimed to investigate whether CPAP improves vascular function in minimally symptomatic OSA.In two centers taking part in the MOSAIC (Multicentre Obstructive Sleep Apnoea Interventional Cardiovascular) trial, 253 patients with minimally symptomatic OSA were randomized to 6 months of CPAP or standard care. Two hundred eight patients attended their follow-up visit within the predefined time window and had complete measurements of arterial stiffness (augmentation index [AIx]), and 64 patients had endothelial function measurements by brachial artery flow-mediated dilatation (FMD). Multivariable analyses adjusting for baseline measurements and minimization factors were performed to assess the effect of CPAP treatment on FMD (% dilatation) and AIx (% augmentation) compared with standard care.The mean ± SD baseline oxygen desaturation index and Epworth Sleepiness Score (ESS) of the 208 patients (age 58 ± 7.3 years, 31 women) were 13.7 ± 12.8 events/h and 8.3 ± 4.2, respectively. There was no CPAP treatment effect on arterial stiffness (AIx, -1.4%; 95% CI, -3.6 to +0.9%; P = .23), but CPAP improved endothelial function (FMD, +2.1%; 95% CI, +1.0 to +3.2%; P < .0001). CPAP reduced daytime sleepiness (ESS, -2.2; 95% CI, -3.0 to -1.5; P < .0001) compared with standard care. There was a larger improvement in FMD in patients using CPAP for > 4 h/night than those who used it less (P = .013).CPAP improves endothelial function, but not arterial stiffness, in minimally symptomatic OSA. Thus, minimally symptomatic OSA may be a cardiovascular risk factor.ISRCTN Register; No.: ISRCTN 34164388; URL: http://isrctn.org.

S14 CPAP improves endothelial function in minimally symptomatic OSA patients: results from the MOSAIC trial

BackgroundCPAP treatment for symptomatic OSA improves surrogate markers of cardiovascular risk, such as endothelial function and arterial stiffness, and may reduce actual cardiovascular events. Minimally symptomatic OSA is far more...

S13 The primary results of the MOSAIC trial: does CPAP for minimally symptomatic OSA reduce daytime sleepiness or calculated vascular risk?

IntroductionCPAP treatment for symptomatic OSA improves sleepiness, and reduces vascular risk by reducing blood pressure (BP) and cholesterol. Minimally symptomatic OSA is far more prevalent than symptomatic disease, and treatment...

Mandibular advancement splint titration in obstructive sleep apnoea

Mandibular advancement splints (MAS) allowing self-adjustment may be better tolerated, but the optimum titration protocol needs systematic study. The aims of the study are to assess the effectiveness of a titratable MAS device in consecutive patients with body mass index (BMI) < 35 kg/m(2) and obstructive sleep apnoea [OSA, apnoea-hypopnoea index (AHI) 10-40/h] and compare two methods of adjustment [self-adjustment or adjustment after polysomnographic (PSG) feedback]. Twenty-eight patients (24 M, mean age 49 years, mean BMI 27.6 kg/m(2)) with symptomatic (Epworth Sleepiness score > 8/24, snoring, choking or poor sleep quality) OSA (mean AHI 25.7/h, range 10-46/h) had a MAS set at 70% maximal protrusion and were randomised to subjective self-adjustment for 6 weeks (n = 16) or objective adjustment (n = 12; fixed position for 3 weeks, then PSG based feedback at 3 weeks with self-adjustment instructions). Primary outcome variable (AHI) and OSA symptoms were compared by t tests and chi-squared tests at baseline and after 6 weeks. Resolution of apnoea was defined as AHI < 5/h; improvement was defined as AHI decreased by >50% but still >5/h. The groups had similar baseline demographics, OSA severity and occlusal type. MAS therapy improved or resolved OSA in 20 out of 28 (71%) and was reportedly used nightly by 91% of the objective group and 63% of the subjective group (p = 0.04). MAS were used all night by 75% of the objective group and 69% of the subjective group (p > 0.05). MAS adjustment following PSG feedback did not lower AHI further from 3 weeks (baseline 26.5 +/- 12.0/h, 3 weeks 15.3 +/- 13.5/h p = 0.01, 6 weeks 11.7 +/- 10.0/h, p = 0.11). The overall improvement was similar to that achieved with subjective adjustment (baseline AHI 25.4 +/- 7.4/h, 6 weeks 14.3 +/- 10.7/h, p = 0.0002). Symptomatic benefit was reported by both groups. In selected patients, titratable MAS improved or resolved OSA in the majority of patients and was well tolerated. PSG-based feedback at 3 weeks allowed objective confirmation of efficacy and increased device use but did not result in greater improvement in AHI or symptoms. Neither titration method was significantly superior for us to provide firm endorsement. However, we recommend a follow-up sleep study to confirm MAS efficacy.

Nasal CPAP Continues to Improve Sleep-Disordered Breathing and Daytime Oxygenation over Long-term Follow-up of Occlusive Sleep Apnea Syndrome

To assess the effects of long-term nasal continuous positive airway pressure (CPAP) in occlusive sleep apnea syndrome (OSA), 17 patients with severe symptomatic OSA had repeated spirometry, arterial blood gases, and nocturnal polysomnograms off nasal CPAP after 3 to 46 months of treatment with nasal CPAP. Without loss of weight or change in respiratory mechanics, the ventilatory disturbance index fell from a mean of 87 events per hour to 57 events per hour (p < 0.0001), correlating with an improvement in mean nocturnal desaturation with sleep-disordered breathing events (r = 0.54, p = 0.03). Moreover, the daytime PaO2 rose significantly from a mean of 69 mm Hg to a mean of 82 mm Hg (P = 0.0001) at follow-up. The rise in daytime PaO2 was not only due to the alleviation of daytime hypercapnea observed in eight of nine hypercapneic subjects since the P(A-a)O2 gradient also decreased significantly. The improvement in PaO2 correlated significantly with the number of months of CPAP therapy, suggesting a continuing effect over time (r = 0.58, p = 0.015). These results indicate that there is a reversible element of the severity of OSA and suggest a result of nasal CPAP therapy may be to reverse the adverse and time-dependent effects of hypoxemia and sleep fragmentation on ventilatory control in severe OSA.