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, ; Watson, Nathaniel F.; Badr, M. Safwan; Belenky, Gregory; Bliwise, Donald L.; Buxton, Orfeu M.; Buysse, Daniel; Dinges, David F.; Gangwisch, James; Grandner, Michael A.; Kushida, Clete; Malhotra, Raman K.; Martin, Jennifer L.; Patel, Sanjay R.;
Halder, Indrani; Matthews, Karen A.; Buysse, Daniel J.; Strollo, Patrick J.; Causer, Victoria; Reis, Steven E.; Hall, Martica H.
doi: 10.5665/sleep.4888pmid: 25845688
AbstractStudy Objectives:The mechanisms that underlie differences in sleep characteristics between European Americans (EA) and African Americans (AA) are not fully known. Although social and psychological processes that differ by race are possible mediators, the substantial heritability of sleep characteristics also suggests genetic underpinnings of race differences. We hypothesized that racial differences in sleep phenotypes would show an association with objectively measured individual genetic ancestry in AAs.Design:Cross sectional.Setting:Community-based study.Participants:Seventy AA adults (mean age 59.5 ± 6.7 y; 62% female) and 101 EAs (mean age 60.5 ± 7 y, 39% female).Measurements and Results:Multivariate tests were used to compare the Pittsburgh Sleep Quality Index (PSQI) and in-home polysomnographic measures of sleep duration, sleep efficiency, apnea-hypopnea index (AHI), and indices of sleep depth including percent visually scored slow wave sleep (SWS) and delta EEG power of EAs and AAs. Sleep duration, efficiency, and sleep depth differed significantly by race. Individual % African ancestry (%AF) was measured in AA subjects using a panel of 1698 ancestry informative genetic markers and ranged from 10% to 88% (mean 67%). Hierarchical linear regression showed that higher %AF was associated with lower percent SWS in AAs (β (standard error) = −4.6 (1.5); P = 0.002), and explained 11% of the variation in SWS after covariate adjustment. A similar association was observed for delta power. No association was observed for sleep duration and efficiency.Conclusion:African genetic ancestry is associated with indices of sleep depth in African Americans. Such an association suggests that part of the racial differences in slow-wave sleep may have genetic underpinnings.
Sanders, Anne E.; Essick, Greg K.; Beck, James D.; Cai, Jianwen; Beaver, Shirley; Finlayson, Tracy L.; Zee, Phyllis C.; Loredo, Jose S.; Ramos, Alberto R.; Singer, Richard H.; Jimenez, Monik C.; Barnhart, Janice M.; Redline, Susan
Abdelsattar, Zaid M.; Hendren, Samantha; Wong, Sandra L.; Campbell, Darrell A.; Ramachandran, Satya Krishna
doi: 10.5665/sleep.4892pmid: 25761980
AbstractStudy Objective:To determine whether preoperatively untreated obstructive sleep apnea (OSA) affects postoperative outcomes.Design:Cohort study of patients undergoing surgery between July 2012 and September 2013, utilizing prospectively collected data from the Michigan Surgical Quality Collaborative. Multivariable regression models were used to compare complication rates between treated and untreated OSA, while adjusting for important patient covariates and clustering within hospitals.Setting:Fifty-two community and academic hospitals in Michigan.Patients:Adult patients undergoing various general or vascular operations were categorized as: (1) no diagnosis or low risk of OSA; (2) documented OSA without therapy or suspicion of OSA; and (3) diagnosis of OSA with treatment (e.g., positive airway pressure).Exposures:OSA, preoperatively treated or untreated, was the exposure variable. Postoperative 30-day cardiopulmonary complications including arrhythmias, cardiac arrest, myocardial infarction, unplanned reintubation, pulmonary embolism, and pneumonia were the outcomes of interest.Measurements and Results:Of 26,842 patients, 2,646 (9.9%) had a diagnosis or suspicion of OSA. Of those, 1,465 (55.4%) were untreated. Patient and procedural risk factors were evenly balanced between treated and untreated groups. Compared with treated OSA, untreated OSA was independently associated with more cardiopulmonary complications (risk-adjusted rates 6.7% versus 4.0%; adjusted odds ratio [aOR] = 1.8, P = 0.001), particularly unplanned reintubations (aOR = 2.5, P = 0.003) and myocardial infarction (aOR = 2.6, P = 0.031).Conclusions:Patients with obstructive sleep apnea (OSA) who are not treated with positive airway pressure preoperatively are at increased risks for cardiopulmonary complications after general and vascular surgery. Improving the recognition of OSA and ensuring adequate treatment may be a strategy to reduce risk for surgical patients with OSA.
Zhang, Zhongxing; Khatami, Ramin
doi: 10.5665/sleep.4894pmid: 25761983
AbstractStudy Objectives:Current knowledge on hemodynamics in sleep is limited because available techniques do not allow continuous recordings and mainly focus on cerebral blood flow while neglecting other important parameters, such as blood volume (BV) and vasomotor activity.Design:Observational study.Participants and Settings:Continuous measures of hemodynamics over the left forehead and biceps were performed using near-infrared spectroscopy (NIRS) during nocturnal polysomnography in 16 healthy participants in sleep laboratory.Measurements and Results:Temporal dynamics and mean values of cerebral and muscular oxygenated hemoglobin (HbO2), deoxygenated hemoglobin (HHb), and BV during different sleep stages were compared. A biphasic change of cerebral BV was observed which contrasted a monotonic increase of muscular BV during non-rapid eye movement sleep. A significant decrement in cerebral HbO2 and BV accompanied by an increase of HHb was recorded at sleep onset (Phase I). Prior to slow wave sleep (SWS) HbO2 and BV turned to increase whereas HHb began to decrease in subsequent Phase II suggested increased brain perfusion during SWS. The cerebral HbO2 slope correlated to BV slope in Phase I and II, but it only correlated to HHb slope in Phase II. The occurrence time of inflection points correlated to SWS latencies.Conclusion:Initial decrease of brain perfusion with decreased blood volume (BV) and oxygenated hemoglobin (HbO2) together with increasing muscular BV fit thermoregulation process at sleep onset. The uncorrelated and correlated slopes of HbO2 and deoxygenated hemoglobin indicate different mechanisms underlying the biphasic hemodynamic process in light sleep and slow wave sleep (SWS). In SWS, changes in vasomotor activity (i.e., increased vasodilatation) may mediate increasing cerebral and muscular BV.
Showing 1 to 10 of 24 Articles
doi: 10.5665/sleep.4886pmid: 26194576
AbstractThe American Academy of Sleep Medicine and Sleep Research Society recently released a Consensus Statement regarding the recommended amount of sleep to promote optimal health in adults. This paper describes the methodology, background literature, voting process, and voting results for the consensus statement. In addition, we address important assumptions and challenges encountered during the consensus process. Finally, we outline future directions that will advance our understanding of sleep need and place sleep duration in the broader context of sleep health.
doi: 10.5665/sleep.4890pmid: 25669183
AbstractStudy Objectives:To investigate the association between sleep disordered breathing (SDB) and severe chronic periodontitis.Design:Cross-sectional data analysis from the Hispanic Community Health Study/Study of Latinos.Setting:Community-based setting with probability sampling from four urban US communities.Participants:12,469 adults aged 18–74 y.Interventions:None.Measurements and Results:Severe chronic periodontitis was defined using the Centers for Disease Control and Prevention/American Academy of Periodontology case classification based on full-mouth periodontal assessments performed by calibrated dentists. SDB was evaluated in standardized home sleep tests, and defined as the number of apnea plus hypopnea events associated with ≥ 3% desaturation, per hour of estimated sleep. SDB was quantified using categories of the apnea-hypopnea index (AHI): 0.0 events (nonapneic); 0.1–4.9 (subclinical); 5.0–14.9 (mild); and ≥ 15 (moderate/severe). Covariates were demographic characteristics and established periodontitis risk factors. C-reactive protein was a potential explanatory variable. Using survey estimation, multivariable binary logistic regression estimated odds ratios (OR) and 95% confidence limits (CL). Following adjustment for confounding, the SDB and periodontitis relationship remained statistically significant, but was attenuated in strength and no longer dose-response. Compared with the nonapneic referent, adjusted odds of severe periodontitis were 40% higher with subclinical SDB (OR = 1.4, 95% CL: 1.0, 1.9), 60% higher with mild SDB (OR = 1.6, 95% CL: 1.1, 2.2) and 50% higher with moderate/severe SDB (OR = 1.5, 95% CL: 1.0, 2.3) demonstrating an independent association between SDB and severe periodontitis.Conclusions:This study identifies a novel association between mild sleep disordered breathing and periodontitis that was most pronounced in young adults.