03943nas a2200397 4500008004100000022001400041245008100055210006900136260001300205300001000218490000700228520285600235653000903091653002203100653001103122653001103133653002003144653000903164653001603173653002603189653001503215653001703230653002603247653002903273100002403302700001903326700001703345700001803362700001703380700001903397700001903416700002303435700002303458710002903481856003503510 2003 eng d a0149-599200aDiabetes and sleep disturbances: findings from the Sleep Heart Health Study.0 aDiabetes and sleep disturbances findings from the Sleep Heart He c2003 Mar a702-90 v263 a
OBJECTIVE: To test the hypothesis that diabetes is independently associated with sleep-disordered breathing (SDB), and in particular that diabetes is associated with sleep abnormalities of a central, rather than obstructive, nature.
RESEARCH DESIGN AND METHODS: Using baseline data from the Sleep Heart Health Study (SHHS), we related diabetes to 1). the respiratory disturbance index (RDI; number of apneas plus hypopneas per h of sleep); 2). obstructive apnea index (OAI; >or=3 apneas/h of sleep associated with obstruction of the upper airway); 3). percent of sleep time < 90% O(2) saturation; 4). central apnea index (CAI; >or=3 apneas [without respiratory effort]/h sleep); 5). occurrence of a periodic breathing (Cheyne Stokes) pattern; and 6) sleep stages. Initial analyses excluding persons with prevalent cardiovascular disease (CVD) were repeated including these participants.
RESULTS: Of the 5874 participants included in this report, 692 (11.8%) reported diabetes or were taking oral hypoglycemic medications or insulin and 1002 had prevalent CVD. Among the 4872 persons without CVD, 470 (9.6%) had diabetes. Diabetic participants had worse CVD risk factor profiles than their nondiabetic counterparts, including higher BMI, waist and neck circumferences, triglycerides, higher prevalence of hypertension, and lower HDL cholesterol (P < 0.001, all). Descriptive analyses indicated differences between diabetic and nondiabetic participants in RDI, sleep stages, sleep time <90% O(2) saturation, CAI, and periodic breathing (P < 0.05, all). However, multivariable regression analyses that adjusted for age, sex, BMI, race, and neck circumference eliminated these differences for all sleep measures except percent time in rapid eye movement (REM) sleep (19.0% among diabetic vs. 20.1% among nondiabetic subjects, P < 0.001) and prevalence of periodic breathing (odds ratio [OR] for diabetic subjects versus nondiabetic subjects 1.80, 95% CI 1.02-3.15). Additionally, adjusted analyses showed diabetes was associated with nonstatistically significant elevations in the odds of an increased central breathing index (OR 1.42, 95% CI 0.80-2.55). Addition to the analysis of the 1002 persons with prevalent CVD (including 222 people with diabetes) did not materially change these results.
CONCLUSIONS: These data suggest that diabetes is associated with periodic breathing, a respiratory abnormality associated with abnormalities in the central control of ventilation. Some sleep disturbances may result from diabetes through the deleterious effects of diabetes on central control of respiration. The high prevalence of SDB in diabetes, although largely explained by obesity and other confounders, suggests the presence of a potentially treatable risk factor for CVD in the diabetic population.
10aAged10aDiabetes Mellitus10aFemale10aHumans10aLogistic Models10aMale10aMiddle Aged10aMultivariate Analysis10aPrevalence10aRisk Factors10aSleep Apnea Syndromes10aSleep Apnea, Obstructive1 aResnick, Helaine, E1 aRedline, Susan1 aShahar, Eyal1 aGilpin, Adele1 aNewman, Anne1 aWalter, Robert1 aEwy, Gordon, A1 aHoward, Barbara, V1 aPunjabi, Naresh, M1 aSleep Heart Health Study uhttps://chs-nhlbi.org/node/72703188nas a2200433 4500008004100000022001400041245010300055210006900158260001600227300000900243490000800252520195400260653000902214653001902223653001102242653002902253653001102282653000902293653001602302653001902318653002002337653002402357653004302381653001002424653002902434653001502463653001902478100002102497700002002518700002702538700001902565700002202584700002002606700002402626700002302650700001702673710002902690856003502719 2003 eng d a1073-449X00aSleep and sleep-disordered breathing in adults with predominantly mild obstructive airway disease.0 aSleep and sleepdisordered breathing in adults with predominantly c2003 Jan 01 a7-140 v1673 aNeither the association between obstructive airways disease (OAD) and sleep apnea-hypopnea (SAH) nor the sleep consequences of each disorder alone and together have been characterized in an adult community setting. Our primary aims were (1) to determine if there is an association between OAD and SAH and (2) identify predictors of oxyhemoglobin desaturation during sleep in persons having OAD with and without SAH. Polysomnography and spirometry results from 5,954 participants in the Sleep Heart Health Study were analyzed. OAD was defined by a FEV1/FVC value less than 70%. Assessment of SAH prevalence in OAD was performed using thresholds of respiratory disturbance index (RDI) greater than 10 and greater than 15. A total of 1,132 participants had OAD that was predominantly mild (FEV1/FVC 63.81 +/- 6.56%, mean +/- SD). SAH was not more prevalent in participants with OAD than in those without OAD (22.32 versus 28.86%, with and without OAD, respectively, at RDI threshold values greater than 10; and 13.97 versus 18.63%, with and without OAD, respectively, at RDI threshold value greater than 15). In the absence of SAH, the adjusted odds ratio for sleep desaturation (> 5% total sleep time with saturation < 90%) was greater than 1.9 when FEV1/FVC was less than 65%. Participants with both OAD and SAH had greater sleep perturbation and desaturation than those with one disorder. Generally mild OAD alone was associated with minimally altered sleep quality. We conclude that (1) there is no association between generally mild OAD and SAH; (2) exclusive of SAH and after adjusting for demographic factors and awake oxyhemoglobin saturation, an FEV1/FVC value less than 65% is associated with increased risk of sleep desaturation; (3) desaturation is greater in persons with both OAD and SAH compared with each of these alone; and (4) individuals with generally mild OAD and without SAH in the community have minimally perturbed sleep.
10aAged10aCohort Studies10aFemale10aForced Expiratory Volume10aHumans10aMale10aMiddle Aged10aOxyhemoglobins10aPolysomnography10aProspective Studies10aPulmonary Disease, Chronic Obstructive10aSleep10aSleep Apnea, Obstructive10aSpirometry10aVital Capacity1 aSanders, Mark, H1 aNewman, Anne, B1 aHaggerty, Catherine, L1 aRedline, Susan1 aLebowitz, Michael1 aSamet, Jonathan1 aO'Connor, George, T1 aPunjabi, Naresh, M1 aShahar, Eyal1 aSleep Heart Health Study uhttps://chs-nhlbi.org/node/71502954nas a2200505 4500008004100000022001400041245010700055210006900162260001600231300001100247490000800258520147700266653000901743653002301752653002201775653002001797653001901817653003901836653002801875653003001903653001201933653001101945653002401956653002701980653001102007653002302018653001802041653000902059653001602068653002602084653001902110653002002129653002002149653001702169653003002186653002602216100002302242700001702265700001902282700002402301700002102325700002402346710004302370856003502413 2004 eng d a0002-926200aSleep-disordered breathing, glucose intolerance, and insulin resistance: the Sleep Heart Health Study.0 aSleepdisordered breathing glucose intolerance and insulin resist c2004 Sep 15 a521-300 v1603 aClinic-based studies suggest that sleep-disordered breathing (SDB) is associated with glucose intolerance and insulin resistance. However, in the available studies, researchers have not rigorously controlled for confounding variables to assess the independent relation between SDB and impaired glucose metabolism. The objective of this study was to determine whether SDB was associated with glucose intolerance and insulin resistance among community-dwelling subjects (n=2,656) participating in the Sleep Heart Health Study (1994-1999). SDB was characterized with the respiratory disturbance index and measurements of oxygen saturation during sleep. Fasting and 2-hour glucose levels measured during an oral glucose tolerance test were used to assess glycemic status. Relative to subjects with a respiratory disturbance index of less than 5.0 events/hour (the reference category), subjects with mild SDB (5.0-14.9 events/hour) and moderate to severe SDB (> or =15 events/hour) had adjusted odds ratios of 1.27 (95% confidence interval: 0.98, 1.64) and 1.46 (95% confidence interval: 1.09, 1.97), respectively, for fasting glucose intolerance (p for trend < 0.01). Sleep-related hypoxemia was also associated with glucose intolerance independently of age, gender, body mass index, and waist circumference. The results of this study suggest that SDB is independently associated with glucose intolerance and insulin resistance and may lead to type 2 diabetes mellitus.
10aAged10aBlood Gas Analysis10aBody Constitution10aBody Mass Index10aCohort Studies10aConfounding Factors, Epidemiologic10aCross-Sectional Studies10aDiabetes Mellitus, Type 210aFasting10aFemale10aGlucose Intolerance10aGlucose Tolerance Test10aHumans10aInsulin Resistance10aLinear Models10aMale10aMiddle Aged10aMultivariate Analysis10aOxyhemoglobins10aPolysomnography10aResearch Design10aRisk Factors10aSeverity of Illness Index10aSleep Apnea Syndromes1 aPunjabi, Naresh, M1 aShahar, Eyal1 aRedline, Susan1 aGottlieb, Daniel, J1 aGivelber, Rachel1 aResnick, Helaine, E1 aSleep Heart Health Study Investigators uhttps://chs-nhlbi.org/node/80003249nas a2200433 4500008004100000022001400041245008500055210006900140260001600209300001000225490000800235520207600243653001602319653000902335653002202344653001802366653002202384653002402406653001102430653002402441653001102465653000902476653001602485653001502501653001502516653002402531653001002555653003102565653001702596653001802613100002402631700002302655700001902678700002402697700001902721700002202740700001802762856003502780 2005 eng d a0003-992600aAssociation of sleep time with diabetes mellitus and impaired glucose tolerance.0 aAssociation of sleep time with diabetes mellitus and impaired gl c2005 Apr 25 a863-70 v1653 aBACKGROUND: Experimental sleep restriction causes impaired glucose tolerance (IGT); however, little is known about the metabolic effects of habitual sleep restriction. We assessed the cross-sectional relation of usual sleep time to diabetes mellitus (DM) and IGT among participants in the Sleep Heart Health Study, a community-based prospective study of the cardiovascular consequences of sleep-disordered breathing.
METHODS: Participants were 722 men and 764 women, aged 53 to 93 years. Usual sleep time was obtained by standardized questionnaire. Diabetes mellitus was defined as a serum glucose level of 126 mg/dL or more (> or =7.0 mmol/L) fasting or 200 mg/dL or more (> or =11.1 mmol/L) 2 hours following standard oral glucose challenge or medication use for DM. Impaired glucose tolerance was defined as a 2-hour postchallenge glucose level of 140 mg/dL or more (> or =7.8 mmol/L) and less than 200 mg/dL. The relation of sleep time to DM and IGT was examined using categorical logistic regression with adjustment for age, sex, race, body habitus, and apnea-hypopnea index.
RESULTS: The median sleep time was 7 hours per night, with 27.1% of subjects sleeping 6 hours or less per night. Compared with those sleeping 7 to 8 hours per night, subjects sleeping 5 hours or less and 6 hours per night had adjusted odds ratios for DM of 2.51 (95% confidence interval, 1.57-4.02) and 1.66 (95% confidence interval, 1.15-2.39), respectively. Adjusted odds ratios for IGT were 1.33 (95% confidence interval, 0.83-2.15) and 1.58 (95% confidence interval, 1.15-2.18), respectively. Subjects sleeping 9 hours or more per night also had increased odds ratios for DM and IGT. These associations persisted when subjects with insomnia symptoms were excluded.
CONCLUSIONS: A sleep duration of 6 hours or less or 9 hours or more is associated with increased prevalence of DM and IGT. Because this effect was present in subjects without insomnia, voluntary sleep restriction may contribute to the large public health burden of DM.
10aAge Factors10aAged10aAged, 80 and over10aBlood Glucose10aDiabetes Mellitus10aDisease Progression10aFemale10aGlucose Intolerance10aHumans10aMale10aMiddle Aged10aOdds Ratio10aPrevalence10aProspective Studies10aSleep10aSurveys and Questionnaires10aTime Factors10aUnited States1 aGottlieb, Daniel, J1 aPunjabi, Naresh, M1 aNewman, Ann, B1 aResnick, Helaine, E1 aRedline, Susan1 aBaldwin, Carol, M1 aNieto, Javier uhttps://chs-nhlbi.org/node/83403456nas a2200445 4500008004100000022001400041245008900055210006900144260001300213300001200226490000700238520224900245653001002494653000902504653002202513653002002535653001902555653001602574653002802590653001102618653001902629653001102648653001702659653000902676653001602685653001502701653002402716653001002740653002902750653002202779653002402801100002402825700001902849700001802868700002202886700002002908700002402928700002302952856003502975 2006 eng d a0161-810500aAssociation of usual sleep duration with hypertension: the Sleep Heart Health Study.0 aAssociation of usual sleep duration with hypertension the Sleep c2006 Aug a1009-140 v293 aSTUDY OBJECTIVES: Limited experimental data suggest that sleep restriction acutely elevates blood pressure; however, little is known about the relationship between usual sleep duration and hypertension. This study assesses the relationship between usual sleep duration and hypertension in a community-based cohort.
DESIGN: Cross-sectional observational study.
SETTING: The Sleep Heart Health Study, a community-based prospective study of the cardiovascular consequences of sleep-disordered breathing.
PARTICIPANTS: Two thousand eight hundred thirteen men and 3097 women, aged 40 to 100 years.
INTERVENTIONS: None.
MEASUREMENTS AND RESULTS: Usual weekday and weekend sleep durations were obtained by questionnaire, and their weighted average were categorized as less than 6, 6 to less than 7, 7 to less than 8, 8 to less than 9, and 9 or more hours per night. Hypertension was defined as a systolic blood pressure of 140 mm Hg or greater, a diastolic blood pressure of 90 mm Hg or greater, or use of medication to treat hypertension. The relationship between sleep duration and hypertension was examined using categorical logistic regression with adjustment for age, sex, race, apnea-hypopnea index, and body mass index. Compared to subjects sleeping 7 to less than 8 hours per night, those sleeping less than 6 and between 6 and 7 hours per night had adjusted odds ratios for hypertension of 1.66 (95% confidence interval 1.35-2.04) and 1.19 (1.02-1.39), respectively, whereas those sleeping between 8 and 9 and 9 or more hours per night had adjusted odds ratios for hypertension of 1.19 (1.04-1.37) and 1.30 (1.04-1.62), respectively (p < .0001 for association of sleep duration with hypertension). These associations persisted when analyses were further adjusted for caffeine and alcohol consumption, current smoking, insomnia symptoms, depression symptoms, sleep efficiency, and prevalent diabetes mellitus or cardiovascular disease.
CONCLUSIONS: Usual sleep duration above or below the median of 7 to less than 8 hours per night is associated with an increased prevalence of hypertension, particularly at the extreme of less than 6 hours per night.
10aAdult10aAged10aAged, 80 and over10aBody Mass Index10aCohort Studies10aComorbidity10aCross-Sectional Studies10aFemale10aHealth Surveys10aHumans10aHypertension10aMale10aMiddle Aged10aOdds Ratio10aProspective Studies10aSleep10aSleep Apnea, Obstructive10aSleep Deprivation10aStatistics as Topic1 aGottlieb, Daniel, J1 aRedline, Susan1 aNieto, Javier1 aBaldwin, Carol, M1 aNewman, Anne, B1 aResnick, Helaine, E1 aPunjabi, Naresh, M uhttps://chs-nhlbi.org/node/91502391nas a2200361 4500008004100000022001400041245005600055210005500111260001600166300001100182490000800193520147400201653000901675653001201684653002801696653001101724653001101735653000901746653001601755653002001771653001501791653002401806653001701830653001701847653002501864653001201889653001801901100001501919700002001934700001701954700002301971856003501994 2006 eng d a0002-926200aCigarette smoking and nocturnal sleep architecture.0 aCigarette smoking and nocturnal sleep architecture c2006 Sep 15 a529-370 v1643 aCigarette smoking has been associated with a high prevalence of sleep-related complaints. However, its effects on sleep architecture have not been fully examined. The primary objective of this investigation was to assess the impact of cigarette smoking on sleep architecture. Polysomnography was used to characterize sleep architecture among 6,400 participants of the Sleep Heart Health Study (United States, 1994-1999). Sleep parameters included total sleep time, latency to sleep onset, sleep efficiency, and percentage of time in each sleep stage. The study sample consisted of 2,916 never smokers, 2,705 former smokers, and 779 current smokers. Compared with never smokers, current smokers had a longer initial sleep latency (5.4 minutes, 95% confidence interval (CI): 2.9, 7.9) and less total sleep time (14.0 minutes, 95% CI: 6.4, 21.7). Furthermore, relative to never smokers, current smokers also had more stage 1 sleep (relative proportion = 1.24, 95% CI: 1.14, 1.33) and less slow wave sleep (relative proportion = 0.86, 95% CI: 0.78, 0.95). Finally, no differences in sleep architecture were noted between former and never smokers. The results of this study show that cigarette smoking is independently associated with disturbances in sleep architecture, including a longer latency to sleep onset and a shift toward lighter stages of sleep. Nicotine in cigarette smoke and acute withdrawal from it may contribute to disturbances in sleep architecture.
10aAged10aArousal10aChi-Square Distribution10aFemale10aHumans10aMale10aMiddle Aged10aPolysomnography10aPrevalence10aRegression Analysis10aRisk Factors10aSleep Stages10aSleep Wake Disorders10aSmoking10aUnited States1 aZhang, Lin1 aSamet, Jonathan1 aCaffo, Brian1 aPunjabi, Naresh, M uhttps://chs-nhlbi.org/node/90402915nas a2200421 4500008004100000022001400041245014000055210006900195260001300264300001100277490000700288520167100295653001901966653002001985653002802005653002502033653002802058653002202086653001102108653001102119653002802130653000902158653001602167653001502183653001902198653003002217653002602247100001902273700002102292700001902313700002102332700002002353700002302373700001902396700002302415700002002438856003502458 2006 eng d a1046-667300aSleep apnea in patients on conventional thrice-weekly hemodialysis: comparison with matched controls from the Sleep Heart Health Study.0 aSleep apnea in patients on conventional thriceweekly hemodialysi c2006 Dec a3503-90 v173 aSleep-disordered breathing (SDB) has been noted commonly in hemodialysis (HD) patients, but it is not known whether this is related directly to the treatment of kidney failure with HD or to the higher prevalence of obesity and older age. Forty-six HD patients were compared with 137 participants from the Sleep Heart Health Study (SHHS) who were matched for age, gender, body mass index (BMI), and race. Home unattended polysomnography was performed and scored using similar protocols. The study sample was 62.7 +/- 10.1 yr, was predominantly male (72%) and white (63%), and had an average BMI of 28 +/- 5.3 kg/m(2). The HD sample had a higher systolic BP (137 versus 121 mmHg; P < 0.01) and a higher prevalence of diabetes (33 versus 9%; P < 0.01) and cardiovascular disease (33 versus 13%; P < 0.01) compared with the SHHS sample. The HD group had significantly less sleep time (320 versus 379 min; P < 0.0001) but similar sleep efficiency. HD patients had a higher frequency of arousals per hour (25.1 versus 17.1; P < 0.0001) and apnea-hypopneas per hour (27.2 versus 15.2; P < 0.0001) and greater percentage of the total sleep time below an oxygen saturation of 90% (7.2 versus 1.8; P < 0.0001). HD patients were more likely to have severe SDB (>30 respiratory events per hour) compared with the SHHS sample (odds ratio 4.07; 95% confidence interval 1.83 to 9.07). There was a strong association of HD with severe SDB and nocturnal hypoxemia independent of age, BMI, and the higher prevalence of chronic disease. The potential mechanisms for the higher likelihood of SDB in the HD population must be identified to provide specific prevention and therapy.
10aBlood Pressure10aBody Mass Index10aCardiovascular Diseases10aCase-Control Studies10aCross-Sectional Studies10aDiabetes Mellitus10aFemale10aHumans10aKidney Failure, Chronic10aMale10aMiddle Aged10aPrevalence10aRenal Dialysis10aSeverity of Illness Index10aSleep Apnea Syndromes1 aUnruh, Mark, L1 aSanders, Mark, H1 aRedline, Susan1 aPiraino, Beth, M1 aUmans, Jason, G1 aHammond, Terese, C1 aSharief, Imran1 aPunjabi, Naresh, M1 aNewman, Anne, B uhttps://chs-nhlbi.org/node/92603455nas a2200421 4500008004100000022001400041245010600055210006900161260001300230300001200243490000700255520228800262653000902550653001802559653002002577653001902597653002802616653003002644653001202674653001102686653001102697653000902708653001602717653001502733653001102748653001902759653002002778653002102798653002902819100002602848700002102874700001702895700002402912700002102936700001702957700002302974856003602997 2008 eng d a0161-810500aFasting glycemia in sleep disordered breathing: lowering the threshold on oxyhemoglobin desaturation.0 aFasting glycemia in sleep disordered breathing lowering the thre c2008 Jul a1018-240 v313 aSTUDY OBJECTIVES: Commonly used definitions of sleep-disordered breathing (SDB) are based on identifying discrete events of breathing abnormalities during sleep that are accompanied by an oxyhemoglobin desaturation (delta SaO2) of at least 4%. However, it is not known whether disordered breathing events with oxyhemoglobin desaturation less than 4% are associated with clinical sequelae such as abnormalities in fasting glycemia.
DESIGN: Cross-sectional study.
SUBJECTS AND SETTING: Participants from the Sleep Heart Health Study (SHHS) with a fasting glucose measurement made within a year of the baseline polysomnogram.
MEASUREMENTS AND RESULTS: SDB severity was defined using the apnea-hypopnea index (AHI) and the hypopnea index (HI) by counting events with different levels of oxyhemoglobin desaturation (0.0%-1.9%, 2.0%-2.9%, 3.0%-3.9%, > or = 4.0%). Fasting glucose levels were used to classify individuals into normal (<100 mg/dL), impaired (100-125 mg/dL), and diabetic (> or = 126 mg/dL) groups. Ordinal logistic regression was used to determine the adjusted relative odds of an abnormal glucose value across quartiles of the hypopnea index, independent of factors such as age, body mass index, waist circumference, and usual sleep duration. The prevalence of impaired and diabetic fasting glucose in the analytical sample was 32.9% and 5.8%, respectively. The covariate-adjusted relative odds of impaired or diabetic fasting glucose in the highest versus the lowest AHI quartile was 1.35 (95% CI: 1.04-1.76) for events with a delta SaO2 > or = 4.0%, 1.72 (95% CI: 1.20-2.48) for events with a delta SaO2 between 3.0%-3.9%, 1.41 (95% CI: 1.07-1.86) for events with a delta SaO2 between 2.0%-2.9%, and 1.07 (95% CI: 0.84-1.37) for events with a delta SaO2 between 0.0%-1.9%. The corresponding odds ratios for the HI were 1.47 (95% CI: 1.13-1.92), 2.25 (95% CI: 1.59-3.19), 1.44 (95% CI: 1.09-1.90), and 1.15 (95% CI: 0.90-1.47), respectively.
CONCLUSIONS: The results of this study indicate that SDB events accompanied by oxyhemoglobin desaturation of between 2% to 4% are associated with fasting hyperglycemia. These findings suggest that milder degrees of SDB may predispose to adverse metabolic outcomes.
10aAged10aBlood Glucose10aBody Mass Index10aCohort Studies10aCross-Sectional Studies10aDiabetes Mellitus, Type 210aFasting10aFemale10aHumans10aMale10aMiddle Aged10aOdds Ratio10aOxygen10aOxyhemoglobins10aPolysomnography10aReference Values10aSleep Apnea, Obstructive1 aStamatakis, Katherine1 aSanders, Mark, H1 aCaffo, Brian1 aResnick, Helaine, E1 aGottlieb, Dan, J1 aMehra, Reena1 aPunjabi, Naresh, M uhttps://chs-nhlbi.org/node/104302728nas a2200313 4500008004100000022001400041245007900055210006900134260001300203300001100216490000800227520186900235653002702104653001102131653001102142653002002153653000902173653001602182653002002198653001002218653001202228653004502240100001502285700002002300700001702320700001902337700002302356856003502379 2008 eng d a0012-369200aPower spectral analysis of EEG activity during sleep in cigarette smokers.0 aPower spectral analysis of EEG activity during sleep in cigarett c2008 Feb a427-320 v1333 aBACKGROUND: Research on the effects of cigarette smoking on sleep architecture is limited. The objective of this investigation was to examine differences in sleep EEG between smokers and nonsmokers.
METHODS: Smokers and nonsmokers who were free of all medical comorbidities were matched on different factors, including age, gender, race, body mass index, and anthropometric measures. Home polysomnography was conducted using a standard recording montage. Sleep architecture was assessed using visual sleep-stage scoring. The discrete fast Fourier transform was used to calculate the EEG power spectrum for the entire night within contiguous 30-s epochs of sleep for the following frequency bandwidths: delta (0.8 to 4.0 Hz); theta (4.1 to 8.0 Hz); alpha (8.1 to 13.0 Hz); and beta (13.1 to 20.0 Hz).
RESULTS: Conventional sleep stages were similar between the two groups. However, spectral analysis of the sleep EEG showed that, compared to nonsmokers, smokers had a lower percentage of EEG power in the delta-bandwidth (59.7% vs 62.6%, respectively; p < 0.04) and higher percentage of EEG power in alpha-bandwidth (15.6% vs 12.5%, respectively; p < 0.001). Differences in the EEG power spectrum between smokers and nonsmokers were greatest in the early part of the sleep period and decreased toward the end. Subjective complaints of lack of restful sleep were also more prevalent in smokers than in nonsmokers (22.5% vs 5.0%, respectively; p < 0.02) and were explained, in part, by the differences in EEG spectral power.
CONCLUSIONS: Cigarette smokers manifest disturbances in the sleep EEG that are not evident in conventional measures of sleep architecture. Nicotine in cigarette smoke and withdrawal from it during sleep may contribute to these changes and the subjective experience of nonrestorative sleep.
10aElectroencephalography10aFemale10aHumans10aLogistic Models10aMale10aMiddle Aged10aPolysomnography10aSleep10aSmoking10aSpectroscopy, Fourier Transform Infrared1 aZhang, Lin1 aSamet, Jonathan1 aCaffo, Brian1 aBankman, Isaac1 aPunjabi, Naresh, M uhttps://chs-nhlbi.org/node/99302453nas a2200337 4500008004100000022001400041245008900055210006900144260001300213300001100226490000800237520153300245653000901778653002101787653002801808653001101836653001101847653000901858653001601867653001501883653001701898653002601915653001801941653001701959653002001976100002701996700001702023700002302040700001702063856003502080 2008 eng d a1879-148400aRelation of sleep-disordered breathing to carotid plaque and intima-media thickness.0 aRelation of sleepdisordered breathing to carotid plaque and inti c2008 Mar a125-310 v1973 aBACKGROUND: Sleep-disordered breathing (SDB) is associated with clinical cardiovascular disease (CVD), but its relation to subclinical atherosclerosis remains to be determined.
METHODS: We analyzed the cross-sectional associations of SDB, measured by the respiratory disturbance index (RDI), a hypoxemia index, and an arousal index, with carotid plaque and carotid intima-media thickness (IMT), measured by ultrasound. The sample included 985 participants in the Sleep Heart Health Study (mean age-62, median RDI-8.7) with no history of coronary heart disease and stroke, of whom 396 had evidence of a carotid plaque.
RESULTS: As compared with the first quartile of the RDI (0-1.2), the crude odds ratio for carotid plaque was 1.14, 1.27, and 1.48 for the second (1.3-4.1), third (4.2-10.7), and fourth (>10.7) quartile, respectively. After adjustment for CVD risk factors, the corresponding odds ratios were reduced (1.00, 1.04, 1.07, and 1.25). Similarly, the unadjusted mean carotid IMT increased with RDI, but adjusted means (mm) were similar (0.84, 0.85, 0.84, 0.85). Spline regression models did not show monotonicity of the dose-response functions at the right end of the RDI distribution. Neither the hypoxemia index nor the arousal index was associated with carotid plaque or carotid IMT.
CONCLUSION: The results of this study suggest that crude, positive associations between SDB and subclinical atherosclerosis can be attributed to confounding by CVD risk factors.
10aAged10aCarotid Arteries10aCarotid Artery Diseases10aFemale10aHumans10aMale10aMiddle Aged10aOdds Ratio10aRisk Factors10aSleep Apnea Syndromes10aTunica Intima10aTunica Media10aUltrasonography1 aWattanakit, Keattiyoat1 aBoland, Lori1 aPunjabi, Naresh, M1 aShahar, Eyal uhttps://chs-nhlbi.org/node/95703134nas a2200349 4500008004100000022001400041245010100055210006900156260001600225300001100241490000800252520216200260653000902422653001002431653002802441653001902469653001102488653001102499653000902510653001602519653001502535653001902550653002002569653002602589653002502615100002302640700002002663700002002683700002402703700002102727856003602748 2008 eng d a1535-497000aSleep-disordered breathing and cardiovascular disease: an outcome-based definition of hypopneas.0 aSleepdisordered breathing and cardiovascular disease an outcomeb c2008 May 15 a1150-50 v1773 aRATIONALE: Epidemiologic studies on the consequences of sleep-disordered breathing invariably use the apnea-hypopnea index as the primary measure of disease severity. Although hypopneas constitute a majority of disordered breathing events, significant controversy remains about the best criteria used to define these events.
OBJECTIVES: The current investigation sought to assess the most appropriate definition for hypopneas that would be best correlated with cardiovascular disease.
METHODS: A community sample of middle-aged and older adults was recruited as part of the Sleep Heart Health Study. Full-montage polysomnography was conducted and hypopneas were defined using different thresholds of oxyhemoglobin desaturation with and without arousals. Prevalent cardiovascular disease was assessed based on self-report. Logistic regression analysis was used to characterize the independent association between the hypopnea index and prevalent cardiovascular disease.
MEASUREMENTS AND MAIN RESULTS: Using a sample of 6,106 adults with complete data on cardiovascular disease status and polysomnography, the current study found that hypopneas associated with an oxyhemoglobin desaturation of 4% or more were associated with prevalent cardiovascular disease independent of confounding covariates. The adjusted prevalent odds ratios for quartiles of the hypopnea index using a 4% desaturation criterion were as follows: 1.00 (<1.10 events/h), 1.10 (1.01-3.20 events/h), 1.33 (3.21-7.69 events/h), and 1.41 (>7.69 events/h). Hypopnea measures based on less than 4% oxyhemoglobin desaturation or presence of arousals showed no association with cardiovascular disease.
CONCLUSIONS: Hypopneas comprise a significant component of sleep-disordered breathing in the general community. By varying the criteria for defining hypopneas, this study demonstrates that hypopneas with a desaturation of at least 4% are independently associated with cardiovascular disease. In contrast, no association was observed between cardiovascular disease and hypopneas associated with milder desaturations or arousals.
10aAged10aApnea10aCardiovascular Diseases10aCohort Studies10aFemale10aHumans10aMale10aMiddle Aged10aOdds Ratio10aOxyhemoglobins10aPolysomnography10aSleep Apnea Syndromes10aTerminology as Topic1 aPunjabi, Naresh, M1 aNewman, Anne, B1 aYoung, Terry, B1 aResnick, Helaine, E1 aSanders, Mark, H uhttps://chs-nhlbi.org/node/101802979nas a2200433 4500008004100000022001400041245014400055210006900199260001300268300001100281490000700292520172800299653000902027653002202036653001602058653002802074653002802102653001102130653002402141653002702165653001102192653000902203653001602212653001202228653001502240653002002255653002102275653002502296100002202321700002102343700002402364700002302388700002102411700001802432700002102450700001902471700001902490856003602509 2008 eng d a1935-554800aSleep-disordered breathing and impaired glucose metabolism in normal-weight and overweight/obese individuals: the Sleep Heart Health Study.0 aSleepdisordered breathing and impaired glucose metabolism in nor c2008 May a1001-60 v313 aOBJECTIVE: To characterize the association between sleep-disordered breathing (SDB) and impaired fasting glucose (IFG), impaired glucose tolerance (IGT), combined IFG and IGT, and occult diabetes in individuals of different body habitus.
RESEARCH DESIGN AND METHODS: Cross-sectional analysis of 2,588 participants (aged 52-96 years; 46% men) without known diabetes. SDB was defined as respiratory disturbance index >or=10 events/h. IFG, IGT, occult diabetes, and body weight were classified according to recent accepted guidelines. Participants with and without SDB were compared on prevalence and odds ratios for measures of impaired glucose metabolism (IGM), adjusting for age, sex, race, BMI, and waist circumference.
RESULTS: SDB was observed in 209 nonoverweight and 1,036 overweight/obese participants. SDB groups had significantly higher adjusted prevalence and adjusted odds of IFG, IFG plus IGT, and occult diabetes. The adjusted odds ratio for all subjects was 1.3 (95% CI 1.1-1.6) for IFG, 1.2 (1.0-1.4) for IGT, 1.4 (1.1-2.7) for IFG plus IGT, and 1.7 (1.1-2.7) for occult diabetes.
CONCLUSIONS: SDB was associated with occult diabetes, IFG, and IFG plus IGT, after adjusting for age, sex, race, BMI, and waist circumference. The magnitude of these associations was similar in nonoverweight and overweight participants. The consistency of associations across all measures of IGM and body habitus groups and the significant association between SDB and IFG plus IGT, a risk factor for rapid progression to diabetes, cardiovascular disease, and mortality, suggests the importance of SDB as a risk factor for clinically important levels of metabolic dysfunction.
10aAged10aAged, 80 and over10aBody Weight10aCardiovascular Diseases10aCross-Sectional Studies10aFemale10aGlucose Intolerance10aGlucose Tolerance Test10aHumans10aMale10aMiddle Aged10aObesity10aOverweight10aPolysomnography10aReference Values10aSleep Wake Disorders1 aSeicean, Sinziana1 aKirchner, Lester1 aGottlieb, Daniel, J1 aPunjabi, Naresh, M1 aResnick, Helaine1 aSanders, Mark1 aBudhiraja, Rohit1 aSinger, Mendel1 aRedline, Susan uhttps://chs-nhlbi.org/node/101603469nas a2200541 4500008004100000022001400041245016700055210006900222260001300291300001100304490000700315520191400322653000902236653002202245653002002267653002802287653002402315653001102339653002202350653001502372653001102387653001402398653002802412653000902440653001602449653001502465653001702480653002002497653001402517653001902531653002602550653001702576653003002593653001002623653002602633653003102659100001902690700002102709700001902730700002102749700002002770700001802790700002102808700002302829700001902852700002002871856003602891 2008 eng d a1523-683800aSubjective and objective sleep quality in patients on conventional thrice-weekly hemodialysis: comparison with matched controls from the sleep heart health study.0 aSubjective and objective sleep quality in patients on convention c2008 Aug a305-130 v523 aBACKGROUND: Studies examining sleep in the hemodialysis (HD) population have largely lacked an adequate comparison group. It therefore is uncertain whether poor sleep quality in the HD population reflects age, chronic health conditions, or effects of conventional HD therapy.
STUDY DESIGN: Cross-sectional matched-group study.
SETTING & PARTICIPANTS: Forty-six in-center HD patients were compared with 137 community participants participating in the Sleep Heart Health Study matched for age, sex, body mass index, and race.
PREDICTOR: HD patients compared with community-dwelling non-HD participants.
OUTCOMES & MEASUREMENTS: Home unattended polysomnography was performed and scored by using similar protocols. Sleep habits and sleepiness were assessed by using the Sleep Habits Questionnaire and Epworth Sleepiness Scale.
RESULTS: Average age of study samples was 63 years, 72% were white, and average body mass index was 28 +/- 5 kg/m(2). HD patients were significantly more likely than community participants to have short sleep (odds ratio, 3.27; 95% confidence interval, 1.16 to 9.25) and decreased sleep efficiency (odds ratio, 5.5; 95% confidence interval, 1.5 to 19.6). HD patients reported more difficulty getting back to sleep (odds ratio, 2.25; 95% confidence interval, 1.11 to 4.60) and waking up too early (odds ratio, 2.39; 95% confidence interval, 1.01 to 5.66). There was no association between polysomnography sleep time and self-reported sleep time (r = 0.09; P = 0.6) or between the Epworth Sleepiness Scale and severity of sleep apnea (r = 0.10; P = 0.5) in the HD population.
LIMITATIONS: The study was limited to participants older than 45 years.
CONCLUSIONS: Kidney failure treated with thrice-weekly HD is significantly associated with poor subjective and objective sleep quality.
10aAged10aAged, 80 and over10aBody Mass Index10aCross-Sectional Studies10aDisease Progression10aFemale10aFollow-Up Studies10aHeart Rate10aHumans10aIncidence10aKidney Failure, Chronic10aMale10aMiddle Aged10aOdds Ratio10aPennsylvania10aPolysomnography10aPrognosis10aRenal Dialysis10aRetrospective Studies10aRisk Factors10aSeverity of Illness Index10aSleep10aSleep Apnea Syndromes10aSurveys and Questionnaires1 aUnruh, Mark, L1 aSanders, Mark, H1 aRedline, Susan1 aPiraino, Beth, M1 aUmans, Jason, G1 aChami, Hassan1 aBudhiraja, Rohit1 aPunjabi, Naresh, M1 aBuysse, Daniel1 aNewman, Anne, B uhttps://chs-nhlbi.org/node/104103483nas a2200457 4500008004100000022001400041245007400055210006900129260001300198300001300211490000600224520223200230653000902462653002802471653001102499653001102510653001202521653000902533653001602542653001502558653003202573653002402605653001702629653001602646653002602662653002202688100002302710700002002733700002202753700002402775700002002799700002402819700002302843700001902866700002402885700002102909700001702930700001902947700002302966856003602989 2009 eng d a1549-167600aSleep-disordered breathing and mortality: a prospective cohort study.0 aSleepdisordered breathing and mortality a prospective cohort stu c2009 Aug ae10001320 v63 aBACKGROUND: Sleep-disordered breathing is a common condition associated with adverse health outcomes including hypertension and cardiovascular disease. The overall objective of this study was to determine whether sleep-disordered breathing and its sequelae of intermittent hypoxemia and recurrent arousals are associated with mortality in a community sample of adults aged 40 years or older.
METHODS AND FINDINGS: We prospectively examined whether sleep-disordered breathing was associated with an increased risk of death from any cause in 6,441 men and women participating in the Sleep Heart Health Study. Sleep-disordered breathing was assessed with the apnea-hypopnea index (AHI) based on an in-home polysomnogram. Survival analysis and proportional hazards regression models were used to calculate hazard ratios for mortality after adjusting for age, sex, race, smoking status, body mass index, and prevalent medical conditions. The average follow-up period for the cohort was 8.2 y during which 1,047 participants (587 men and 460 women) died. Compared to those without sleep-disordered breathing (AHI: <5 events/h), the fully adjusted hazard ratios for all-cause mortality in those with mild (AHI: 5.0-14.9 events/h), moderate (AHI: 15.0-29.9 events/h), and severe (AHI: >or=30.0 events/h) sleep-disordered breathing were 0.93 (95% CI: 0.80-1.08), 1.17 (95% CI: 0.97-1.42), and 1.46 (95% CI: 1.14-1.86), respectively. Stratified analyses by sex and age showed that the increased risk of death associated with severe sleep-disordered breathing was statistically significant in men aged 40-70 y (hazard ratio: 2.09; 95% CI: 1.31-3.33). Measures of sleep-related intermittent hypoxemia, but not sleep fragmentation, were independently associated with all-cause mortality. Coronary artery disease-related mortality associated with sleep-disordered breathing showed a pattern of association similar to all-cause mortality.
CONCLUSIONS: Sleep-disordered breathing is associated with all-cause mortality and specifically that due to coronary artery disease, particularly in men aged 40-70 y with severe sleep-disordered breathing. Please see later in the article for the Editors' Summary.
10aAged10aCoronary Artery Disease10aFemale10aHumans10aHypoxia10aMale10aMiddle Aged10aOdds Ratio10aProportional Hazards Models10aProspective Studies10aRisk Factors10aSex Factors10aSleep Apnea Syndromes10aSurvival Analysis1 aPunjabi, Naresh, M1 aCaffo, Brian, S1 aGoodwin, James, L1 aGottlieb, Daniel, J1 aNewman, Anne, B1 aO'Connor, George, T1 aRapoport, David, M1 aRedline, Susan1 aResnick, Helaine, E1 aRobbins, John, A1 aShahar, Eyal1 aUnruh, Mark, L1 aSamet, Jonathan, M uhttps://chs-nhlbi.org/node/112202822nas a2200637 4500008004100000022001400041245011200055210006900167260001300236300001000249490000700259520095900266653002301225653001101248653002901259653003801288653001801326653003401344653001101378653000901389653001801398653000901416653002701425653003601452653001501488653001901503100002101522700002201543700001901565700002001584700002001604700002601624700002301650700003001673700001901703700001701722700002501739700002101764700002201785700002001807700002301827700002201850700002801872700001901900700002301919700002601942700002401968700002101992700001902013700002302032700001902055700002502074700002402099700002502123856003602148 2010 eng d a1546-171800aMeta-analyses of genome-wide association studies identify multiple loci associated with pulmonary function.0 aMetaanalyses of genomewide association studies identify multiple c2010 Jan a45-520 v423 aSpirometric measures of lung function are heritable traits that reflect respiratory health and predict morbidity and mortality. We meta-analyzed genome-wide association studies for two clinically important lung-function measures: forced expiratory volume in the first second (FEV(1)) and its ratio to forced vital capacity (FEV(1)/FVC), an indicator of airflow obstruction. This meta-analysis included 20,890 participants of European ancestry from four CHARGE Consortium studies: Atherosclerosis Risk in Communities, Cardiovascular Health Study, Framingham Heart Study and Rotterdam Study. We identified eight loci associated with FEV(1)/FVC (HHIP, GPR126, ADAM19, AGER-PPT2, FAM13A, PTCH1, PID1 and HTR4) and one locus associated with FEV(1) (INTS12-GSTCD-NPNT) at or near genome-wide significance (P < 5 x 10(-8)) in the CHARGE Consortium dataset. Our findings may offer insights into pulmonary function and pathogenesis of chronic lung disease.
10aDatabases, Genetic10aFemale10aForced Expiratory Volume10aGenetic Predisposition to Disease10aGenome, Human10aGenome-Wide Association Study10aHumans10aLung10aLung Diseases10aMale10aMeta-Analysis as Topic10aPolymorphism, Single Nucleotide10aSpirometry10aVital Capacity1 aHancock, Dana, B1 aEijgelsheim, Mark1 aWilk, Jemma, B1 aGharib, Sina, A1 aLoehr, Laura, R1 aMarciante, Kristin, D1 aFranceschini, Nora1 avan Durme, Yannick, M T A1 aChen, Ting-Hsu1 aBarr, Graham1 aSchabath, Matthew, B1 aCouper, David, J1 aBrusselle, Guy, G1 aPsaty, Bruce, M1 aDuijn, Cornelia, M1 aRotter, Jerome, I1 aUitterlinden, André, G1 aHofman, Albert1 aPunjabi, Naresh, M1 aRivadeneira, Fernando1 aMorrison, Alanna, C1 aEnright, Paul, L1 aNorth, Kari, E1 aHeckbert, Susan, R1 aLumley, Thomas1 aStricker, Bruno, H C1 aO'Connor, George, T1 aLondon, Stephanie, J uhttps://chs-nhlbi.org/node/115002243nas a2200361 4500008004100000022001400041245014200055210006900197260001300266300001100279490000700290520121600297653001601513653000901529653001501538653002001553653001901573653001101592653001101603653000901614653001601623653003001639653001701669653001401686653002601700653001201726653002401738100001701762700002301779700002301802700002001825856003601845 2010 eng d a0161-810500aA novel approach to prediction of mild obstructive sleep disordered breathing in a population-based sample: the Sleep Heart Health Study.0 anovel approach to prediction of mild obstructive sleep disordere c2010 Dec a1641-80 v333 aThis manuscript considers a data-mining approach for the prediction of mild obstructive sleep disordered breathing, defined as an elevated respiratory disturbance index (RDI), in 5,530 participants in a community-based study, the Sleep Heart Health Study. The prediction algorithm was built using modern ensemble learning algorithms, boosting in specific, which allowed for assessing potential high-dimensional interactions between predictor variables or classifiers. To evaluate the performance of the algorithm, the data were split into training and validation sets for varying thresholds for predicting the probability of a high RDI (≥7 events per hour in the given results). Based on a moderate classification threshold from the boosting algorithm, the estimated post-test odds of a high RDI were 2.20 times higher than the pre-test odds given a positive test, while the corresponding post-test odds were decreased by 52% given a negative test (sensitivity and specificity of 0.66 and 0.70, respectively). In rank order, the following variables had the largest impact on prediction performance: neck circumference, body mass index, age, snoring frequency, waist circumference, and snoring loudness.
10aAge Factors10aAged10aAlgorithms10aBody Mass Index10aCohort Studies10aFemale10aHumans10aMale10aMiddle Aged10aPredictive Value of Tests10aRisk Factors10aROC Curve10aSleep Apnea Syndromes10aSnoring10aWaist Circumference1 aCaffo, Brian1 aDiener-West, Marie1 aPunjabi, Naresh, M1 aSamet, Jonathan uhttps://chs-nhlbi.org/node/125202992nas a2200445 4500008004100000022001400041245008800055210006900143260001600212300001100228490000800239520174000247653000901987653001101996653001102007653002502018653000902043653001602052653002002068653003202088653002402120653003002144653001602174653002902190653001102219100001902230700002102249700002402270700001702294700002402311700002402335700002302359700002102382700002002403700002502423700001702448700002202465700002302487856003602510 2010 eng d a1535-497000aObstructive sleep apnea-hypopnea and incident stroke: the sleep heart health study.0 aObstructive sleep apneahypopnea and incident stroke the sleep he c2010 Jul 15 a269-770 v1823 aRATIONALE: Although obstructive sleep apnea is associated with physiological perturbations that increase risk of hypertension and are proatherogenic, it is uncertain whether sleep apnea is associated with increased stroke risk in the general population.
OBJECTIVES: To quantify the incidence of ischemic stroke with sleep apnea in a community-based sample of men and women across a wide range of sleep apnea.
METHODS: Baseline polysomnography was performed between 1995 and 1998 in a longitudinal cohort study. The primary exposure was the obstructive apnea-hypopnea index (OAHI) and outcome was incident ischemic stroke.
MEASUREMENTS AND MAIN RESULTS: A total of 5,422 participants without a history of stroke at the baseline examination and untreated for sleep apnea were followed for a median of 8.7 years. One hundred ninety-three ischemic strokes were observed. In covariate-adjusted Cox proportional hazard models, a significant positive association between ischemic stroke and OAHI was observed in men (P value for linear trend: P = 0.016). Men in the highest OAHI quartile (>19) had an adjusted hazard ratio of 2.86 (95% confidence interval, 1.1-7.4). In the mild to moderate range (OAHI, 5-25), each one-unit increase in OAHI in men was estimated to increase stroke risk by 6% (95% confidence interval, 2-10%). In women, stroke was not significantly associated with OAHI quartiles, but increased risk was observed at an OAHI greater than 25.
CONCLUSIONS: The strong adjusted association between ischemic stroke and OAHI in community-dwelling men with mild to moderate sleep apnea suggests that this is an appropriate target for future stroke prevention trials.
10aAged10aFemale10aHumans10aLongitudinal Studies10aMale10aMiddle Aged10aPolysomnography10aProportional Hazards Models10aProspective Studies10aSeverity of Illness Index10aSex Factors10aSleep Apnea, Obstructive10aStroke1 aRedline, Susan1 aYenokyan, Gayane1 aGottlieb, Daniel, J1 aShahar, Eyal1 aO'Connor, George, T1 aResnick, Helaine, E1 aDiener-West, Marie1 aSanders, Mark, H1 aWolf, Philip, A1 aGeraghty, Estella, M1 aAli, Tauqeer1 aLebowitz, Michael1 aPunjabi, Naresh, M uhttps://chs-nhlbi.org/node/118102972nas a2200433 4500008004100000022001400041245013400055210006900189260001600258300001100274490000800285520171800293653001002011653000902021653002102030653001102051653001802062653001102080653002502091653000902116653001602125653002002141653003202161653002402193653002902217653002202246100002402268700002102292700002002313700002402333700002302357700002002380700001902400700002402419700001902443700002302462700001702485856003602502 2010 eng d a1524-453900aProspective study of obstructive sleep apnea and incident coronary heart disease and heart failure: the sleep heart health study.0 aProspective study of obstructive sleep apnea and incident corona c2010 Jul 27 a352-600 v1223 aBACKGROUND: Clinic-based observational studies in men have reported that obstructive sleep apnea is associated with an increased incidence of coronary heart disease. The objective of this study was to assess the relation of obstructive sleep apnea to incident coronary heart disease and heart failure in a general community sample of adult men and women.
METHODS AND RESULTS: A total of 1927 men and 2495 women > or =40 years of age and free of coronary heart disease and heart failure at the time of baseline polysomnography were followed up for a median of 8.7 years in this prospective longitudinal epidemiological study. After adjustment for multiple risk factors, obstructive sleep apnea was a significant predictor of incident coronary heart disease (myocardial infarction, revascularization procedure, or coronary heart disease death) only in men < or =70 years of age (adjusted hazard ratio 1.10 [95% confidence interval 1.00 to 1.21] per 10-unit increase in apnea-hypopnea index [AHI]) but not in older men or in women of any age. Among men 40 to 70 years old, those with AHI > or =30 were 68% more likely to develop coronary heart disease than those with AHI <5. Obstructive sleep apnea predicted incident heart failure in men but not in women (adjusted hazard ratio 1.13 [95% confidence interval 1.02 to 1.26] per 10-unit increase in AHI). Men with AHI > or =30 were 58% more likely to develop heart failure than those with AHI <5.
CONCLUSIONS: Obstructive sleep apnea is associated with an increased risk of incident heart failure in community-dwelling middle-aged and older men; its association with incident coronary heart disease in this sample is equivocal.
10aAdult10aAged10aCoronary Disease10aFemale10aHeart Failure10aHumans10aLongitudinal Studies10aMale10aMiddle Aged10aPolysomnography10aProportional Hazards Models10aProspective Studies10aSleep Apnea, Obstructive10aSurvival Analysis1 aGottlieb, Daniel, J1 aYenokyan, Gayane1 aNewman, Anne, B1 aO'Connor, George, T1 aPunjabi, Naresh, M1 aQuan, Stuart, F1 aRedline, Susan1 aResnick, Helaine, E1 aTong, Elisa, K1 aDiener-West, Marie1 aShahar, Eyal uhttps://chs-nhlbi.org/node/121502828nas a2200349 4500008004100000022001400041245010500055210006900160260001600229300001300245490000800258520184300266653000902109653003802118653001102156653001102167653000902178653001602187653002002203653002002223653001002243653002602253653001502279100002102294700002202315700002202337700001602359700002002375700002302395700002402418856003602442 2010 eng d a1535-497000aSleepiness, quality of life, and sleep maintenance in REM versus non-REM sleep-disordered breathing.0 aSleepiness quality of life and sleep maintenance in REM versus n c2010 May 01 a997-10020 v1813 aRATIONALE: The impact of REM-predominant sleep-disordered breathing (SDB) on sleepiness, quality of life (QOL), and sleep maintenance is uncertain.
OBJECTIVE: To evaluate the association of SDB during REM sleep with daytime sleepiness, health-related QOL, and difficulty maintaining sleep, in comparison to their association with SDB during non-REM sleep in a community-based cohort.
METHODS: Cross-sectional analysis of 5,649 Sleep Heart Health Study participants (mean age 62.5 [SD = 10.9], 52.6% women, 22.6% ethnic minorities). SDB during REM and non-REM sleep was quantified using polysomnographically derived apnea-hypopnea index in REM (AHI(REM)) and non-REM (AHI(NREM)) sleep. Sleepiness, sleep maintenance, and QOL were respectively quantified using the Epworth Sleepiness Scale (ESS), the Sleep Heart Health Study Sleep Habit Questionnaire, and the physical and mental composites scales of the Medical Outcomes Study Short Form (SF)-36.
MEASUREMENTS AND MAIN RESULTS: AHI(REM) was not associated with the ESS scores or the physical and mental components scales scores of the SF-36 after adjusting for demographics, body mass index, and AHI(NREM) x AHI(REM) was not associated with frequent difficulty maintaining sleep or early awakening from sleep. AHI(NREM) was associated with the ESS score (beta = 0.25; 95% confidence interval [CI], 0.16 to 0.34) and the physical (beta = -0.12; 95% CI, -0.42 to -0.01) and mental (beta = -0.20; 95% CI, -0.20 to -0.01) components scores of the SF-36 adjusting for demographics, body mass index, and AHI(REM).
CONCLUSIONS: In a community-based sample of middle-aged and older adults, REM-predominant SDB is not independently associated with daytime sleepiness, impaired health-related QOL, or self-reported sleep disruption.
10aAged10aDisorders of Excessive Somnolence10aFemale10aHumans10aMale10aMiddle Aged10aPolysomnography10aQuality of Life10aSleep10aSleep Apnea Syndromes10aSleep, REM1 aChami, Hassan, A1 aBaldwin, Carol, M1 aSilverman, Angela1 aZhang, Ying1 aRapoport, David1 aPunjabi, Naresh, M1 aGottlieb, Daniel, J uhttps://chs-nhlbi.org/node/116103091nas a2200361 4500008004100000022001400041245007000055210006900125260001300194300001100207490000700218520213900225653001602364653000902380653001202389653002002401653001902421653001102440653001102451653000902462653001602471653002002487653003002507653001702537653001602554653001702570653002502587100001902612700001702631700002202648700002302670856003602693 2010 eng d a0161-810500aUtility of sleep stage transitions in assessing sleep continuity.0 aUtility of sleep stage transitions in assessing sleep continuity c2010 Dec a1681-60 v333 aSTUDY OBJECTIVES: Sleep continuity is commonly assessed with polysomnographic measures such as sleep efficiency, sleep stage percentages, and the arousal index. The aim of this study was to examine whether the transition rate between different sleep stages could be used as an index of sleep continuity to predict self-reported sleep quality independent of other commonly used metrics.
DESIGN AND SETTING: Analysis of the Sleep Heart Health Study polysomnographic data.
PARTICIPANTS: A community cohort.
MEASUREMENTS AND RESULTS: Sleep recordings on 5,684 participants were deemed to be of sufficient quality to allow visual scoring of NREM and REM sleep. For each participant, we tabulated the frequency of transitions between wake, NREM sleep, and REM sleep. An overall transition rate was determined as the number of all transitions per hour sleep. Stage-specific transition rates between wake, NREM sleep, and REM sleep were also determined. A 5-point Likert scale was used to assess the subjective experience of restless and light sleep the morning after the sleep study. Multivariable regression models showed that a high overall sleep stage transition rate was associated with restless and light sleep independent of several covariates including total sleep time, percentages of sleep stages, wake time after sleep onset, and the arousal index. Compared to the lowest quartile of the overall transition rate (<7.76 events/h), the odds ratios for restless sleep were 1.27, 1.42, and 1.38, for the second (7.77-10.10 events/h), third (10.11-13.34 events/h), and fourth (≥13.35 events/h) quartiles, respectively. Analysis of stage-specific transition rates showed that transitions between wake and NREM sleep were also independently associated with restless and light sleep.
CONCLUSIONS: Assessing overall and stage-specific transition rates provides a complementary approach for assessing sleep continuity. Incorporating such measures, along with conventional metrics, could yield useful insights into the significance of sleep continuity for clinical outcomes.
10aAge Factors10aAged10aArousal10aBody Mass Index10aCohort Studies10aFemale10aHumans10aMale10aMiddle Aged10aPolysomnography10aPredictive Value of Tests10aRisk Factors10aSex Factors10aSleep Stages10aSleep Wake Disorders1 aLaffan, Alison1 aCaffo, Brian1 aSwihart, Bruce, J1 aPunjabi, Naresh, M uhttps://chs-nhlbi.org/node/125302266nas a2200241 4500008004100000022001400041245010800055210006900163260001600232300001200248490000600260520153300266100001901799700002201818700002301840700001701863700002001880700002301900700002401923700002101947700002001968856003601988 2011 eng d a2160-677300aThe Impact of Sleep-Disordered Breathing on Body Mass Index (BMI): The Sleep Heart Health Study (SHHS).0 aImpact of SleepDisordered Breathing on Body Mass Index BMI The S c2011 Dec 08 a159-1680 v33 aINTRODUCTION: It is well known that obesity is a risk factor for sleep-disordered breathing (SDB). However, whether SDB predicts increase in BMI is not well defined. Data from the Sleep Heart Health Study (SHHS) were analyzed to determine whether SDB predicts longitudinal increase in BMI, adjusted for confounding factors. METHODS: A full-montage unattended home polysomnogram (PSG) and body anthropometric measurements were obtained approximately five years apart in 3001 participants. Apnea-hypopnea index (AHI) was categorized using clinical thresholds: < 5 (normal), ≥ 5 to <15 (mild sleep apnea), and ≥ 15 (moderate to severe sleep apnea). Linear regression was used to examine the association between the three AHI groups and increased BMI. The model included age, gender, race, baseline BMI, and change in AHI as covariates. RESULTS: Mean (SD) age was 62.2 years (10.14), 55.2% were female and 76.1% were Caucasian. Five-year increase in BMI was modest with a mean (SD) change of 0.53 (2.62) kg/m(2) (p=0.071). A multivariate regression model showed that subjects with a baseline AHI between 5-15 had a mean increase in BMI of 0.22 kg/m(2) (p=0.055) and those with baseline AHI ≥ 15 had a BMI increase of 0.51 kg/m(2) (p<0.001) compared to those with baseline AHI of <5. CONCLUSION: Our findings suggest that there is a positive association between severity of SDB and subsequent increased BMI over approximately 5 years. This observation may help explain why persons with SDB have difficulty losing weight.
1 aBrown, Mark, A1 aGoodwin, James, L1 aSilva, Graciela, E1 aBehari, Ajay1 aNewman, Anne, B1 aPunjabi, Naresh, M1 aResnick, Helaine, E1 aRobbins, John, A1 aQuan, Stuart, F uhttps://chs-nhlbi.org/node/156602775nas a2200385 4500008004100000022001400041245009300055210006900148260001300217300001200230490000800242520174600250653001601996653000902012653001302021653002502034653001102059653002002070653002202090653001102112653001102123653000902134653001602143653002002159653001502179653002602194653001602220653002602236653000802262100001802270700002502288700001702313700002302330856003602353 2012 eng d a1931-354300aSleep-disordered breathing and caffeine consumption: results of a community-based study.0 aSleepdisordered breathing and caffeine consumption results of a c2012 Sep a631-6380 v1423 aBACKGROUND: Sleepiness is one of the most burdensome symptoms of sleep-disordered breathing (SDB). While caffeine is frequently used to avert sleepiness, the association between SDB and caffeine use has not been thoroughly explored. The current study examined whether SDB is associated with caffeine consumption and if factors such as sex, age, and daytime sleepiness explain or modify the association.
METHODS: Data from the Sleep Heart Health Study, a community-based study on the consequences of SDB, were used to characterize the association between SDB and caffeine intake. SDB was assessed with full-montage polysomnography. Caffeine use was quantified as the number of cans of soda or the cups of coffee or tea consumed daily. The Epworth Sleepiness Scale was used to assess daytime sleepiness. Multivariable negative binomial regression models were used to characterize the independent association between SDB and caffeine use.
RESULTS: Caffeinated soda, but not tea or coffee, intake was independently associated with SDB severity. Compared with participants without SDB, the relative ratios for caffeinated soda consumption in women with mild, moderate, and severe SDB were 1.20 (CI, 1.03-1.41), 1.46 (CI, 1.14-1.87), and 1.73 (CI, 1.23-2.42), respectively. For men, an association was only noted with severe SDB and caffeinated soda use. Age did not modify the SDB-caffeine association, and sleepiness could not explain the observed associations.
CONCLUSIONS: SDB is independently associated with caffeinated soda use in the general community. Identifying excessive caffeine used in SDB has potential significance given the cardiovascular effects of caffeine and untreated SDB.
10aAge Factors10aAged10aCaffeine10aCarbonated Beverages10aCoffee10aData Collection10aDrinking Behavior10aFemale10aHumans10aMale10aMiddle Aged10aPolysomnography10aPrevalence10aRetrospective Studies10aSex Factors10aSleep Apnea Syndromes10aTea1 aAurora, Nisha1 aCrainiceanu, Ciprian1 aCaffo, Brian1 aPunjabi, Naresh, M uhttps://chs-nhlbi.org/node/154003530nas a2200565 4500008004100000022001400041245010700055210006900162260001300231300001100244490000700255520189800262653001802160653002102178653002002199653002802219653003002247653004002277653001202317653001102329653003802340653002202378653001302400653002402413653002602437653001102463653002302474653000902497653001602506653003602522653001702558653001002575653003102585653001702616653001802633100001802651700002402669700001902693700002302712700001902735700002302754700002502777700002002802700002002822700002402842700002502866700001902891700001802910856003602928 2014 eng d a1432-042800aSleep duration does not mediate or modify association of common genetic variants with type 2 diabetes.0 aSleep duration does not mediate or modify association of common c2014 Feb a339-460 v573 aAIMS/HYPOTHESIS: Short and long sleep duration are associated with increased risk of type 2 diabetes. We aimed to investigate whether genetic variants for fasting glucose or type 2 diabetes associate with short or long sleep duration and whether sleep duration modifies the association of genetic variants with these traits.
METHODS: We examined the cross-sectional relationship between self-reported habitual sleep duration and prevalence of type 2 diabetes in individuals of European descent participating in five studies included in the Candidate Gene Association Resource (CARe), totalling 1,474 cases and 8,323 controls. We tested for association of 16 fasting glucose-associated variants, 27 type 2 diabetes-associated variants and aggregate genetic risk scores with continuous and dichotomised (≤5 h or ≥9 h) sleep duration using regression models adjusted for age, sex and BMI. Finally, we tested whether a gene × behaviour interaction of variants with sleep duration had an impact on fasting glucose or type 2 diabetes risk.
RESULTS: Short sleep duration was significantly associated with type 2 diabetes in CARe (OR 1.32; 95% CI 1.08, 1.61; p = 0.008). Variants previously associated with fasting glucose or type 2 diabetes and genetic risk scores were not associated with sleep duration. Furthermore, no study-wide significant interaction was observed between sleep duration and these variants on glycaemic traits. Nominal interactions were observed for sleep duration and PPARG rs1801282, CRY2 rs7943320 and HNF1B rs4430796 in influencing risk of type 2 diabetes (p < 0.05).
CONCLUSIONS/INTERPRETATION: Our findings suggest that differences in habitual sleep duration do not mediate or modify the relationship between common variants underlying glycaemic traits (including in circadian rhythm genes) and diabetes.
10aBlood Glucose10aBody Composition10aBody Mass Index10aCross-Sectional Studies10aDiabetes Mellitus, Type 210aEuropean Continental Ancestry Group10aFasting10aFemale10aGenetic Predisposition to Disease10aGenetic Variation10aGenotype10aGlucose Intolerance10aGlycated Hemoglobin A10aHumans10aInsulin Resistance10aMale10aMiddle Aged10aPolymorphism, Single Nucleotide10aRisk Factors10aSleep10aSurveys and Questionnaires10aTime Factors10aUnited States1 aTare, Archana1 aLane, Jacqueline, M1 aCade, Brian, E1 aGrant, Struan, F A1 aChen, Ting-Hsu1 aPunjabi, Naresh, M1 aLauderdale, Diane, S1 aZee, Phyllis, C1 aGharib, Sina, A1 aGottlieb, Daniel, J1 aScheer, Frank, A J L1 aRedline, Susan1 aSaxena, Richa uhttps://chs-nhlbi.org/node/627003096nas a2200541 4500008004100000022001400041245008500055210006900140260001500209300001100224490000700235520160100242653001901843653001801862653001101880653003601891653002001927653002701947653001001974653001701984100001902001700002402020700002502044700002202069700002102091700002202112700002402134700002102158700001702179700002002196700001902216700001402235700002002249700001902269700001902288700002302307700001502330700002002345700002302365700001402388700002002402700002002422700002102442700001802463700001902481700001802500856003602518 2016 eng d a1460-208300aCommon variants in DRD2 are associated with sleep duration: the CARe consortium.0 aCommon variants in DRD2 are associated with sleep duration the C c2016 Jan 1 a167-790 v253 aSleep duration is implicated in the etiologies of chronic diseases and premature mortality. However, the genetic basis for sleep duration is poorly defined. We sought to identify novel genetic components influencing sleep duration in a multi-ethnic sample. Meta-analyses were conducted of genetic associations with self-reported, habitual sleep duration from seven Candidate Gene Association Resource (CARe) cohorts of over 25 000 individuals of African, Asian, European and Hispanic American ancestry. All individuals were genotyped for ∼50 000 SNPs from 2000 candidate heart, lung, blood and sleep genes. African-Americans had additional genome-wide genotypes. Four cohorts provided replication. A SNP (rs17601612) in the dopamine D2 receptor gene (DRD2) was significantly associated with sleep duration (P = 9.8 × 10(-7)). Conditional analysis identified a second DRD2 signal with opposite effects on sleep duration. In exploratory analysis, suggestive association was observed for rs17601612 with polysomnographically determined sleep latency (P = 0.002). The lead DRD2 signal was recently identified in a schizophrenia GWAS, and a genetic risk score of 11 additional schizophrenia GWAS loci genotyped on the IBC array was also associated with longer sleep duration (P = 0.03). These findings support a role for DRD2 in influencing sleep duration. Our work motivates future pharmocogenetics research on alerting agents such as caffeine and modafinil that interact with the dopaminergic pathway and further investigation of genetic overlap between sleep and neuro-psychiatric traits.
10aCohort Studies10aEthnic Groups10aHumans10aPolymorphism, Single Nucleotide10aPolysomnography10aReceptors, Dopamine D210aSleep10aTime Factors1 aCade, Brian, E1 aGottlieb, Daniel, J1 aLauderdale, Diane, S1 aBennett, David, A1 aBuchman, Aron, S1 aBuxbaum, Sarah, G1 aDe Jager, Philip, L1 aEvans, Daniel, S1 aFulop, Tibor1 aGharib, Sina, A1 aJohnson, Craig1 aKim, Hyun1 aLarkin, Emma, K1 aLee, Seung, Ku1 aLim, Andrew, S1 aPunjabi, Naresh, M1 aShin, Chol1 aStone, Katie, L1 aTranah, Gregory, J1 aWeng, Jia1 aYaffe, Kristine1 aZee, Phyllis, C1 aPatel, Sanjay, R1 aZhu, Xiaofeng1 aRedline, Susan1 aSaxena, Richa uhttps://chs-nhlbi.org/node/712104625nas a2201021 4500008004100000022001400041245006600055210006500121260001300186300001200199490000700211520174100218100001601959700002501975700002502000700002802025700001502053700002402068700002202092700001602114700002402130700001802154700002502172700002302197700002602220700001902246700001602265700001802281700001902299700002102318700001802339700002302357700002202380700002302402700002002425700001602445700002102461700002002482700002002502700002402522700001902546700001802565700001702583700002602600700002002626700002002646700002302666700001202689700002402701700002502725700003002750700002402780700002402804700002302828700002802851700002602879700003002905700002502935700002502960700001902985700002403004700001903028700002003047700002403067700002103091700002603112700002103138700001903159700002303178700001903201700002003220700002103240700001903261700002303280700002403303700002303327700002403350700001603374700002203390700002803412700002303440700002103463700002203484700001703506700002103523700002303544856003603567 2016 eng d a1476-543800aGenetic variants in RBFOX3 are associated with sleep latency.0 aGenetic variants in RBFOX3 are associated with sleep latency c2016 Oct a1488-950 v243 aTime to fall asleep (sleep latency) is a major determinant of sleep quality. Chronic, long sleep latency is a major characteristic of sleep-onset insomnia and/or delayed sleep phase syndrome. In this study we aimed to discover common polymorphisms that contribute to the genetics of sleep latency. We performed a meta-analysis of genome-wide association studies (GWAS) including 2 572 737 single nucleotide polymorphisms (SNPs) established in seven European cohorts including 4242 individuals. We found a cluster of three highly correlated variants (rs9900428, rs9907432 and rs7211029) in the RNA-binding protein fox-1 homolog 3 gene (RBFOX3) associated with sleep latency (P-values=5.77 × 10(-08), 6.59 × 10(-)(08) and 9.17 × 10(-)(08)). These SNPs were replicated in up to 12 independent populations including 30 377 individuals (P-values=1.5 × 10(-)(02), 7.0 × 10(-)(03) and 2.5 × 10(-)(03); combined meta-analysis P-values=5.5 × 10(-07), 5.4 × 10(-07) and 1.0 × 10(-07)). A functional prediction of RBFOX3 based on co-expression with other genes shows that this gene is predominantly expressed in brain (P-value=1.4 × 10(-316)) and the central nervous system (P-value=7.5 × 10(-)(321)). The predicted function of RBFOX3 based on co-expression analysis with other genes shows that this gene is significantly involved in the release cycle of neurotransmitters including gamma-aminobutyric acid and various monoamines (P-values<2.9 × 10(-11)) that are crucial in triggering the onset of sleep. To conclude, in this first large-scale GWAS of sleep latency we report a novel association of variants in RBFOX3 gene. Further, a functional prediction of RBFOX3 supports the involvement of RBFOX3 with sleep latency.
1 aAmin, Najaf1 aAllebrandt, Karla, V1 avan der Spek, Ashley1 aMüller-Myhsok, Bertram1 aHek, Karin1 aTeder-Laving, Maris1 aHayward, Caroline1 aEsko, Tõnu1 avan Mill, Josine, G1 aMbarek, Hamdi1 aWatson, Nathaniel, F1 aMelville, Scott, A1 aDel Greco, Fabiola, M1 aByrne, Enda, M1 aOole, Edwin1 aKolcic, Ivana1 aChen, Ting-Hsu1 aEvans, Daniel, S1 aCoresh, Josef1 aVogelzangs, Nicole1 aKarjalainen, Juha1 aWillemsen, Gonneke1 aGharib, Sina, A1 aZgaga, Lina1 aMihailov, Evelin1 aStone, Katie, L1 aCampbell, Harry1 aBrouwer, Rutger, Ww1 aDemirkan, Ayse1 aIsaacs, Aaron1 aDogas, Zoran1 aMarciante, Kristin, D1 aCampbell, Susan1 aBorovecki, Fran1 aLuik, Annemarie, I1 aLi, Man1 aHottenga, Jouke Jan1 aHuffman, Jennifer, E1 avan den Hout, Mirjam, Cgn1 aCummings, Steven, R1 aAulchenko, Yurii, S1 aGehrman, Philip, R1 aUitterlinden, André, G1 aWichmann, Heinz-Erich1 aMüller-Nurasyid, Martina1 aFehrmann, Rudolf, Sn1 aMontgomery, Grant, W1 aHofman, Albert1 aKao, Wen Hong Linda1 aOostra, Ben, A1 aWright, Alan, F1 aVink, Jacqueline, M1 aWilson, James, F1 aPramstaller, Peter, P1 aHicks, Andrew, A1 aPolasek, Ozren1 aPunjabi, Naresh, M1 aRedline, Susan1 aPsaty, Bruce, M1 aHeath, Andrew, C1 aMerrow, Martha1 aTranah, Gregory, J1 aGottlieb, Daniel, J1 aBoomsma, Dorret, I1 aMartin, Nicholas, G1 aRudan, Igor1 aTiemeier, Henning1 avan IJcken, Wilfred, Fj1 aPenninx, Brenda, W1 aMetspalu, Andres1 aMeitinger, Thomas1 aFranke, Lude1 aRoenneberg, Till1 aDuijn, Cornelia, M uhttps://chs-nhlbi.org/node/7168