Background Sleep-disordered breathing is prevalent in the generalpopulation and has been linked to chronically elevated bloodpressure in cross-sectional epidemiologic studies. We performeda prospective, population-based study of the association betweenobjectively measured sleep-disordered breathing and hypertension(defined as a laboratory-measured blood pressure of at least140/90 mm Hg or the use of antihypertensive medications).
Methods We analyzed data on sleep-disordered breathing, bloodpressure, habitus, and health history at base line and afterfour years of follow-up in 709 participants of the WisconsinSleep Cohort Study (and after eight years of follow-up in thecase of 184 of these participants). Participants were assessedovernight by 18-channel polysomnography for sleep-disorderedbreathing, as defined by the apnea–hypopnea index (thenumber of episodes of apnea and hypopnea per hour of sleep).The odds ratios for the presence of hypertension at the four-yearfollow-up study according to the apnea–hypopnea indexat base line were estimated after adjustment for base-line hypertensionstatus, body-mass index, neck and waist circumference, age,sex, and weekly use of alcohol and cigarettes.
Results Relative to the reference category of an apnea–hypopneaindex of 0 events per hour at base line, the odds ratios forthe presence of hypertension at follow-up were 1.42 (95 percentconfidence interval, 1.13 to 1.78) with an apnea–hypopneaindex of 0.1 to 4.9 events per hour at base line as comparedwith none, 2.03 (95 percent confidence interval, 1.29 to 3.17)with an apnea–hypopnea index of 5.0 to 14.9 events perhour, and 2.89 (95 percent confidence interval, 1.46 to 5.64)with an apnea–hypopnea index of 15.0 or more events perhour.
Conclusions We found a dose–response association betweensleep-disordered breathing at base line and the presence ofhypertension four years later that was independent of knownconfounding factors. The findings suggest that sleep-disorderedbreathing is likely to be a risk factor for hypertension andconsequent cardiovascular morbidity in the general population.
Screening studies in the United States, Europe, and Australiahave shown that a substantial proportion of the adult populationhas mild-to-moderate sleep-disordered breathing, a conditioncharacterized by repeated episodes of apnea and hypopnea duringsleep.1,2,3,4,5,6 Apnea and hypopnea cause temporary elevationsin blood pressure in association with blood oxygen desaturation,arousal, and sympathetic activation and may cause elevated bloodpressure during the daytime and, ultimately, sustained hypertension.7Recent reviews judged the epidemiologic evidence relating sleep-disorderedbreathing to hypertension to be inconclusive, but they notedthat study designs were inappropriate, that there was inadequatecontrol for confounding factors such as obesity, and that therewas a dearth of prospective studies.8,9 Since sleep-disorderedbreathing is prevalent and treatable and the morbidity and costsof hypertension are profound, a rigorous assessment of the relationbetween the two conditions remains a priority.
We assessed the association between sleep-disordered breathingand hypertension in a prospective analysis of data from theWisconsin Sleep Cohort Study. The Sleep Cohort Study is a population-based,longitudinal study of the natural history of sleep-disorderedbreathing in adults. Participants complete overnight sleep studiesat four-year intervals. These studies include assessment ofsleep-disordered breathing (by monitored polysomnography), bloodpressure, and many potential confounding factors.
Methods
Overview
The protocols for the Wisconsin Sleep Cohort Study and informed-consentdocuments were approved by the institutional review board ofthe University of Wisconsin Medical School. In 1989, a subgroupof employees of four Wisconsin state agencies was mailed a four-pagequestionnaire on sleep habits, health history, and demographicinformation. A stratified random sample of respondents was invitedto participate in the study. Participants completed a base-lineovernight protocol that included assessments of the physiologiccharacteristics of sleep by polysomnography, blood pressure,habitus, health history, and other information. Approximatelyevery four years thereafter, participants have been invitedfor follow-up studies.
Exclusion criteria included pregnancy, unstable or decompensatedcardiopulmonary disease, airway cancers, and recent surgeryof the upper respiratory tract. For this report, participantswere also excluded if they had sleep studies with unusable physiologicmeasurements, an inadequate period of sleep (less than fourhours), no episodes of rapid-eye-movement sleep, or a historyof physician-diagnosed stroke or cardiovascular disease, orif they were receiving medical treatment for sleep-disorderedbreathing.
Participants
As of September 1999, a total of 1189 participants had completeda base-line sleep study and 957 of these participants had beeninvited for four-year follow-up studies. Of those invited, 709(74 percent) participated in a follow-up study, 233 (24 percent)declined, and 15 (2 percent) could not be contacted (becausethey had moved or died). Of the 709 who completed four-yearfollow-up studies, 219 had been invited for eight-year follow-upstudies at the time of our analysis. Of these, 184 (84 percent)completed the second follow-up study, 30 (14 percent) declined,and 5 (2 percent) could not be contacted. Table 1 compares keybase-line variables among the participants who completed thebase-line sleep study, those who completed the four-year follow-upstudy, and those who completed the eight-year follow-up study.There were no substantial differences among the three groups,although the percentage of female participants was slightlylower in the subgroup that completed the eight-year follow-upstudy.
Table 1. Base-Line Characteristics of the Participants Who Completed the Base-Line Sleep Study, the Four-Year Follow-up Study, and the Eight-Year Follow-up Study.
Collection of Data
The overnight sleep studies were conducted at the Universityof Wisconsin General Clinical Research Center in rooms resemblingtypical bedrooms. Participants arrived in the early evening.Sleep technicians obtained written informed consent and administeredhealth-history and lifestyle questionnaires. The use of antihypertensivemedication was determined on the basis of participants' answersto questions concerning the current use of -adrenergic antagonists,beta-blockers, calcium-channel blockers, diuretics, and angiotensin-converting–enzymeinhibitors for the treatment of hypertension. After administrationof the questionnaires and after participants had been seatedfor at least 15 minutes, two or three readings of systolic anddiastolic (phase V) blood pressure were obtained at 5-minuteintervals with the use of conventional mercury sphygmomanometryaccording to the recommendations of the American Society ofHypertension.10 Habitus was assessed with the use of standardprocedures11 and included measurements of height (in meters)and weight (in kilograms); waist, hip, and neck circumference(in centimeters); skin-fold thickness (in millimeters) of thebiceps, triceps, and subscapular and suprailiac areas with useof a caliper; and body-mass index, which was calculated as theweight in kilograms divided by the square of the height in meters.
After the assessment of blood pressure and habitus, techniciansaffixed polysomnography leads to each participant and performedcalibrations. An 18-channel polysomnographic recording system(model 78, Grass Instruments, Quincy, Mass.) was used to assesssleep state and respiratory and cardiac variables. Sleep statewas measured with electroencephalography, electrooculography,and chin electromyography. These signals were used to determinethe sleep stage for each 30-second interval of the polysomnographicrecord, according to conventional criteria.12 Arterial oxyhemoglobinsaturation, oral and nasal airflow, nasal air pressure, andrib-cage and abdominal respiratory motion were used to assessepisodes of sleep-disordered breathing. Oxyhemoglobin saturationwas continuously recorded with a pulse oximeter (model 3740,Ohmeda, Englewood, Colo.). Stalk-mounted thermocouples (ProTec,Hendersonville, Tenn.) detected oral and nasal airflow. A pressuretransducer (Validyne Engineering, Northridge, Calif.) measuredair pressure at the nares. Respiratory inductance plethysmography(Respitrace, Ambulatory Monitoring, Ardsley, N.Y.) recordedrib-cage and abdominal excursions. Sleep stage and respiratoryevents were assessed by trained sleep technicians and reviewedby an expert polysomnographer. Each 30-second interval of thepolysomnographic record was inspected visually for episodesof abnormal breathing. Cessation of airflow for at least 10seconds was defined as an episode of apnea. A discernible reductionin the sum amplitude of the rib-cage plus the abdominal excursionson respiratory inductance plethysmography that lasted at least10 seconds and that was associated with a reduction in the oxyhemoglobinsaturation of at least 4 percent was defined as an episode ofhypopnea. The apnea–hypopnea index was defined as theaverage number of episodes of apnea and hypopnea per hour ofobjectively measured sleep and was the summary measurement ofthe occurrence of sleep-disordered breathing.
Statistical Analysis
The primary goal of the study was to estimate the associationof sleep-disordered breathing at base line with the presenceof hypertension four years later. With this approach, an interpretationof a positive association might be that greater initial degreesof sleep-disordered breathing accelerate the development ofhypertension. Actual changes in blood-pressure levels were notmodeled, because the prevalent use of antihypertensive medicationin the cohort obscures underlying blood-pressure levels in thosewho use medications, possibly biasing associations.13 Participantswhose blood pressure exceeded a specified cutoff point or whoused antihypertensive medication at the time of their studieswere classified as being hypertensive. In defining hypertension,we examined cutoff points for blood pressure ranging from 130/85to 180/110 mm Hg. The cutoff point of primary interest was 140/90mm Hg, which was defined as stage 1 hypertension by the sixthreport of the Joint National Committee on Prevention, Detection,Evaluation, and Treatment of High Blood Pressure.14 Other cutoffpoints were also examined to determine whether the associationsdepended on the choice of cutoff point.
Among 709 participants who completed base-line and four-yearfollow-up sleep studies, 184 also completed eight-year follow-upstudies, yielding data on 893 sets of four-year sleep studiesfor analysis. We used logistic-regression analysis with theSAS GENMOD procedure15 to estimate the odds ratios for the presenceof hypertension at follow-up according to the level of sleep-disorderedbreathing at base line. We used the generalized-estimating-equationsapproach16,17 to incorporate correlations between observationsresulting from the inclusion of the 184 participants assessedat all three times. The significance of logistic-regressioncoefficients was determined with two-sided P values with useof an level of 0.05 for main effects and of 0.01 for interactionsbetween the covariates and the apnea–hypopnea index.
The degree of sleep-disordered breathing was characterized bythe apnea–hypopnea index. We examined whether untransformedvalues for the apnea–hypopnea index at base line, log-transformedvalues (apnea–hypopnea index + 1), the square of the values,and categorization of values (0, 0.1 to 4.9, 5.0 to 14.9, and15.0 or more events per hour) were predictors of the presenceof hypertension at follow-up. The category of 0 events per hourwas included because a substantial proportion of the participantshad no episodes of apnea or hypopnea at base line. The cutoffpoints of 5.0 and 15.0 events per hour have been used in previousepidemiologic studies of sleep-disordered breathing. Furthersubdivision of the highest category was impractical becausefew participants had more than 15.0 events per hour.
Because of variability within subjects and measurement errorin assessing blood pressure, some misclassification of hypertensionstatus was inevitable. Thus, we could not precisely identifya cohort of participants who were free of hypertension at baseline to follow for a determination of the incidence of hypertension.Instead, in all models, we controlled for hypertension statusat base line. This approach allowed us simultaneously to examinethe association between sleep-disordered breathing at base lineand hypertension at follow-up in participants classified asnormotensive at base line and the association between sleep-disorderedbreathing and persistent hypertension in participants classifiedas hypertensive at base line. We used an interaction term toassess whether these two associations were different. As a checkfor a possible bias resulting from the misclassification ofhypertension, we performed Monte Carlo simulations in whicha random error was added to the measurement of participants'blood pressure. Using conservative (larger than likely) estimatesof the error in blood-pressure measurements calculated fromthe variability between participants' base-line and follow-upmeasurements, we determined that the misclassification of hypertensionmight lead to slight underestimates of the odds ratios for thelikelihood of hypertension at follow-up.
We examined the following base-line variables as covariates:age, sex, body-mass index, neck circumference, waist circumference,waist-to-hip ratio, skin-fold measurements, smoking status (currentsmoker, former smoker, or no history of smoking; the numberof pack-years; and the current number of packs smoked per week),extent of alcohol use (based on the participant's usual weeklyconsumption), hours of regular exercise per week, and menopausalstatus. Base-line covariates that substantially altered regressioncoefficients for the apnea–hypopnea index at base linewere included in the final models. Interactions between thecovariates and the apnea–hypopnea index were tested forstatistical significance.
Results
Table 2 presents key characteristics at base line and follow-upaccording to the apnea–hypopnea index at base line. Whendata on all 893 follow-up studies were analyzed, there was adecrease in mean blood pressure from base line to follow-up(from 125/82 mm Hg to 123/79 mm Hg) and an increase in the prevalenceof stage 1 or worse hypertension (from 28 percent to 31 percent).These changes were due, in part, to a net increase in the useof antihypertensive medications (from 10 percent to 17 percent).
Table 2. Characteristics of the Participants Who Completed One or Both Follow-up Sleep Studies, According to the Apnea–Hypopnea Index at Base Line.
Odds ratios for the presence of hypertension at follow-up accordingto the apnea–hypopnea index at base line are given inTable 3. Results from four models are presented. The first modeladjusted for hypertension status at base line, the second controlledfor this variable as well as for age and sex (nonmodifiablerisk factors), the third controlled for all these variablesas well as for habitus, and the fourth controlled for all thepreceding variables as well as for weekly alcohol consumptionand cigarette use. Within each model there was a linear increasein the logarithm of the odds ratios for successively higherstrata of the apnea–hypopnea index. These models fit betterthan alternative models that used continuous measures of theapnea–hypopnea index. No higher-order terms (e.g., linearsquared or cubed) for the strata of the apnea–hypopneaindex were statistically significant.
Table 3. Adjusted Odds Ratios for Hypertension at a Follow-up Sleep Study, According to the Apnea–Hypopnea Index at Base Line.
Table 3 reveals that age and sex minimally confounded the associationbetween sleep-disordered breathing and hypertension: the oddsratios remained essentially unchanged after adjustment for ageand sex. Adjustment for habitus variables did reduce the oddsratios, but further adjustment for alcohol and cigarette usedid not. Other variables examined did not appreciably alterthe odds ratios. No interaction terms for sleep-disordered breathingand the covariates examined, including base-line hypertensionstatus, were significant.
Odds ratios obtained with the use of a more conservative definitionof hypertension (blood pressure of at least 160/100 mm Hg orthe use of antihypertensive medications) were similar to thosein Table 3. After adjustment for base-line hypertension status,age, sex, body-mass index, waist and neck circumference, andweekly alcohol and cigarette use, the odds ratio associatedwith an apnea–hypopnea index of 0.1 to 4.9 events perhour as compared with none was 1.39 (95 percent confidence interval,1.04 to 1.84), the odds ratio associated with an apnea–hypopneaindex of 5.0 to 14.9 events per hour was 1.92 (95 percent confidenceinterval, 1.09 to 3.39), and the odds ratio associated withan apnea–hypopnea index of 15.0 or more events per hourwas 2.66 (95 percent confidence interval, 1.13 to 6.25). Oddsratios based on other cutoff points for blood pressure (rangingfrom 130/85 to 180/110 mm Hg) were similar.
As a check for possible bias resulting from the dropout of participantsfrom the study, we analyzed data after excluding all eight-yearfollow-up data and adjusting for base-line hypertension status,age, sex, body-mass index, waist and neck circumference, andweekly alcohol and cigarette use. The resulting odds ratiosfor the presence of hypertension at the four-year follow-upstudy were 1.40 (95 percent confidence interval, 1.09 to 1.81)with an apnea–hypopnea index of 0.1 to 4.9 events perhour at base line, 1.97 (95 percent confidence interval, 1.19to 3.27) with an apnea–hypopnea index of 5.0 to 14.9 eventsper hour at base line, and 2.77 (95 percent confidence interval,1.30 to 5.92) with an apnea–hypopnea index of 15.0 ormore events per hour at base line. In each case the referencecategory was an apnea–hypopnea index of 0 events per hour.These odds ratios were similar to those in Table 3.
Discussion
We found a relation between sleep-disordered breathing and hypertension,measured over a four-year period, after adjustment for habitus,age, sex, and cigarette and alcohol use. Persons with few episodesof apnea or hypopnea (0.1 to 4.9 events per hour) at base linehad 42 percent greater odds of having hypertension at follow-upthan did persons with no episodes. Persons with mild sleep-disorderedbreathing (as defined by an apnea–hypopnea index of 5.0to 14.9 events per hour) and those with more severe sleep-disorderedbreathing (as defined by an apnea–hypopnea index of 15.0or more events per hour) had approximately two and three times,respectively, the odds of having hypertension at follow-up ofthose with no episodes of apnea or hypopnea. Our findings, ifaccurate and reflective of a causal relation, are particularlyimportant because of the high prevalences of sleep-disorderedbreathing and hypertension.
Dropout of participants, the possibility of confounding, anderror in assessing key study factors are important featuresof our study that may be relevant to the accuracy of our results.Among the participants who were invited for the four-year andeight-year follow-up studies, 74 percent and 84 percent, respectively,completed the studies. The odds ratios for hypertension at follow-upthat were calculated from base-line and all follow-up data weresimilar to those that excluded eight-year follow-up data, indicatingthat factors influencing participation in the eight-year follow-upstudies did not lead to biased associations. If similar factorsinfluenced participation in the four-year follow-up studies,then it would be unlikely that an important bias related todropout affected the findings.
The associations between sleep-disordered breathing and hypertensionmay be confounded by variables that cause both sleep-disorderedbreathing and hypertension. We measured and controlled for establishedconfounding factors (age, sex, and habitus) as well as severaladditional variables. In our sample, measures of habitus, butnot age or sex, were strong confounding variables. Previouscross-sectional studies of sleep-disordered breathing and hypertensionhave been faulted for not adjusting for smoking or alcohol use.8We found no evidence that these factors were important confounders.
Measurement error in assessing sleep-disordered breathing, bloodpressure, or other covariates may have reduced the accuracyof our findings. Random error in measuring sleep-disorderedbreathing is likely to produce a bias toward the absence ofan association.18 Our Monte Carlo simulations indicated thata random error in blood-pressure measurement might also producea bias toward a reduced association. If the accuracy of theclassification of hypertension was related to the degree ofsleep-disordered breathing or to important covariates such asobesity, then underestimates or overestimates of associationcould occur. Incomplete control of confounding due to, for example,measurement error in assessing habitus may produce a bias towardan overestimate of associations between sleep-disordered breathingand hypertension.18
The fact that our study was prospective lends support to theevidence of a causal role of sleep-disordered breathing in hypertension.We found that the presence of sleep-disordered breathing waspredictive of the presence of hypertension four years later.This finding may indicate that sleep-disordered breathing acceleratesthe progression of blood-pressure levels commonly present inmiddle-aged adults in the United States. However, our findingsdo not offer comprehensive insight into the natural historyof the association. Sleep-disordered breathing changes bloodpressures acutely.19,20,21,22 Nocturnal exposure to sleep-disorderedbreathing may lead to elevations in blood pressure that lastthroughout the morning or the entire day.23 A daytime pressorresponse that outlasts experimentally induced nocturnal hypoxiahas been demonstrated in humans.24 It has also been hypothesizedthat sleep-disordered breathing could cause permanent changesin blood pressure by remodeling the systemic vasculature.25
We did not have data that could be used to model the dynamicrelation between sleep-disordered breathing, habitus, and hypertension.For example, although there have been few relevant studies,there has been speculation that sleep-disordered breathing hasa causal role in obesity.26 If this is the case, then our effortsto control for confounding by including measures of obesityin our models may have led to a partial overadjustment of theassociation between sleep-disordered breathing and hypertensionand thus to an underestimate of the association.
We found no evidence of a threshold of the apnea–hypopneaindex below which hypertension was not related to sleep-disorderedbreathing. Even persons with minimal sleep-disordered breathing(as defined by an apnea–hypopnea index of 0.1 to 4.9 eventsper hour) had higher odds of hypertension than those with noepisodes of sleep-disordered breathing. If even those with minimalsleep-disordered breathing are at higher risk for hypertension,then the proportion of cases of hypertension that are attributableto this factor may be substantial.
Previous epidemiologic studies of sleep-disordered breathingand hypertension that focused on subjects from the general populationand patients from sleep-disorders clinics have reached conflictingconclusions, although none have precluded the existence of amoderate association.9 Studies that involved cross-sectionalsamples from sleep-disorders clinics26,27,28,29,30,31,32,33,34have typically used high-quality methods to assess sleep-disorderedbreathing (multichannel polysomnography). However, unknown factorsthat influence referral to a sleep-disorders clinic may havemade these studies incapable of accurately assessing the relations.Conversely, most cross-sectional population-based studies5,35,36,37,38,39,40,41,42,43have used samples that were epidemiologically more rigorousbut used instruments with poor or unknown validity to assesssleep-disordered breathing. Two recent population-based cross-sectionalanalyses from the Wisconsin Sleep Cohort Study44 and the SleepHeart Health Study,45 which used polysomnography to assess sleep-disorderedbreathing, reported moderate, statistically significant associationsbetween sleep-disordered breathing and hypertension. In a recentprospective study, Hu and colleagues46 assessed a large numberof normotensive women and found that snoring, a cardinal (butnonspecific) symptom of sleep-disordered breathing, significantlyincreased the risk of hypertension. As compared with the riskin nonsnorers, the risk of hypertension was increased by 29percent in occasional snorers and by 55 percent in those whosnored regularly.
As evidence builds of a causal role of sleep-disordered breathingin hypertension and other health outcomes, there is a growingneed to understand the natural history of and risk factors forsleep-disordered breathing. Continued development and refinementof medical treatments for sleep-disordered breathing are alsopriorities. Available treatments, such as continuous positiveairway pressure, can be effective. However, these therapiesmay be overly burdensome for the treatment of mild cases ofasymptomatic sleep-disordered breathing. Little is known aboutthe effectiveness of risk-factor intervention for mild-to-moderatesleep-disordered breathing, and this is an important area forfuture research.
In this prospective analysis, we found an association betweenlaboratory-assessed sleep-disordered breathing and hypertension.Important elevations in the odds of hypertension were observedeven in participants with mild-to-moderate sleep-disorderedbreathing. Because sleep-disordered breathing is highly prevalent,afflicting as many as 9 percent of women and 24 percent of menin the United States,1 a causal association could be responsiblefor a substantial number of cases of hypertension and its sequelae,such as cardiovascular and cerebrovascular morbidity and mortality.
Supported by grants (R01HL62252, P01HL42242, RR03186, and R01CA53786)from the National Institutes of Health.
We are indebted to Jerome Dempsey, Ph.D., Steven Weber, Ph.D.,Laurel Finn, Tony Jacques, Linda Evans, Kathy Pluff, DeborahBrown, Andrea Darner, Kathy Kenison, Leah Steinberg, Marty Kanarek,Ph.D., and Richard Chappell, Ph.D., for their contributionsand technical expertise.
Source Information
From the Departments of Preventive Medicine (P.E.P., T.Y., M.P.), Medicine (J.S.), and Biostatistics and Medical Informatics (M.P.), University of Wisconsin School of Medicine, Madison.
Address reprint requests to Dr. Peppard at the Department of Preventive Medicine, University of Wisconsin, 502 N. Walnut St., Madison, WI 53705, or at ppeppard{at}facstaff.wisc.edu.
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16: 169-182
[Abstract][Full Text]
-adrenergic antagonists, beta-blockers, calcium-channel blockers, diuretics, and angiotensin-converting–enzyme inhibitors for the treatment of hypertension. After administration of the questionnaires and after participants had been seated for at least 15 minutes, two or three readings of systolic and diastolic (phase V) blood pressure were obtained at 5-minute intervals with the use of conventional mercury sphygmomanometry according to the recommendations of the American Society of Hypertension.10 Habitus was assessed with the use of standard procedures11 and included measurements of height (in meters) and weight (in kilograms); waist, hip, and neck circumference (in centimeters); skin-fold thickness (in millimeters) of the biceps, triceps, and subscapular and suprailiac areas with use of a caliper; and body-mass index, which was calculated as the weight in kilograms divided by the square of the height in meters. 
