Obstructive Sleep Apnea as a Risk Factor for Stroke and Death
H. Klar Yaggi, M.D., M.P.H., John Concato, M.D., M.P.H., Walter N. Kernan, M.D., Judith H. Lichtman, Ph.D., M.P.H., Lawrence M. Brass, M.D., and Vahid Mohsenin, M.D.
Background Previous studies have suggested that the obstructivesleep apnea syndrome may be an important risk factor for stroke.It has not been determined, however, whether the syndrome isindependently related to the risk of stroke or death from anycause after adjustment for other risk factors, including hypertension.
Methods In this observational cohort study, consecutive patientsunderwent polysomnography, and subsequent events (strokes anddeaths) were verified. The diagnosis of the obstructive sleepapnea syndrome was based on an apnea–hypopnea index of5 or higher (five or more events per hour); patients with anapnea–hypopnea index of less than 5 served as the comparisongroup. Proportional-hazards analysis was used to determine theindependent effect of the obstructive sleep apnea syndrome onthe composite outcome of stroke or death from any cause.
Results Among 1022 enrolled patients, 697 (68 percent) had theobstructive sleep apnea syndrome. At baseline, the mean apnea–hypopneaindex in the patients with the syndrome was 35, as comparedwith a mean apnea–hypopnea index of 2 in the comparisongroup. In an unadjusted analysis, the obstructive sleep apneasyndrome was associated with stroke or death from any cause(hazard ratio, 2.24; 95 percent confidence interval, 1.30 to3.86; P=0.004). After adjustment for age, sex, race, smokingstatus, alcohol-consumption status, body-mass index, and thepresence or absence of diabetes mellitus, hyperlipidemia, atrialfibrillation, and hypertension, the obstructive sleep apneasyndrome retained a statistically significant association withstroke or death (hazard ratio, 1.97; 95 percent confidence interval,1.12 to 3.48; P=0.01). In a trend analysis, increased severityof sleep apnea at baseline was associated with an increasedrisk of the development of the composite end point (P=0.005).
Conclusions The obstructive sleep apnea syndrome significantlyincreases the risk of stroke or death from any cause, and theincrease is independent of other risk factors, including hypertension.
Stroke is the second leading cause of death worldwide and theleading cause of long-term disability.1,2 Strategies for strokeprevention, including the control of hypertension, treatmentof atrial fibrillation, and smoking cessation, have reducedthe disease burden, but stroke still remains an important publichealth challenge. A better understanding of the risk factorsfor stroke is needed to develop additional preventive strategies.
The obstructive sleep apnea syndrome is a treatable form ofdisordered breathing in which the upper airway closes repeatedlyduring sleep. The syndrome is associated with vascular riskfactors and with substantial cardiovascular morbidity and mortality.3Several studies have shown a prevalence of the syndrome amongpatients with stroke that exceeds 60 percent,4,5,6,7 as comparedwith 4 percent in the middle-aged adult population.8
Whether the relation between the syndrome and stroke is independentof confounding risk factors, such as hypertension, hyperlipidemia,diabetes mellitus, and smoking, is not clear. Several cross-sectionalanalyses6,9,10,11,12,13,14 have shown an increase in the riskof stroke with sleep-disordered breathing that is similar inmagnitude to the effect of other cardiovascular risk factors.A study of patients with acute stroke7 demonstrated that obstructiveapnea persisted despite neurologic recovery, suggesting thatthe obstructive sleep apnea syndrome may have predated the developmentof stroke. We therefore hypothesized that patients with thesyndrome have an increased risk of stroke or death from anycause that is independent of other cerebrovascular risk factors.
Methods
Study Population
We conducted an observational cohort study. The cohort consistedof patients who were referred to the Yale Center for Sleep Medicinespecifically for the evaluation of sleep-disordered breathing,underwent at least two hours of attended sleep monitoring, completeda 10-page questionnaire on their sleep and medical history,and were 50 or more years old. The exposure group was defineda priori as having an apnea–hypopnea index of 5 or higher(five or more events per hour of sleep); patients with an apnea–hypopneaindex of less than 5 constituted the comparison group.
Patients were excluded if they had been referred for reasonsother than the evaluation of suspected sleep-disordered breathing(e.g., narcolepsy or movement disorder); if they had a historyof stroke, myocardial infarction, or tracheostomy; or if theentire polysomnographic study was performed with airway pressurization(e.g., continuous positive airway pressure for therapeutic purposes).
Participants or their family members gave either written ororal informed consent at the time of follow-up ascertainment.The study was approved by the Human Investigation Committeeat Yale University School of Medicine.
Baseline Assessment
Data on demographic characteristics, sleep and medical history,medication use, and habits were obtained with the use of a standardizedquestionnaire administered by a trained technologist beforethe initiation of overnight polysomnography; the questionnaireswere reviewed by a physician. Each patient's height and weightwere recorded at the time of polysomnography and used to calculatethe body-mass index.
Sleep-history data included a validated measure of daytime sleepiness(the Epworth Sleepiness Scale)15 and self-reported habitualsnoring, which was defined as loud snoring occurring "frequently"or "constantly." Data regarding medications included the dailyuse of beta-blockers, angiotensin-converting–enzyme inhibitors,other antihypertensive medications, antiplatelet therapy, anticoagulants,oral medications for the treatment of diabetes, insulin, andlipid-lowering medications. Risk-factor data included a historyof hypertension, atrial fibrillation, diabetes mellitus, orhyperlipidemia, either reported by the patient on the baselinemedical questionnaire or noted by the referring physician. Inaddition, atrial fibrillation on electrocardiography duringpolysomnography was considered sufficient evidence to establishthat diagnosis.
Patients were classified according to whether they were currentor former smokers or had never smoked; data were elicited, ifapplicable, on the number of pack-years of smoking. The historyof alcohol consumption was based on the average number of drinksper day and the number of years of drinking.
Polysomnography
Participants underwent attended overnight polysomnography withthe use of Grass data-acquisition systems (Astro-Med) on thebasis of a protocol described previously.4 A single, attendedpolysomnographic study that was conducted during an entire nightwas used to establish the presence of sleep apnea.16 Sleep stageswere scored in 30-second epochs according to standard criteria.17Total cessation of airflow at the nose and mouth for at least10 seconds was classified as apnea (as obstructive apnea ifrespiratory efforts were present and as central apnea if respiratoryefforts were absent). Partial airway closure, resulting in adiminution of airflow by more than 30 percent for at least 10seconds and associated with oxygen desaturation of 4 percentor more, was termed hypopnea.18 Calculated polysomnographicvariables included the apnea–hypopnea index and the arousalindex (the number of arousals per hour of sleep).
Outcomes
Each patient was sent a follow-up questionnaire, which includedquestions regarding current state of health, occurrence of stroke,hospitalizations, and treatment of sleep disorders since thebaseline assessment. Strokes and transient ischemic attacks(TIA) were ascertained with the use of a validated questionnairedesigned to be a practical and reliable means of ascertainingstroke status.19 Attempts were made to telephone patients whohad not responded to the initial mailed questionnaire. Familymembers were asked to provide information about patients whowere not able to participate owing to death, illness, or dementia.
A physician investigator who was unaware of the patient's statuswith regard to the obstructive sleep apnea syndrome validatedreported strokes and TIAs by reviewing medical records. Diagnoseswere determined according to criteria of the National Instituteof Neurological Disorders and Stroke20 for the classificationof cerebrovascular events. The exact date of the stroke or TIAwas recorded. Vital records from the Connecticut Departmentof Public Health (regarding in-state deaths) and the SocialSecurity Administration Death Master File21,22 (regarding out-of-statedeaths) were used to determine or confirm death. The exact dateof death was recorded.
Statistical Analysis
The primary outcome was the composite end point of incidentstroke (including TIA, which hereafter will be reported as stroke)or death from any cause. With the assumption of a prevalenceof 60 percent for sleep apnea in our cohort and an incidenceof stroke per year of 1.5 percent23 during a four-year follow-upperiod, a sample of 840 patients was required in order to achieve80 percent power to detect a relative risk of 2.0 at the 5 percent(two-tailed) significance level.
A series of prespecified time-to-event analyses were performedto examine the effect of the obstructive sleep apnea syndromeon the outcome. The time until the composite end point was takento be the time until stroke, if the patient was contacted andfound to have had a stroke, and the time until death, if thepatient was not reached but was found to have died. Data werecensored at the time of the contact if the patient was reachedand was found not to have had a stroke and were censored atday 1 if the patient was not reached (or unwilling to be contacted)and was not found to have died.
The Kaplan–Meier method and the log-rank test were usedto compare event-free survival among patients with and thosewithout the obstructive sleep apnea syndrome. With the use ofproportional-hazards analysis, hazard ratios and 95 percentconfidence intervals were generated for the unadjusted associationbetween sleep-apnea status or other baseline characteristicsand the end point of stroke or death from any cause. Hazardratios were then adjusted for the confounding effects of otherbaseline characteristics, including age, sex, race, smokingstatus, alcohol-consumption status, body-mass index, and thepresence or absence of diabetes mellitus, hyperlipidemia, atrialfibrillation, and hypertension. Because of the possibility thatcontrolling for hypertension could constitute "overadjustment"(i.e., accounting for a variable on the causal pathway),24 modelswere created both with and without the inclusion of hypertension.Finally, a trend analysis, with the use of the chi-square testfor linear trend, was performed to analyze whether an increasedseverity of the obstructive sleep apnea syndrome (on the basisof quartiles of the apnea–hypopnea index) was associatedwith an increased risk of stroke or death from any cause.
Student's t-test was used to compare mean values at baselineamong patients who had the obstructive sleep apnea syndromewith those in the comparison group. Categorical data were comparedwith the use of the chi-square test. All statistical tests wereperformed with the use of SAS software (SAS Institute). Allreported P values are two-sided, and no interim analyses wereconducted. S-Plus software was used to generate the Kaplan–Meiersurvival curves (Mathsoft Engineering and Education).
Results
Between January 1, 1997, and December 31, 2000, 3635 consecutivepatients were referred to the sleep center, of whom 1022 wereeligible to participate in the study. A total of 2402 patientswere ineligible because they were less than 50 years of age,and 159 patients were ineligible because they had clinical evidenceof previous myocardial infarction or stroke at entry. Another52 patients were excluded because of unavailability of baselinedata, having undergone a tracheostomy, or having been referredfor conditions other than sleep-disordered breathing.
A total of 697 of the 1022 study participants (68 percent) wereclassified as having the obstructive sleep apnea syndrome (Table 1).The mean (±SD) apnea–hypopnea index among thepatients with the syndrome was 35±29, as compared with2.0±1.5 in the comparison group. As expected, the prevalenceof hypertension and diabetes mellitus was higher in the groupwith the syndrome than in the comparison group (Table 1). Patientswith the syndrome also were more obese, as reflected by thehigher body-mass index, and had lower nadir oxygen saturationsand a higher arousal index. Obstructive apnea was the predominantapneic event; central apnea was rare.
Table 1. Baseline Characteristics of Patients with the Obstructive Sleep Apnea Syndrome and Controls.
Many patients with the obstructive sleep apnea syndrome receivedsome type of treatment for sleep apnea after the initial evaluation.Thirty-one percent achieved a weight reduction of 10 percentor more; 58 percent were using airway pressurization for atleast four hours per night for five nights or more per week;15 percent underwent upper-airway surgery.
Follow-up after the single sleep study took place between June1, 2002, and December 31, 2003. Patients with the syndrome hada median duration of follow-up of 3.4 years (interquartile range,2.6 to 3.9), and the comparison group had a median durationof follow-up of 3.3 years (interquartile range, 2.8 to 4.2).Among the 1022 study patients, data on stroke events and deathfrom any cause were obtained for 842 patients (82 percent).Investigators were unable to contact the remaining 180 patients(18 percent), and the vital-records search did not indicatethat they had died. This group included 124 patients with thesyndrome and 56 patients in the comparison group. The baselinecharacteristics of these patients were similar to the characteristicsof the group with complete follow-up (data not shown).
Incident stroke or death from any cause occurred in 88 patients(9 percent). The 88 confirmed events among these patients included22 strokes and 50 deaths in the group with the obstructive sleepapnea syndrome (3.48 events per 100 person-years), as comparedwith 2 strokes and 14 deaths in the comparison group (1.60 eventsper 100 person-years). Figure 1 shows the Kaplan–Meierestimates of the time to the composite event of stroke or death.The probability of event-free survival was significantly lowerfor patients with the syndrome than for the comparison group(P=0.003 by the log-rank test). A time-to-event analysis fordeath only showed a similar result (P=0.02 by the log-rank test)(Figure 2).
Figure 2. Kaplan–Meier Estimates of the Probability of Overall Survival among Patients with the Obstructive Sleep Apnea Syndrome and Controls.
In an unadjusted analysis (Table 2), a significant associationwas found between the obstructive sleep apnea syndrome and strokeor death from any cause (hazard ratio, 2.24; 95 percent confidenceinterval, 1.30 to 3.86; P=0.004). The associations of age anddiabetes with the composite outcome were also statisticallysignificant. The unadjusted hazard ratios for smoking, hypertension,and atrial fibrillation were in the expected direction, althoughnot statistically significant. After adjustment for age, sex,race, smoking status, alcohol-consumption status, body-massindex, and the presence or absence of diabetes mellitus, hyperlipidemia,atrial fibrillation, and even hypertension, the obstructivesleep apnea syndrome retained a statistically significant associationwith stroke or death (hazard ratio, 1.97; 95 percent confidenceinterval, 1.12 to 3.48; P=0.01). The association of age withthe outcomes also persisted after adjustment, but no statisticallysignificant association was detected for other covariates. Theinclusion of antiplatelet therapy in the model also did notinfluence the adjusted hazard ratio for the syndrome (data notshown).
Table 2. Unadjusted and Adjusted Hazard Ratios for the Risk of Stroke or Death from Any Cause.
A significant unadjusted association was found between the syndromeand death as a single end point (hazard ratio, 2.0; 95 percentconfidence interval, 1.11 to 3.60; P=0.02). Adjusting for age,sex, race, smoking status, alcohol-consumption status, body-massindex, and the presence or absence of diabetes mellitus, hyperlipidemia,atrial fibrillation, and hypertension resulted in an attenuationof the hazard ratio for sleep apnea (1.70; 95 percent confidenceinterval, 0.92 to 3.16; P=0.09).
A trend analysis (Table 3) revealed a stepwise increase in therisk of stroke or death from any cause as a function of increasedseverity of sleep apnea (P=0.005). The risk of stroke or deathin patients in the most severe quartile of sleep apnea was threetimes that in the controls.
Table 3. Trend Analysis for the Relationship between Increased Severity of the Obstructive Sleep Apnea Syndrome and the Composite Outcome of Stroke or Death from Any Cause (N=1022).
Discussion
We conducted a large observational cohort study examining therole of the obstructive sleep apnea syndrome in the developmentof a first stroke or death from any cause. Our results demonstratethat the syndrome is associated with an increased incidenceof stroke or death from any cause and that the association isindependent of other cardiovascular and cerebrovascular riskfactors, including hypertension.
Our findings are consistent with recent data showing that severeobstructive sleep apnea syndrome increases the risk of fataland nonfatal cardiovascular events.25 The broad range of severityof the syndrome in our study population allowed us to demonstratean association between increased severity of the syndrome andincreased risk of stroke or death from any cause. This correlationconfirms the results of previous cross-sectional data showingthat the risk of stroke appears to increase progressively withincreased severity of the syndrome.14
In contrast to cross-sectional studies14 and studies that donot exclude preexisting cerebrovascular disease25 (which mightreflect reverse causal pathways with the obstructive sleep apneasyndrome as the consequence, rather than the cause, of stroke),our study addressed the temporal relationship between the syndromeand stroke by including only first-time cerebrovascular eventsthat occurred after initially abnormal results of a sleep study.The study also provides an assessment of the independent effectof sleep apnea. After an adjustment was made for cardiovascularrisk factors in the multivariable model, the hazard ratio forstroke or death from any cause among patients with the obstructivesleep apnea syndrome remained significant. Although the associationof the syndrome and death as a single end point was not statisticallysignificant, the lower number of deaths as compared with thecomposite outcome probably reduced the ability to detect anindependent effect. Overall, our results regarding the increasedrisk of death among patients with the obstructive sleep apneasyndrome are consistent with previous reports.26,27
The addition of hypertension to the model did not significantlyattenuate the hazard ratio, suggesting that additional pathogeneticmechanisms (other than increased blood pressure) contributeto the increased risk of stroke and death. Possible mechanismsinclude acute hemodynamic changes during episodes of apnea,28,29decreased cerebral blood flow,30,31,32 paradoxical embolization,33hypercoagulability,34,35 hypoxia-related cerebral ischemia,36and atherosclerosis.37
Several studies have demonstrated that airway pressurization(the main medical therapy for the syndrome) can reverse hypercoagulability34,35and hemodynamic changes38,39,40,41,42 and even reduce the riskof cardiovascular events.25 The present study was not designedor powered to address adherence with treatment or the effectof treatment on outcomes. Nonetheless, our study demonstratedan increased risk of stroke or death from any cause among patientswith the obstructive sleep apnea syndrome despite the administrationof various therapies. Several explanations may account for thisfinding. First, it is likely that many of our patients had haduntreated obstructive sleep apnea for years before seeking treatment,resulting in a prolonged exposure to cardiovascular risk. Themedian 3.4 years of follow-up may not have been a sufficientlength of time to derive the potential cardiovascular therapeuticbenefits. Second, reduced compliance with continuous positiveairway pressure and limited efficacy of other treatments mayhave played a role in the failure of therapy to reduce the riskto baseline levels. Third, in contrast to the patients in arecent study that suggested a beneficial effect of treatmenton outcomes,25 our population was older and had a higher prevalenceof cardiovascular risk factors.
Several methodologic issues should be considered in the interpretationof our results. First, the ascertainment of stroke outcome wasnot possible in all patients. Some patients for whom death wasreported as the outcome event may have had earlier, unreportedstrokes. The consequences of this methodologic limitation arereduced by an analysis that focuses on the combined end pointof stroke or death, but it is nonetheless possible that strokesoccurring much earlier in patients who died would alter thetime-dependent character of the findings. A related issue involvespossible nonfatal strokes among patients who were alive butwere not contacted. However, the distribution of the obstructivesleep apnea syndrome between patients with and those withoutconfirmed follow-up was nearly identical, suggesting that theresults in patients who were lost to follow-up would be similarto those for the study population as a whole.
Second, it is possible that residual confounding factors affectedour adjusted hazard ratios, despite our attempts to controlfor major cardiovascular risk factors. All the major known riskfactors for stroke were considered in our analysis, so we thinkit is unlikely that an important confounder was overlooked.
Finally, some of the hazard ratios for known cardiovascularrisk factors did not achieve statistical significance in ourmodeling. There are several possible reasons. First, patientswith previous cardiovascular and cerebrovascular events wereexcluded from our cohort and the median 3.4 years of follow-upmay not have been long enough for new events related to thesetraditional risk factors to develop in this cohort. Second,the concurrent treatment of these conditions probably reducedtheir effect on the composite outcome. Third, deaths from noncardiovascularcauses (which were included in our composite outcome) may havereduced the measurable effect of traditional cardiovascularrisk factors.
In conclusion, the obstructive sleep apnea syndrome is significantlyassociated with the risk of stroke or death from any cause,and this association is independent of other risk factors, includinghypertension. Increased severity of the syndrome is associatedwith an incremental increase in the risk of this composite outcome.
Supported by a National Research Service Award InstitutionalResearch Training Grant from the National Institutes of Health(5T32HL07778), by the Yale Center for Sleep Medicine, and bya career development award from the Veterans Affairs HealthServices Research and Development Service (to Dr. Yaggi).
We are indebted to the staff of the Yale Center for Sleep Medicinefor their valuable technical assistance; to the participants,whose cooperation made this study possible; and to Birol Emir,Ph.D., for his assistance in the preparation of the graphs.
Source Information
From the Section of Pulmonary and Critical Care Medicine, Yale Center for Sleep Medicine (H.K.Y., V.M.), the Section of General Medicine (J.C., W.N.K.), and the Departments of Epidemiology and Public Health (J.H.L., L.M.B.) and Neurology (L.M.B.), Yale University School of Medicine, New Haven, Conn.; and the Section of Pulmonary and Critical Care Medicine (H.K.Y.), the Clinical Epidemiology Research Center (H.K.Y., J.C.), and the Section of Neurology (L.M.B.), Veterans Affairs Connecticut Healthcare System, West Haven, Conn.
Address reprint requests to Dr. Mohsenin at the Yale Center for Sleep Medicine, 300 Cedar St., TAC 441, P.O. Box 208057, New Haven, CT 06520.
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Sleep Apnea and Heart Disease
Sinha A.-M., Skobel E. C., Breithardt O.-A., Zheng H., Zhan H., Wilcox I., Booth V., Lattimore J., Chhajed P. N., Tamm M., Strobel W., Neuberger H.-R., Böhm M., Mewis C., Bradley T. D., Floras J. S., Logan A. G., Yaggi H. K., Concato J., Mohsenin V.
Extract |
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N Engl J Med 2006;
354:1086-1089, Mar 9, 2006.
Correspondence
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