0
Original Research: Sleep Disorders |

OSA Is Common and Independently Associated With Hypertension and Increased Arterial Stiffness in Consecutive Perimenopausal WomenOSA Increases Arterial Stiffness in Perimenopause FREE TO VIEW

Rodrigo P. Pedrosa, MD, PhD; Isly M. L. Barros, MD; Luciano F. Drager, MD, PhD; Marcio S. Bittencourt, MD, MPH; Ana Kelley L. Medeiros, RN; Liana L. Carvalho, RN; Thais C. Lustosa, RpT; Martinha M. B. Carvalho, RpT; Moacir N. L. Ferreira, MD, PhD; Geraldo Lorenzi-Filho, MD, PhD; Laura O. B. F. Costa, MD, PhD
Author and Funding Information

From the Sleep and Heart Laboratory (Drs Pedrosa, Barros, and Ferreira and Mss Medeiros, L. L. Carvalho, Lustosa, and M. M. B. Carvalho), Pronto Socorro Cardiológico de Pernambuco (PROCAPE) da Universidade de Pernambuco, and PROCAPE da Universidade de Pernambuco (Drs Barros and Costa), Pernambuco; Sleep Laboratory (Drs Drager and Lorenzi-Filho), Pulmonary Division, Heart Institute (InCor) do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo; and University Hospital (Dr Bittencourt), University of São Paulo, São Paulo, Brazil.

CORRESPONDENCE TO: Rodrigo P. Pedrosa, MD, PhD, Sleep and Heart Laboratory, PROCAPE da Universidade de Pernambuco, Rua dos Palmares, SN, Recife, Pernambuco, Brazil; e-mail: rppedrosa@terra.com.br


This study has been presented in poster form at the American Thoracic Society International Conference, May 17-22, 2013, Philadelphia, PA.

FUNDING/SUPPORT: This work was supported by the Fundação de Amparo à Ciência e Tecnologia do Estado de Pernambuco.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;146(1):66-72. doi:10.1378/chest.14-0097
Text Size: A A A
Published online

BACKGROUND:  Perimenopause is associated with increased cardiovascular risk. OSA is an emerging risk factor for cardiovascular disease, particularly among men, but the independent contribution of OSA to cardiovascular risk in climacteric women is not clear.

METHODS:  We evaluated 277 consecutive women (age, 56 [52-61] years; BMI, 28 [25-32] kg/m2) without manifest cardiovascular disease (heart failure, coronary disease, or stroke). All women underwent 24-h ambulatory BP monitoring, arterial stiffness evaluation (pulse wave velocity), and portable sleep study.

RESULTS:  OSA (apnea-hypopnea index ≥ 5 events/h) and moderate to severe OSA (apnea-hypopnea index ≥ 15 events/h) were diagnosed in 111 (40.1%) and 31 (11.1%) women, respectively. None of the participants had received a previous diagnosis of OSA. Women with moderate to severe OSA vs those without OSA had a higher prevalence of hypertension, were prescribed more medications for hypertension, had higher awake BP (systolic, 133 [125-142] vs 126 [119-134] mm Hg [P < .01]; diastolic, 82 [78-88] vs 79 [74-85] mm Hg [P = .07]), higher nocturnal BP (systolic, 125 [118-135] vs 115 [109-124] mm Hg [P < .01]; diastolic, 73 [69-79] vs 69 [62-75] mm Hg [P < .01]), and more arterial stiffness (pulse wave velocity, 11.5 [10.1-12.3] m/s vs 9.5 [8.6-10.8] m/s, P < .001). Oxygen desaturation index during the night was independently associated with 24-h arterial BP and arterial stiffness (per five-unit increase in oxygen desaturation index, β = 1.30 [95% CI, 0.02-2.54; P = .04] vs 0.22 [95% CI, 0.03-0.40; P = .02] in women with vs without OSA, respectively).

CONCLUSIONS:  OSA is common, underdiagnosed, and independently associated with high BP and increased arterial stiffness in perimenopausal women.

Figures in this Article

Despite improvements in the awareness, treatment, and prevention of cardiovascular disease in women, deaths resulting from cardiovascular diseases in this group are still highly prevalent.1 For instance, it was estimated that cardiovascular disease caused approximately one death per minute among women in the United States in 2007.1 This is particularly true for women in perimenopause, a physiologic process characterized by age-related changes in the female organism associated with reduced estrogen production and increased cardiovascular risk.2 Because hormone replacement therapy is not associated with a reduction in cardiovascular risk,3 the only means of improving prognosis in this population is by adequate diagnosis and control of known and emerging cardiovascular risk factors.

OSA is characterized by repetitive episodes of upper airway obstruction promoting intermittent hypoxia and disrupted sleep.4 OSA is a common condition in the general population regardless of sex,5,6 with a higher prevalence with increasing age. There is growing evidence that OSA independently contributes to poor cardiovascular outcome.7 OSA is independently associated with several cardiovascular diseases, such as hypertension, atherosclerosis, and heart remodeling.8 Moreover, its effects on the occurrence of cardiac remodeling and vascular injury are additive to those of hypertension.9 Severe OSA and hypertension are associated with arterial stiffness, a strong predictor of cardiovascular morbidity and mortality,10,11 and heart structure abnormalities of similar magnitude, with additive effects when both conditions coexist.12

Most studies have included predominantly middle-age men, so the association of OSA and cardiovascular disease in women remains controversial. Although one study demonstrated that OSA was associated with an increased risk of myocardial infarction in men but not women,13 observational data demonstrated that severe and untreated OSA is associated with a 3.5-fold increased mortality among women.14 Thus, we hypothesized that OSA is common and associated with increased BP and arterial stiffness in perimenopausal women.

Subjects

We recruited 304 consecutive women aged 45 to 65 years with menstrual irregularity (amenorrhea > 60 days)15 from two primary care gynecologic clinics between May 2011 and June 2012. Patients who had a hysterectomy were included if they presented follicle-stimulating hormone (FSH) levels > 35 mIU/mL.15 We excluded from the study women with a history of smoking in the past 5 years, use of hormone replacement therapy, heart failure symptoms, prior coronary disease, or stroke. All participants underwent specific evaluations in the morning after the sleep study. The local ethics committee approved the protocol (Complexo Hospitalar, Hospital Universitário Oswaldo Cruz, Universidade de Pernambuco/PROCAPE, approval no. CAAE-0135.0.106.000-10), and all participants gave written informed consent.

Blood Samples

All samples were collected from venous blood in the early morning (7:00-9:00 am) after 12 h of fasting for measurement of glucose, total cholesterol, low-density lipoprotein, high-density lipoprotein, serum creatinine, and FSH levels according to standard protocols.

Office BP

BP was measured after 5 min of rest. The mean of two readings obtained at 5-min intervals with an automatic digital sphygmomanometer (Omron BP742) was used in the analysis.16 The same procedure was used to measure BP during pulse wave velocity (PWV) analysis.

24-H Ambulatory BP Monitoring

Twenty-four-hour ambulatory BP monitoring (ABPM) was evaluated using a Spacelabs Healthcare model 90207 device. BP was measured every 10 min during the day and every 20 min during the night with an appropriate cuff placed on the nondominant arm. Participants were instructed to perform their ordinary daily activities and not to move their arm during the measurement. Bedtime and time of awakening were recorded in diaries; thus, data are based on 24-h ABPM using actual sleep and wake times recorded by participants and not arbitrary preset times as previously described.17 Patients were classified as having normal awake BP if the corresponding value was < 135 mm Hg systolic and < 85 mm Hg diastolic. The normal sleep BP was considered to be < 120/70 mm Hg.18 The normal BP dip was defined separately for systolic and diastolic BP as a ≥ 10% reduction in BP during sleep compared with the awake period. Nondipping was defined as a decrease of < 10%.

PWV Measurement

With participants lying supine, PWV was measured by the foot-to-foot velocity method with the previously validated Complior SP system (Artech Medical)19 in the same week of the other examinations. Waveforms were obtained transcutaneously using the right-side common carotid and femoral arteries simultaneously during a minimum period of 10 to 15 s. Time delay (t) in seconds was measured between the two waveforms, and the distance (D) in meters covered by the waves was measured directly between the femoral recording site and the suprasternal notch. PWV was calculated as D/t. Three consecutive readings were obtained, and the PWV is reported as the mean of those readings.

Sleep Evaluation

All patients underwent a portable overnight sleep recording in the sleep laboratory using a validated device20 (Resmed Embletta PDS; Medcare). Oxygen saturation, body position, airflow (pressure cannula), and rib cage and abdominal movements during breathing using impedance belts were measured. Apnea was defined as a total absence of oronasal flow for ≥ 10 s and hypopnea as a clear decrease (> 30%) in amplitude of oronasal flow for ≥ 10 s followed by a 4% desaturation.21 The apnea-hypopnea index (AHI) was calculated by dividing the total number of apneas and hypopneas by total time in bed. OSA and moderate to severe OSA were defined as AHI ≥ 5 events/h and AHI ≥ 15 events/h, respectively. The oxygen desaturation index (ODI) was calculated as the total number of desaturations divided by the total time in bed. In addition, subjective daytime sleepiness was evaluated using the Epworth Sleepiness Scale. A total score > 10 was considered excessive daytime sleepiness.22

Statistical Analysis

Continuous variables are expressed as mean ± SD or median (interquartile range [IQR]) as appropriate. Qualitative variables are expressed as percentages. A two-tailed unpaired t test or Mann-Whitney U test for independent samples was used to compare variables between patients without and with OSA when appropriate. χ2 Test was used for qualitative variables. One-way analysis of variance or Kruskal-Wallis test was used to compare variables among patients without OSA, with mild OSA, and with moderate to severe OSA. When necessary, post hoc tests were performed to identify differences between subgroups. All subgroup analyses were performed using Bonferroni correction to adjust for multiple comparisons. Univariate and multivariable linear regression models were used to estimate the association of sleep parameters derived from sleep studies with BP and PWV. The multivariable models were adjusted for known confounders from the literature,12 including age, diabetes, BMI, family history of hypertension, and hypertension and dyslipidemia drug therapy for the BP analysis and mean BP, age, hypertension, diabetes, and BMI for the PWV analysis. Data were analyzed with SPSS, version 17.0 (IBM) and Stata 12.0 (StataCorp LP) statistical software. A two-sided P < .05 was considered significant.

From the initially screened population of 304 women, 26 refused to participate, and 21 had a poor-quality biologic signal during the sleep study (oximeter or impedance belt problems). Of these 21, 20 repeated the sleep study, and one was excluded due to another inadequate sleep study (oximeter malfunction). The final sample was 277 participants. The participants were predominantly middle-aged and overweight (Table 1). OSA (AHI ≥ 5 events/h) and moderate to severe OSA (AHI ≥ 15 events/h) were diagnosed in 111 (40.1%) and 31 (11.1%), respectively. None of the participants had received a previous diagnosis of OSA. The anthropometrics and clinical characteristics of the entire sample as well as according to the absence or presence of OSA are summarized in Table 1. Compared with participants without OSA, those with OSA were older and more obese. The lipid profile and glucose, creatinine, and FSH levels of participants with and without OSA were similar (Table 2).

Table Graphic Jump Location
TABLE 1  ] Baseline Anthropometrics and Clinical Characteristics

Data are presented as median (interquartile range), mean ± SD, or No. (%).

a 

Based on National Cholesterol Education Program, Adult Treatment Panel III.

Table Graphic Jump Location
TABLE 2  ] Baseline Laboratory and Sleep Study Characteristics

Data are presented as median (interquartile range). AHI = apnea-hypopnea index; FSH = follicle-stimulating hormone; HDL = high-density lipoprotein; LDL = low-density lipoprotein; ODI = oxygen desaturation index; Sao2 = arterial oxygen saturation.

Participants with moderate to severe OSA had higher 24-h ABPM than those without OSA (systolic awake BP, 133 [IQR, 125-142] mm Hg vs 126 [IQR, 119-134] mm Hg [P < .01]; diastolic awake BP, 82 [IQR, 78 -88] mm Hg vs 79 [IQR, 74-85] mm Hg [P = .07]; nocturnal systolic BP, 125 [IQR, 118-135] mm Hg vs 115 [IQR, 109-124] mm Hg [P < .01]; nocturnal diastolic BP, 73 [IQR, 69-79] mm Hg vs 69 [IQR, 62-75] mm Hg [P < .01]) (Fig 1). The proportion of abnormal systolic and diastolic nocturnal BP dipping among women with and without moderate to severe OSA was similar for systolic BP (74% vs 67%, P = .34), and diastolic BP (48% vs 38%, P = .09, respectively). The AHI and ODI were independently and positively associated with 24-h systolic arterial BP in the multivariate analysis (Table 3).

Figure Jump LinkFigure 1  Twenty-four-hour ambulatory BP monitoring according to the presence and absence of OSA. Data are presented as mean ± SD.Grahic Jump Location
Table Graphic Jump Location
TABLE 3  ] Univariate and Multivariate Linear Regression of Sleep Measures and 24-H Systolic Arterial BP

Each multivariable model is adjusted for age, diabetes, BMI, family history of hypertension, and hypertension and dyslipidemia drug therapy.

Spo2 = oxygen saturation as measured by pulse oximetry. See Table 2 legend for expansion of other abbreviations.

Although PWV was significantly higher in participants with moderate to severe OSA (Fig 2), AHI and desaturation variables were not associated with PWV. Only ODI was independently associated with PWV when adjusted for known confounders (Table 4).

Figure Jump LinkFigure 2  Pulse wave velocity according to OSA severity. Mod = moderate.Grahic Jump Location
Table Graphic Jump Location
TABLE 4  ] Univariate and Multivariate Linear Regression of Sleep Measures and Pulse Wave Velocity

Each multivariable model is adjusted for mean BP, age, hypertension, diabetes, and BMI. See Table 2 and 3 legends for expansion of abbreviations.

To our knowledge, this study is the first to specifically evaluate the potential vascular consequences of OSA in consecutive perimenopausal women. We were able to identify a number of important novel findings. First, although OSA was present in more than one-third of the sample, none of the participants had received a previous diagnosis of OSA, suggesting the low awareness of OSA in this population. Second, women with moderate to severe OSA were more likely to be hypertensive, use more medications to reduce BP, and have higher awake and nocturnal BP and increased arterial stiffness. Finally, the OSA severity was independently associated with increased BP and arterial stiffness. These findings suggest that OSA is common and may contribute to poor cardiovascular outcome among perimenopausal women.

OSA has been considered to be predominantly a disease of obese middle-aged men, and it is generally accepted that the disorder is twice as common in men as in women.6 An ominous trend is the ongoing increase in average body weight, with nearly two of every three US women aged > 20 years being overweight or obese.2 The rise in obesity is a key contributor to the burgeoning epidemic of OSA among men, whereas increasing age is the main risk factor among women,6 and the perimenopause period marks this increase in OSA diagnosis.23 Several studies have attempted to explain the male predominance in OSA prevalence, including differences in the anatomic size of the airway,24 greater collapsibility of the upper airway,25 and greater increase in upper airway resistance in men26 and hormonal changes in women.27,28 In addition to the fact that OSA is more prevalent and well recognized among men,29 the Wisconsin Sleep Cohort Study estimated that OSA was undiagnosed in > 90% of women with moderate to severe OSA.30 One reason for this underdiagnosis may be a lack of daytime somnolence, as indicated by the relatively low Epworth Sleepiness Scale scores in the present sample. This symptom, one of the main reasons for referral to sleep laboratories to rule out OSA, was not a predictor of OSA in the present study or in a hypertensive population.31 Because few studies have specifically investigated the association between OSA and cardiovascular risk in women,14,32 the knowledge in this field comes mainly from studies conducted predominantly or exclusively in men.33,34 Although, these findings may not apply to women because women may have a different cardiovascular risk profile associated with OSA,35 the present study shows that OSA is associated with increased daytime and nocturnal BP among climacteric women. OSA is a well-known cause of secondary hypertension, and CPAP therapy has been shown to decrease BP in patients with prehypertension and masked hypertension,36 hypertension,37 and resistant hypertension,38 although most data are derived from studies predominantly in men. The present study extends previous findings by showing an association between moderate to severe OSA with markers of poor cardiovascular outcome in perimenopausal women. Interestingly, there was no association between abnormal nocturnal BP dipping with OSA in this study. These results are similar to those observed in patients with resistant hypertension.39

PWV, a validated measure of arterial stiffness, is an important predictor of cardiovascular events.40 The present study demonstrates an association between OSA severity and PWV, even after adjustment for known confounders. Several factors contribute to changes in arterial stiffness, such as age, sex, mean BP, and BMI.41 In this study, we adjusted the PWV values for the known covariates associated to PWV (mean BP, age, hypertension, diabetes, and BMI). It is difficult, however, to completely exclude some residual factors in the observed results. A systematic review of factors associated with PWV concluded that the traditional cardiovascular risk factors, with the exception of BP and age, are poorly correlated with PWV.37 Among the 54 studies included, only a few reported small, positive, and independent associations between PWV and BMI, and only one evaluated OSA as an independent contributor to PWV.37 The positive and independent relationship between PWV and ODI in the present study stresses the importance of OSA in perimenopause and raises the possibility of new targets to decrease cardiovascular risk among women.

Strengths of this study include recruiting from a large non-sleep clinic population. Previous studies42,43 have recruited from sleep clinic populations, which biases toward a larger number of OSA diagnoses. A further strength is the use of gold standard techniques to assess hypertension (ABPM) and arterial stiffness (PWV).

The study also has several potential limitations. First, we used a four-channel recording device that does not measure sleep; thus, the measurements of AHI were based on total recording time rather than on total sleep time, although, this device has been validated against full polysomnography.20 Moreover, using an easier-to-perform test in populations with a high prevalence of OSA increases the feasibility of implementing the findings in clinical practice. Second, because of the cross-sectional nature of the present study, we cannot infer any causality other than an association between OSA and cardiovascular parameters. Third, because we included consecutive patients, it is not surprising that patients with OSA were older and heavier. These potential confounders may help to explain the worst cardiovascular profile among women with OSA. However, arterial BP and PWV were independently associated with OSA severity in multivariate analysis after carefully controlling for several variables.

This study demonstrates that OSA is common, underdiagnosed, and may contribute to cardiovascular risk in perimenopausal women. Efforts to increase recognition and treatment of OSA in perimenopausal women may help to reduce their cardiovascular risk, although more evidence is necessary to support a systematic evaluation of OSA in this population.

Author contributions: R. P. P. had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. R. P. P, I. M. L. B., M. N. L. F., and L. O. B. F. C. contributed to the study design; R. P. P., I. M. L. B., A. K. L. M., L. L. C., T. C. L., M. M. B. C., and L. O. B. F. C. contributed to data collection; R. P. P., L. F. D., M. S. B., and G. L.-F. contributed to data analysis; R. P. P., L. F. D., M. S. B., and G. L.-F. contributed to the drafting of the manuscript; and I. M. L. B., A. K. L. M., L. L. C., T. C. L., M. M. B. C., M. N. L. F., and L. O. B. F. C. contributed to the revision of the manuscript.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Role of sponsors: The sponsor had no role in the design of the study, the collection and analysis of the data, or the preparation of the manuscript.

ABPM

ambulatory BP monitoring

AHI

apnea-hypopnea index

FSH

follicle-stimulating hormone

IQR

interquartile range

ODI

oxygen desaturation index

PWV

pulse wave velocity

Roger VL, Go AS, Lloyd-Jones DM, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2011 update: a report from the American Heart Association. Circulation. 2011;123(4):e18-e209. [CrossRef] [PubMed]
 
Mosca L, Benjamin EJ, Berra K, et al. Effectiveness-based guidelines for the prevention of cardiovascular disease in women—2011 update: a guideline from the American Heart Association. Circulation. 2011;123(11):1243-1262. [CrossRef] [PubMed]
 
Manson JE, Hsia J, Johnson KC, et al; Women’s Health Initiative Investigators. Estrogen plus progestin and the risk of coronary heart disease. N Engl J Med. 2003;349(6):523-534. [CrossRef] [PubMed]
 
Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The report of an American Academy of Sleep Medicine Task Force. Sleep. 1999;22(5):667-689. [PubMed]
 
Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol. 2013;177(9):1006-1014. [CrossRef] [PubMed]
 
Tufik S, Santos-Silva R, Taddei JA, Bittencourt LR. Obstructive sleep apnea syndrome in the Sao Paulo Epidemiologic Sleep Study. Sleep Med. 2010;11(5):441-446. [CrossRef] [PubMed]
 
Kohler M, Stradling JR. Mechanisms of vascular damage in obstructive sleep apnea. Nat Rev Cardiol. 2010;7(12):677-685. [PubMed]
 
Drager LF, Togeiro SM, Polotsky VY, Lorenzi-Filho G. Obstructive sleep apnea: a cardiometabolic risk in obesity and the metabolic syndrome. J Am Coll Cardiol. 2013;62(7):569-576. [CrossRef] [PubMed]
 
Drager LF, Bortolotto LA, Krieger EM, Lorenzi-Filho G. Additive effects of obstructive sleep apnea and hypertension on early markers of carotid atherosclerosis. Hypertension. 2009;53(1):64-69. [CrossRef] [PubMed]
 
Laurent S, Boutouyrie P, Asmar R, et al. Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients. Hypertension. 2001;37(5):1236-1241. [CrossRef] [PubMed]
 
Mattace-Raso FU, van der Cammen TJ, Hofman A, et al. Arterial stiffness and risk of coronary heart disease and stroke: the Rotterdam Study. Circulation. 2006;113(5):657-663. [CrossRef] [PubMed]
 
Drager LF, Bortolotto LA, Figueiredo AC, Silva BC, Krieger EM, Lorenzi-Filho G. Obstructive sleep apnea, hypertension, and their interaction on arterial stiffness and heart remodeling. Chest. 2007;131(5):1379-1386. [CrossRef] [PubMed]
 
Gottlieb DJ, Yenokyan G, Newman AB, et al. Prospective study of obstructive sleep apnea and incident coronary heart disease and heart failure: the sleep heart health study. Circulation. 2010;122(4):352-360. [CrossRef] [PubMed]
 
Campos-Rodriguez F, Martinez-Garcia MA, de la Cruz-Moron I, Almeida-Gonzalez C, Catalan-Serra P, Montserrat JM. Cardiovascular mortality in women with obstructive sleep apnea with or without continuous positive airway pressure treatment: a cohort study. Ann Intern Med. 2012;156(2):115-122. [CrossRef] [PubMed]
 
Harlow SD, Gass M, Hall JE, et al; STRAW 10 Collaborative Group. Executive summary of the Stages of Reproductive Aging Workshop + 10: addressing the unfinished agenda of staging reproductive aging. Menopause. 2012;19(4):387-395. [CrossRef] [PubMed]
 
Chobanian AV, Bakris GL, Black HR, et al; National Heart, Lung, and Blood Institute Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National High Blood Pressure Education Program Coordinating Committee. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289(19):2560-2572. [CrossRef] [PubMed]
 
Drager LF, Diegues-Silva L, Diniz PM, et al. Obstructive sleep apnea, masked hypertension, and arterial stiffness in men. Am J Hypertens. 2010;23(3):249-254. [CrossRef] [PubMed]
 
Pickering TG, Hall JE, Appel LJ, et al. Recommendations for blood pressure measurement in humans and experimental animals: part 1: blood pressure measurement in humans: a statement for professionals from the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research. Circulation. 2005;111(5):697-716. [CrossRef] [PubMed]
 
Asmar R, Benetos A, Topouchian J, et al. Assessment of arterial distensibility by automatic pulse wave velocity measurement. Validation and clinical application studies. Hypertension. 1995;26(3):485-490. [CrossRef] [PubMed]
 
Ng SS, Chan TO, To KW, et al. Validation of Embletta portable diagnostic system for identifying patients with suspected obstructive sleep apnoea syndrome (OSAS). Respirology. 2010;15(2):336-342. [CrossRef] [PubMed]
 
Iber C, Ancoli-Israel S, Chesson A, et al. American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. Westchester, IL: American Academy of Sleep Medicine; 2007.
 
Johns MW. A new method for measuring daytime sleepiness: the Epworth Sleepiness Scale. Sleep. 1991;14(6):540-545. [PubMed]
 
Young T, Finn L, Austin D, Peterson A. Menopausal status and sleep-disordered breathing in the Wisconsin Sleep Cohort Study. Am J Respir Crit Care Med. 2003;167(9):1181-1185. [CrossRef] [PubMed]
 
Brooks LJ, Strohl KP. Size and mechanical properties of the pharynx in healthy men and women. Am Rev Respir Dis. 1992;146(6):1394-1397. [CrossRef] [PubMed]
 
Mohsenin V. Gender differences in the expression of sleep-disordered breathing: role of upper airway dimensions. Chest. 2001;120(5):1442-1447. [CrossRef] [PubMed]
 
Trinder J, Kay A, Kleiman J, Dunai J. Gender differences in airway resistance during sleep. J Appl Physiol (1985). 1997;83(6):1986-1997. [PubMed]
 
Bixler EO, Vgontzas AN, Lin HM, et al. Prevalence of sleep-disordered breathing in women: effects of gender. Am J Respir Crit Care Med. 2001;163(3):608-613. [CrossRef] [PubMed]
 
Fogel RB, Malhotra A, Pillar G, Pittman SD, Dunaif A, White DP. Increased prevalence of obstructive sleep apnea syndrome in obese women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2001;86(3):1175-1180. [PubMed]
 
Shepertycky MR, Banno K, Kryger MH. Differences between men and women in the clinical presentation of patients diagnosed with obstructive sleep apnea syndrome. Sleep. 2005;28(3):309-314. [PubMed]
 
Young T, Evans L, Finn L, Palta M. Estimation of the clinically diagnosed proportion of sleep apnea syndrome in middle-aged men and women. Sleep. 1997;20(9):705-706. [PubMed]
 
Drager LF, Genta PR, Pedrosa RP, et al. Characteristics and predictors of obstructive sleep apnea in patients with systemic hypertension. Am J Cardiol. 2010;105(8):1135-1139. [CrossRef] [PubMed]
 
Hermans MP, Ahn SA, Mahadeb YP, Rousseau MF. Sleep apnoea syndrome and 10-year cardiovascular risk in females with type 2 diabetes: relationship with insulin secretion and insulin resistance. Diabetes Metab Res Rev. 2013;29(3):227-234. [CrossRef] [PubMed]
 
Lavie P, Lavie L, Herer P. All-cause mortality in males with sleep apnoea syndrome: declining mortality rates with age. Eur Respir J. 2005;25(3):514-520. [CrossRef] [PubMed]
 
Punjabi NM, Caffo BS, Goodwin JL, et al. Sleep-disordered breathing and mortality: a prospective cohort study. PLoS Med. 2009;6(8):e1000132. [CrossRef] [PubMed]
 
Faulx MD, Larkin EK, Hoit BD, Aylor JE, Wright AT, Redline S. Sex influences endothelial function in sleep-disordered breathing. Sleep. 2004;27(6):1113-1120. [PubMed]
 
Drager LF, Pedrosa RP, Diniz PM, et al. The effects of continuous positive airway pressure on prehypertension and masked hypertension in men with severe obstructive sleep apnea. Hypertension. 2011;57(3):549-555. [CrossRef] [PubMed]
 
Bazzano LA, Khan Z, Reynolds K, He J. Effect of nocturnal nasal continuous positive airway pressure on blood pressure in obstructive sleep apnea. Hypertension. 2007;50(2):417-423. [CrossRef] [PubMed]
 
Pedrosa RP, Drager LF, de Paula LK, Amaro AC, Bortolotto LA, Lorenzi-Filho G. Effects of OSA treatment on BP in patients with resistant hypertension: a randomized trial. Chest. 2013;144(5):1487-1494. [CrossRef] [PubMed]
 
Pedrosa RP, Drager LF, Gonzaga CC, et al. Obstructive sleep apnea: the most common secondary cause of hypertension associated with resistant hypertension. Hypertension. 2011;58(5):811-817. [CrossRef] [PubMed]
 
Cecelja M, Chowienczyk P. Dissociation of aortic pulse wave velocity with risk factors for cardiovascular disease other than hypertension: a systematic review. Hypertension. 2009;54(6):1328-1336. [CrossRef] [PubMed]
 
de Lima Santos PC, Alvim Rde O, Ferreira NE, et al. Ethnicity and arterial stiffness in Brazil. Am J Hypertens. 2011;24(3):278-284. [CrossRef] [PubMed]
 
Barreiro B, Garcia L, Lozano L, et al. Obstructive sleep apnea and metabolic syndrome in Spanish population. Open Respir Med J. 2013;7:71-76. [CrossRef] [PubMed]
 
Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V. Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med. 2005;353(19):2034-2041. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1  Twenty-four-hour ambulatory BP monitoring according to the presence and absence of OSA. Data are presented as mean ± SD.Grahic Jump Location
Figure Jump LinkFigure 2  Pulse wave velocity according to OSA severity. Mod = moderate.Grahic Jump Location

Tables

Table Graphic Jump Location
TABLE 1  ] Baseline Anthropometrics and Clinical Characteristics

Data are presented as median (interquartile range), mean ± SD, or No. (%).

a 

Based on National Cholesterol Education Program, Adult Treatment Panel III.

Table Graphic Jump Location
TABLE 2  ] Baseline Laboratory and Sleep Study Characteristics

Data are presented as median (interquartile range). AHI = apnea-hypopnea index; FSH = follicle-stimulating hormone; HDL = high-density lipoprotein; LDL = low-density lipoprotein; ODI = oxygen desaturation index; Sao2 = arterial oxygen saturation.

Table Graphic Jump Location
TABLE 3  ] Univariate and Multivariate Linear Regression of Sleep Measures and 24-H Systolic Arterial BP

Each multivariable model is adjusted for age, diabetes, BMI, family history of hypertension, and hypertension and dyslipidemia drug therapy.

Spo2 = oxygen saturation as measured by pulse oximetry. See Table 2 legend for expansion of other abbreviations.

Table Graphic Jump Location
TABLE 4  ] Univariate and Multivariate Linear Regression of Sleep Measures and Pulse Wave Velocity

Each multivariable model is adjusted for mean BP, age, hypertension, diabetes, and BMI. See Table 2 and 3 legends for expansion of abbreviations.

References

Roger VL, Go AS, Lloyd-Jones DM, et al; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2011 update: a report from the American Heart Association. Circulation. 2011;123(4):e18-e209. [CrossRef] [PubMed]
 
Mosca L, Benjamin EJ, Berra K, et al. Effectiveness-based guidelines for the prevention of cardiovascular disease in women—2011 update: a guideline from the American Heart Association. Circulation. 2011;123(11):1243-1262. [CrossRef] [PubMed]
 
Manson JE, Hsia J, Johnson KC, et al; Women’s Health Initiative Investigators. Estrogen plus progestin and the risk of coronary heart disease. N Engl J Med. 2003;349(6):523-534. [CrossRef] [PubMed]
 
Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The report of an American Academy of Sleep Medicine Task Force. Sleep. 1999;22(5):667-689. [PubMed]
 
Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol. 2013;177(9):1006-1014. [CrossRef] [PubMed]
 
Tufik S, Santos-Silva R, Taddei JA, Bittencourt LR. Obstructive sleep apnea syndrome in the Sao Paulo Epidemiologic Sleep Study. Sleep Med. 2010;11(5):441-446. [CrossRef] [PubMed]
 
Kohler M, Stradling JR. Mechanisms of vascular damage in obstructive sleep apnea. Nat Rev Cardiol. 2010;7(12):677-685. [PubMed]
 
Drager LF, Togeiro SM, Polotsky VY, Lorenzi-Filho G. Obstructive sleep apnea: a cardiometabolic risk in obesity and the metabolic syndrome. J Am Coll Cardiol. 2013;62(7):569-576. [CrossRef] [PubMed]
 
Drager LF, Bortolotto LA, Krieger EM, Lorenzi-Filho G. Additive effects of obstructive sleep apnea and hypertension on early markers of carotid atherosclerosis. Hypertension. 2009;53(1):64-69. [CrossRef] [PubMed]
 
Laurent S, Boutouyrie P, Asmar R, et al. Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients. Hypertension. 2001;37(5):1236-1241. [CrossRef] [PubMed]
 
Mattace-Raso FU, van der Cammen TJ, Hofman A, et al. Arterial stiffness and risk of coronary heart disease and stroke: the Rotterdam Study. Circulation. 2006;113(5):657-663. [CrossRef] [PubMed]
 
Drager LF, Bortolotto LA, Figueiredo AC, Silva BC, Krieger EM, Lorenzi-Filho G. Obstructive sleep apnea, hypertension, and their interaction on arterial stiffness and heart remodeling. Chest. 2007;131(5):1379-1386. [CrossRef] [PubMed]
 
Gottlieb DJ, Yenokyan G, Newman AB, et al. Prospective study of obstructive sleep apnea and incident coronary heart disease and heart failure: the sleep heart health study. Circulation. 2010;122(4):352-360. [CrossRef] [PubMed]
 
Campos-Rodriguez F, Martinez-Garcia MA, de la Cruz-Moron I, Almeida-Gonzalez C, Catalan-Serra P, Montserrat JM. Cardiovascular mortality in women with obstructive sleep apnea with or without continuous positive airway pressure treatment: a cohort study. Ann Intern Med. 2012;156(2):115-122. [CrossRef] [PubMed]
 
Harlow SD, Gass M, Hall JE, et al; STRAW 10 Collaborative Group. Executive summary of the Stages of Reproductive Aging Workshop + 10: addressing the unfinished agenda of staging reproductive aging. Menopause. 2012;19(4):387-395. [CrossRef] [PubMed]
 
Chobanian AV, Bakris GL, Black HR, et al; National Heart, Lung, and Blood Institute Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National High Blood Pressure Education Program Coordinating Committee. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289(19):2560-2572. [CrossRef] [PubMed]
 
Drager LF, Diegues-Silva L, Diniz PM, et al. Obstructive sleep apnea, masked hypertension, and arterial stiffness in men. Am J Hypertens. 2010;23(3):249-254. [CrossRef] [PubMed]
 
Pickering TG, Hall JE, Appel LJ, et al. Recommendations for blood pressure measurement in humans and experimental animals: part 1: blood pressure measurement in humans: a statement for professionals from the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research. Circulation. 2005;111(5):697-716. [CrossRef] [PubMed]
 
Asmar R, Benetos A, Topouchian J, et al. Assessment of arterial distensibility by automatic pulse wave velocity measurement. Validation and clinical application studies. Hypertension. 1995;26(3):485-490. [CrossRef] [PubMed]
 
Ng SS, Chan TO, To KW, et al. Validation of Embletta portable diagnostic system for identifying patients with suspected obstructive sleep apnoea syndrome (OSAS). Respirology. 2010;15(2):336-342. [CrossRef] [PubMed]
 
Iber C, Ancoli-Israel S, Chesson A, et al. American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. Westchester, IL: American Academy of Sleep Medicine; 2007.
 
Johns MW. A new method for measuring daytime sleepiness: the Epworth Sleepiness Scale. Sleep. 1991;14(6):540-545. [PubMed]
 
Young T, Finn L, Austin D, Peterson A. Menopausal status and sleep-disordered breathing in the Wisconsin Sleep Cohort Study. Am J Respir Crit Care Med. 2003;167(9):1181-1185. [CrossRef] [PubMed]
 
Brooks LJ, Strohl KP. Size and mechanical properties of the pharynx in healthy men and women. Am Rev Respir Dis. 1992;146(6):1394-1397. [CrossRef] [PubMed]
 
Mohsenin V. Gender differences in the expression of sleep-disordered breathing: role of upper airway dimensions. Chest. 2001;120(5):1442-1447. [CrossRef] [PubMed]
 
Trinder J, Kay A, Kleiman J, Dunai J. Gender differences in airway resistance during sleep. J Appl Physiol (1985). 1997;83(6):1986-1997. [PubMed]
 
Bixler EO, Vgontzas AN, Lin HM, et al. Prevalence of sleep-disordered breathing in women: effects of gender. Am J Respir Crit Care Med. 2001;163(3):608-613. [CrossRef] [PubMed]
 
Fogel RB, Malhotra A, Pillar G, Pittman SD, Dunaif A, White DP. Increased prevalence of obstructive sleep apnea syndrome in obese women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2001;86(3):1175-1180. [PubMed]
 
Shepertycky MR, Banno K, Kryger MH. Differences between men and women in the clinical presentation of patients diagnosed with obstructive sleep apnea syndrome. Sleep. 2005;28(3):309-314. [PubMed]
 
Young T, Evans L, Finn L, Palta M. Estimation of the clinically diagnosed proportion of sleep apnea syndrome in middle-aged men and women. Sleep. 1997;20(9):705-706. [PubMed]
 
Drager LF, Genta PR, Pedrosa RP, et al. Characteristics and predictors of obstructive sleep apnea in patients with systemic hypertension. Am J Cardiol. 2010;105(8):1135-1139. [CrossRef] [PubMed]
 
Hermans MP, Ahn SA, Mahadeb YP, Rousseau MF. Sleep apnoea syndrome and 10-year cardiovascular risk in females with type 2 diabetes: relationship with insulin secretion and insulin resistance. Diabetes Metab Res Rev. 2013;29(3):227-234. [CrossRef] [PubMed]
 
Lavie P, Lavie L, Herer P. All-cause mortality in males with sleep apnoea syndrome: declining mortality rates with age. Eur Respir J. 2005;25(3):514-520. [CrossRef] [PubMed]
 
Punjabi NM, Caffo BS, Goodwin JL, et al. Sleep-disordered breathing and mortality: a prospective cohort study. PLoS Med. 2009;6(8):e1000132. [CrossRef] [PubMed]
 
Faulx MD, Larkin EK, Hoit BD, Aylor JE, Wright AT, Redline S. Sex influences endothelial function in sleep-disordered breathing. Sleep. 2004;27(6):1113-1120. [PubMed]
 
Drager LF, Pedrosa RP, Diniz PM, et al. The effects of continuous positive airway pressure on prehypertension and masked hypertension in men with severe obstructive sleep apnea. Hypertension. 2011;57(3):549-555. [CrossRef] [PubMed]
 
Bazzano LA, Khan Z, Reynolds K, He J. Effect of nocturnal nasal continuous positive airway pressure on blood pressure in obstructive sleep apnea. Hypertension. 2007;50(2):417-423. [CrossRef] [PubMed]
 
Pedrosa RP, Drager LF, de Paula LK, Amaro AC, Bortolotto LA, Lorenzi-Filho G. Effects of OSA treatment on BP in patients with resistant hypertension: a randomized trial. Chest. 2013;144(5):1487-1494. [CrossRef] [PubMed]
 
Pedrosa RP, Drager LF, Gonzaga CC, et al. Obstructive sleep apnea: the most common secondary cause of hypertension associated with resistant hypertension. Hypertension. 2011;58(5):811-817. [CrossRef] [PubMed]
 
Cecelja M, Chowienczyk P. Dissociation of aortic pulse wave velocity with risk factors for cardiovascular disease other than hypertension: a systematic review. Hypertension. 2009;54(6):1328-1336. [CrossRef] [PubMed]
 
de Lima Santos PC, Alvim Rde O, Ferreira NE, et al. Ethnicity and arterial stiffness in Brazil. Am J Hypertens. 2011;24(3):278-284. [CrossRef] [PubMed]
 
Barreiro B, Garcia L, Lozano L, et al. Obstructive sleep apnea and metabolic syndrome in Spanish population. Open Respir Med J. 2013;7:71-76. [CrossRef] [PubMed]
 
Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V. Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med. 2005;353(19):2034-2041. [CrossRef] [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

Find Similar Articles
CHEST Journal Articles
PubMed Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543