Issue Navigator

Volume 15 No. 07
Earn CME
Accepted Papers

Scientific Investigations

Nondipping Nocturnal Blood Pressure Predicts Sleep Apnea in Patients With Hypertension

Sophie J. Crinion, PhD1,2; Silke Ryan, PhD1,2; Jana Kleinerova, MB, BCh1; Brian D. Kent, MB, BCh1,2; Joseph Gallagher, MB, BCh3; Mark Ledwidge, MD3; Kenneth McDonald, MD2,3; Walter T. McNicholas, MD1,2,4
1Department of Respiratory and Sleep Medicine, St. Vincent's University Hospital, Dublin, Ireland; 2School of Medicine, University College Dublin, Dublin, Ireland; 3Department of Cardiology, St. Michael's Hospital, Dublin, Ireland; 4First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China


Study Objectives:

Systemic hypertension is highly prevalent in obstructive sleep apnea (OSA) but there are limited data on OSA prevalence in cohorts with hypertension comparing dippers and nondippers. We investigated this relationship in a clinic-based cohort of patients with hypertension who were not screened for any pretest possibility of OSA.


A total of 100 patients with hypertension aged (mean ± SD) 58 ± 10 years, body mass index 30.5 ± 6.1 kg/m2, and Epworth Sleepiness Scale score 6 ± 4 were included. All underwent overnight attended sleep studies and 24-hour ambulatory blood pressure monitoring. The primary study end-point was OSA prevalence based on the standard criteria of apnea-hypopnea index (AHI) ≥ 15 events/h in patients with dipping and nondipping nocturnal blood pressure.


Results showed 10.5% of dippers and 43.5% of nondippers had an AHI ≥ 15 (chi-square P = .001). In univariate analysis, AHI correlated significantly with blood pressure dip (r = −.26, P < .05), as did ESS (r = −.28, P < .05). In linear regression, AHI predicted the magnitude of blood pressure dip (standardised β = −.288, P = .03), whereas age, body mass index, systolic blood pressure and diastolic blood pressure did not.


Patients with nondipping nocturnal blood pressure are at high risk of OSA, regardless of symptom profile, which supports the recommendation that such patients should be assessed for co-existing OSA.


Crinion SJ, Ryan S, Kleinerova J, Kent BD, Gallagher J, Ledwidge M, McDonald K, McNicholas WT. Nondipping nocturnal blood pressure predicts sleep apnea in patients with hypertension. J Clin Sleep Med. 2019;15(7):957–963.


Current Knowledge/Study Rationale: Although the strong association of hypertension with obstructive sleep apnea (OSA) is widely recognized, there are only limited data on OSA prevalence in hypertensive cohorts comparing dippers and nondippers. We investigated this relationship in a hypertension clinic-based cohort of patients who were not screened for any pretest possibility of OSA.

Study Impact: The study finds a four-fold higher prevalence of OSA in nondipping hypertensive patients compared to dippers, which indicates that these patients are at high risk of the disorder, regardless of symptoms. These data support the recommendation that nondipping hypertensive patients should be assessed for OSA.


Obstructive sleep apnea (OSA) is highly prevalent throughout the world and is increasingly recognized as an independent risk factor for a range of cardiovascular disorders.1,2 Systemic hypertension is common in newly diagnosed patients with OSA,3 as is OSA in patients with hypertension,4,5 which could be anticipated due to the spectrum of common risk factors for both disorders.2 Blood pressure (BP) normally follows a diurnal pattern in which the daytime mean is more than 10% higher than the night-time mean, with those achieving this normal nocturnal dip called dippers and those not, called nondippers. Hypertension and a nondipping BP pattern share many pathogenetic mechanisms, are both risk factors for future cardiovascular events,6 and are both especially common in patients with OSA.7,8 Importantly, OSA is a treatable cause of hypertension, and is the most prevalent secondary cause of resistant hypertension.9

Systemic hypertension affects about 26% of the adult world population with some variation in prevalence due to ethnicity, sex and lifestyle.10 More recently, 24-hour ambulatory blood pressure monitoring (ABPM) has become established as the optimal mode of assessing hypertension and its control11,12 and, with the increasing use of 24-hour BP monitoring in OSA, there has been growing recognition of the importance of a nondipping BP pattern in the disorder.13 Reports have indicated a dose response relationship between severity of OSA and nondipping BP in the Wisconsin Sleep Cohort study,14,15 and also in a cardiovascular clinic population.16 Furthermore, in patients with OSA, a nondipping BP profile has been associated with evidence of systemic inflammation,17 and cardiovascular events are also more frequent in patients with OSA with a nondipping BP profile.18

While there is extensive literature on the relationship between OSA and nondipping BP,13 there are few published data on the relationship between a nondipping BP profile and the prevalence of OSA in patients with systemic hypertension.19 Thus, the primary aim of this study was to determine the extent to which a nondipping BP status was associated with an increased prevalence of significant OSA, defined by the standard sleep-disordered breathing (SDB) criteria of an apneahypopnea index (AHI) ≥ 15 events/h as recommended by the American Academy of Sleep Medicine,20 in a clinical cohort of patients with established hypertension.


Patient Recruitment

Male participants with a clinician diagnosis of hypertension based on standard criteria were considered for enrolment to the study.21 Participants were consecutively recruited from two different sources; the blood pressure unit in St Michael's Hospital, Dun Laoghaire, Dublin, or two local general practitioner (GP) practices, with no clinical differences between the GP and hospital cohorts. Hospital hypertension clinic patients came from the STOP-HF project, which is a relatively non-select population in that they represent a primary care referral of patients with at least one cardiovascular risk factor.22 Suitability for participation required that the participants have a clinical diagnosis of hypertension and be aged between 18–70 years. Exclusion criteria included being outside the participation age window, history of stroke, or previous investigation or treatment for a sleep disorder. Recruitment procedures did not seek any clinical features to suggest the likelihood of OSA such as a history of snoring or daytime sleepiness, and participants were recruited consecutively from each of the recruitment sites. The study population was restricted to males because of concern that the sample size would be insufficient to account for possible sex differences in the association of OSA with hypertension.23 A total of 161 individuals were screened for inclusion of whom 24 did not fulfil the inclusion criteria, 6 had prior investigation for OSA, 28 declined to participate, and 2 failed to complete the study protocol after enrolment. Approval from the Ethics and Medical Research Committee of St Vincent's Healthcare Group was obtained prior to commencement of the study, and all participants provided written informed consent.

Sleep Studies

Following enrolment, all participants were admitted overnight to the sleep laboratory for an inpatient, attended cardiorespiratory polygraphy. At the time of the sleep study, self-reported sleepiness was assessed using the Epworth Sleepiness Scale (ESS),24 and current medication use was assessed by the lead investigator.

Hypopneas were defined using the 3% desaturation criterion.25

Ambulatory Blood Pressure Monitor

Participants underwent a 24-hour ambulatory blood pressure monitor (ABPM) measurement within four months of the cardio-respiratory polygraphy, with self-reported sleep and wake times at the time of monitoring used to calculate the average daytime and night time BP. The time interval between ABPM measurements and sleep studies (average 96 days) reflected the waiting period for sleep studies in our sleep center as patients were recruited for the study in the hypertension clinic and then placed on the waiting list for sleep studies in our sleep laboratory. BP was measured every fifteen minutes during daytime hours and at 20-minute intervals through the night. To calculate the BP dip (%), the difference between the daytime and night time mean systolic BP measurements (Δ) was divided by the mean daytime systolic BP using the following standard equation26:

A rise of night time BP was recorded as a negative percentage (%) dip value.


Participants underwent an Echocardiogram performed by a single trained technician using a Phillips iE33 Ultrasound Machine (Philips Healthcare, Andover, USA). Ejection fraction (EF) was calculated by dividing the stroke volume by the end-diastolic volume. Left atrial volume index (LAVI) was recorded as left atrial volume indexed to body surface area as a measure of left ventricular diastolic function. Finally, E/E' was measured as a ratio of peak velocity of blood flow through the mitral valve in early diastole (E) to the peak velocity of the mitral annulus (E') to assess the left ventricular filling pressure.

Statistical Analysis

Following 24-hour ABPM measurement, the study population was dichotomised according to BP dipping status into dippers and nondippers. The primary outcome measure was the prevalence of significant OSA in dippers and nondippers, defined according to the criteria of the American Academy of Sleep Medicine for SDB in isolation as an AHI ≥ 15 events/h.20 Secondary outcome measures were the prevalence of any OSA (AHI ≥ 5 events/h) and severe OSA (AHI ≥ 30 events/h) in dippers and nondippers, as well as the role of OSA in cardiac function (measured by brain natriuretic peptide [BNP] and echocardiography) in this cohort with hypertension.

The relationship between the BP dip and AHI and other anthropometric and clinical variables was examined using Pearson's correlation coefficient. Logistic regression was carried to determine the odds ratio (OR) of having clinically significant OSA (AHI ≥ 15 events/h) if a nondipping BP profile (< 10% nocturnal BP dip) was present. This was then adjusted for age and BMI, as well as systolic and diastolic BP in subsequent models. Linear regression analysis was also performed comparing SDB with nocturnal dipping as continuous variables.


Patient Characteristics

One hundred patients were studied with a mean age of 58 ± 10 years and BMI of 30.5 ± 6.1 kg/m2. The mean ESS score in the cohort was 6 ± 4. The mean BP dip of the cohort was 8.2 ± 7.4% with 38 (38%) classified as dippers, and 62 (62%) classified as nondippers. Mean BP dip in the dippers and nondippers was 15.7 ± 4.0% and 3.5 ± 4.7% respectively. The mean AHI among the dippers was 9.1 ± 10.8 events/h and 16.9 ± 17.9 events/h among the nondippers. Patient characteristics are demonstrated in Table 1.

Patient characteristics stratified by blood pressure dipping status.


table icon
Table 1

Patient characteristics stratified by blood pressure dipping status.

(more ...)

Prevalence of Significant OSA in Nocturnal Dippers and Nondippers

Using the standard AHI threshold of ≥ 15 events/h for clinically significant OSA,20 10.5% of the dippers and 43.5% of the nondippers were positive (chi-square P = .001; Figure 1A). Using the lower threshold of AHI ≥ 5 events/h to identify participants with any OSA, 60.5% of the dippers and 71.0% of the nondippers were positive (chi-square P = .281). Severe OSA (based on an AHI ≥ 30 events/h) was identified in 2.6% of the dippers and 14.5% of the nondippers (chi-square P = .054) (Figure 1B).

Prevalence of OSA among dipper and nondipper participants with hypertension.

(A) Prevalence of significant OSA (AHI > 15 events/h) among dipper and nondipper participants with hypertension. (B) Prevalence of any SDB (AHI > 5 events/h) and severe OSA (AHI > 30 events/h) among dipper and nondipper participants with hypertension. Data are presented as percentage of cohort (%). * P = .054, ** P = .001. AHI = apnea-hypopnea index, OSA = obstructive sleep apnea, SDB = sleep-disordered breathing.


Figure 1

Prevalence of OSA among dipper and nondipper participants with hypertension.

(more ...)

We also evaluated relationships between oxygen desaturation measures and dipping status. These data indicate significantly higher oxygen desaturation index (ODI) and lower minimum saturation in nondippers with a trend towards higher values for time spent below 90% SaO2 (T < 90%) in nondippers (Table 1).

Relationship of Blood Pressure Dip With Clinical Variables

In this hypertensive cohort, BP dip showed a stronger relationship with OSA severity than any of the anthropometric or clinical variables. In univariate correlation analysis, BP dip correlated significantly with AHI (r = −.26, P = .01), ESS (r = −.28, P = .01) and age (r = −.262, P = .01). However, nonsignificant correlation with magnitude of BP dip (%) was seen with BMI and 24hr mean BP measurements. BP dip (%) also correlated significantly with ODI and minimum oxygen saturation with a trend towards significance for TST < 90% (Table 2).

Univariate correlations of BP dip (%) with OSA severity, anthropometric, demographic and clinical variables.


table icon
Table 2

Univariate correlations of BP dip (%) with OSA severity, anthropometric, demographic and clinical variables.

(more ...)

BP dip did not correlate with BNP or any echocardiographic measurements (Table 2). Stratification of the sample according to OSA severity was not feasible as there were only 4 participants with an AHI ≥ 15 events/h (out of 31 total) who were dippers. For the remaining 69 participants with AHI < 15 events/h, there was no difference in the BNP or echocardiographic measurements comparing dippers and nondippers.

Logistic regression was carried out to further clarify the relationship between a nondipping pattern and likelihood of clinically significant OSA. In the unadjusted model, having a nondipping BP profile increased the odds of having an AHI of ≥ 15 events/h (OR 4.72 [1.62–13.75], P = .001). This remained significant when age, BMI and systolic and diastolic BP were further added to the above model (model 2 and model 3, Table 3). The independent relationship between AHI and nondipping BP was further confirmed by linear regression analysis, which remained significant for % dip after adjustment for age and BMI (r = −.149 [−.262 to −.037], P = .010). Furthermore, partial correlation between AHI and % dip as linear variables demonstrated that AHI (adjusted for age and BMI) still correlated with %dip (r = −.263, P = .010).

Crude and adjusted odds ratios of AHI ≥ 15 events/h by presence of nondipping BP.


table icon
Table 3

Crude and adjusted odds ratios of AHI ≥ 15 events/h by presence of nondipping BP.

(more ...)

Within the subgroup of nondipping hypertensive participants, the presence of AHI ≥ 15 events/h did not significantly influence antihypertensive medication requirement (2.6 ± 1.2 versus 2.4 ± 1.1 medications in nondippers and dippers respectively, P = .539). Furthermore, there was no difference in the proportion of patients with resistant hypertension between dippers and nondippers in that 19% (12/62) of the nondippers had resistant hypertension and 18% (17/38) of the dippers had resistant hypertension based on the standard definition for resistant hypertension of 24-hour BP > 140/90 despite 3 antihypertensives or controlled but requiring > 3 antihypertensives.9 Indices of cardiac function based on echocardiography, including left ventricular ejection fraction, LAVI and E/E', showed no difference in the nondippers with and without significant OSA (data not shown).


The most interesting and important finding of this report is the substantially higher prevalence of OSA based on standard criteria in the nondipper group with hypertension, which represents a poorly explored area in cohorts with hypertension. As evidence of the pathophysiological consequences of OSA grows, the identification of patients at high risk of the disorder becomes more important. Given how common a nondipping profile is in cohorts with hypertension, identifying a high prevalence of OSA in this subgroup carries special clinical significance.

The BP dipping pattern is important in the risk stratification of patients with hypertension, and a nondipping pattern independently predicts cardiovascular events in those with no previous significant cardiovascular disease even after adjustment for 24-hour BP.6 Patients with hypertension, high nocturnal BP, and nondipping profile have more cardiovascular risk factors and evidence of current disease (including clinical evidence of cardiovascular disease and reduced renal function) than nocturnal dippers with hypertension, nocturnal dippers without hypertension and nondippers without hypertension.27 Thus, nondippers with hypertension represent a cohort with a particularly challenging cardiovascular risk profile. The presence of OSA is also recognized to carry a higher burden of cardiovascular risk,28 and the high prevalence of OSA in nondippers with hypertension may indicate a mechanism that could contribute to this compounded cardiovascular risk profile.

While a high frequency of nondipping BP status is established in cohorts with OSA, the difference in prevalence of OSA between dippers and nondippers in a cohort with hypertension has only been explored previously with small numbers. Portaluppi et al described an AHI > 10 events/h in 10 of 11 participants with a nondipping blood pressure pattern, confirmed with continuous blood pressure measurement using a Finapres device.29 Our data in a larger cohort of participants with hypertension and a nondipping BP profile shows a prevalence of significant OSA (AHI ≥ 15 events/h) of 42%, and a prevalence of 71% using an AHI cutoff level of ≥ 5 events/h. Our data are also in agreement with the recent report of Jenner and coauthors who found a higher prevalence of nondipping hypertension in a cohort of men and women with hypertension and OSA compared to those without OSA.19 Further to this observation of a significantly higher prevalence of significant OSA in nondippers, we also showed that the magnitude of nocturnal BP dip significantly correlated with the severity of OSA.

The mechanisms of hypertension in OSA are likely multifactorial and key factors relating to OSA that may promote nocturnal BP elevation include intermittent hypoxia and recurring micro-arousals from sleep.30,31 Our findings of a stronger association of nondipping status with ODI rather than TST < 90% supports the potential role of intermittent hypoxia in this relationship. Since we performed sleep studies by overnight cardiorespiratory polygraphy, we cannot comment on the potential role of recurring arousals in this patient cohort.

The present data support and confirm the high prevalence of OSA in a cohort with hypertension, with 67% of the total cohort having at least mild OSA (AHI ≥ 5 events/h). This prevalence figure is similar to previous reports showing a prevalence of 56% in one report and another showing a prevalence of 75.6%.4,32 A nondipping BP profile was found in 62% of our population being treated for hypertension, which is higher than that reported in some other reports.33 We recognize that patients attending a hospital-based clinic represent a selected population, but patients were referred to this hypertension clinic from primary care centers as part of an ongoing prospective cardiovascular project (STOP-HF) led by one of the present principal investigators (KMcD). The STOP-HF cohort is a relatively non-selected population in that they represent a primary care referral of patients with at least one cardiovascular risk factor.22 Furthermore, to broaden the selection process, we also included patients from a local primary care practice. However, the proportion of nondippers in our cohort compares more closely with results of the large Spanish Society of Hypertension Registry showing a nondipping prevalence of 53% in those being treated for hypertension.34 Furthermore, there was no difference in the proportion of patients with drug-rest hypertension between dippers and nondippers in our cohort.

A strength of this study is the recruitment of participants from multiple sources, reflecting a real-life sample of outpatient hypertensive patients. Of note is that there was minimal self-reported sleepiness based on the ESS questionnaire suggesting that these represent a cohort of asymptomatic patients who would otherwise have no reason to undergo testing for SDB. We included only male patients because of concern that the study sample size might not be enough to account for possible sex disparities in the relationships between OSA and hypertension. Previous reports have indicated that hypertension is more common in male patients with OSA than females.23

A limitation of the present study was the use of cardio-respiratory sleep studies instead of full polysomnography. However, these studies were performed inpatient in our sleep laboratory and were attended by a trained sleep physiologist. This was the best available testing modality given that these 100 participants were tested within the space and time constraints of a clinical sleep laboratory. Furthermore, cardiorespiratory polygraphy represents the most common modality of sleep studies in major European sleep centers. In any event, the use of cardiorespiratory polygraphy as the diagnostic test would likely have underestimated the prevalence of OSA when compared to full polysomnography.35

We included data on echocardiography and BNP to explore potential relationships between OSA, hypertension and cardiac function as a secondary outcome. Natriuretic peptide is a recognized biochemical marker of hypertensive heart disease.36 Our hypothesis in this respect was that co-existing OSA and hypertension (dipping and nondipping) may have greater detrimental effects on cardiac function compared to hypertension alone. However, the data indicate no difference in echocardiography variables or BNP between those patients with both OSA and hypertension compared to those with hypertension alone.

Given the very high prevalence of OSA reported in cohorts with hypertension,4,32 the presence of hypertension is gaining importance as an independent predictor of the presence of clinically significant OSA.30 Importantly, clinical variables including the presence of hypertension have been studied in clinical prediction models of OSA that may not include self-reported symptoms such as sleepiness.37 Thus, the increasing use of 24-hour ABPM measurements of blood pressure provides the opportunity to include the presence of nocturnal BP nondipping as an additional variable in the prediction of OSA. These data may complement other predictive data obtained from screening tools for OSA such as STOP-Bang.38

However, the finding of a nondipping BP profile in association with OSA does not necessarily imply that CPAP therapy is the treatment of choice, especially in non-sleepy patients, and adjustment of anti-hypertensive medications may be a more appropriate intervention depending on the clinical indication. This consideration is especially relevant as CPAP therapy alone results in relatively small reductions in BP levels in the region of 2 mmHg diastolic BP.39 While the present report is focused on OSA prevalence in a cross-sectional study, the findings should be viewed in the overall context of optimum BP control in a nondipping population with hypertension, which may involve adjustment of antihypertensive therapy with or without the addition of CPAP. The addition of CPAP to antihypertensive therapy may be especially relevant in patients with severe or drug-resistant hypertension and not surprisingly, benefits are most evident in treatment adherent patients.33,40,41


These data indicate that nondipping patients with hypertension should be screened for the presence of OSA, especially if other clinical features support this possibility, as clinically significant OSA is highly prevalent in patients with a nondip-ping nocturnal BP profile. These data further support the concept that dipping status may be a useful indicator of undetected OSA and may be a useful tool in the identification of populations who would benefit from screening for OSA.


All authors have seen and approved the manuscript. This study was supported by the Health Research Board (Ireland). Work for this study was performed in St. Vincent's University Hospital and University College Dublin, Dublin, Ireland. The authors report no conflicts of interest.



24-hour ambulatory blood pressure monitoring


apnea-hypopnea index


body mass index


blood pressure


ejection fraction


Epworth Sleepiness Scale


general practitioner


left atrial volume index


odds ratio


obstructive sleep apnea


sleep-disordered breathing


The authors thank Audrey Russell and the staff of the sleep laboratory at St. Vincent's University Hospital and the Hypertension Clinic at St. Michael's Hospital for their help in completing the study, and the patients who participated.



Lévy P, Kohler M, McNicholas WT, et al. Obstructive sleep apnoea syndrome. Nat Rev Dis Primers. 2015;1:15015[PubMed]


McNicholas WT, Bonsignore MR. Sleep apnoea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities. Eur Respir J. 2007;29(1):156–178. [PubMed]


Nieto FJ, Young TB, Lind BK, et al. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA. 2000;283(14):1829–1836. [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. [PubMed]


Worsnop CJ, Naughton MT, Barter CE, Morgan TO, Anderson AI, Pierce RJ. The prevalence of obstructive sleep apnea in hypertensives. Am J Respir Crit Care Med. 1998;157(1):111–115. [PubMed]


Fagard RH, Thijs L, Staessen JA, Clement DL, De Buyzere ML, De Bacquer DA. Night-day blood pressure ratio and dipping pattern as predictors of death and cardiovascular events in hypertension. J Hum Hypertens. 2009;23(10):645–653. [PubMed]


Loredo JS, Ancoli-Israel S, Dimsdale JE. Sleep quality and blood pressure dipping in obstructive sleep apnea. Am J Hypertens. 2001;14(9 Pt 1):887–892. [PubMed]


Ancoli-Israel S, Stepnowsky C, Dimsdale J, Marler M, Cohen-Zion M, Johnson S. The effect of race and sleep-disordered breathing on nocturnal BP “dipping”: analysis in an older population. Chest. 2002;122(4):1148–1155. [PubMed]


Calhoun DA, Jones D, Textor S, et al. Resistant hypertension: diagnosis, evaluation, and treatment: a scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research. Circulation. 2008;117(25):e510–e526. [PubMed]


Cutler JA, Sorlie PD, Wolz M, Thom T, Fields LE, Roccella EJ. Trends in hypertension prevalence, awareness, treatment, and control rates in United States adults between 1988-1994 and 1999-2004. Hypertension. 2008;52(5):818–827. [PubMed]


Kain HK, Hinman AT, Sokolow M. Arterial blood pressure measurements with a portable recorder in hypertensive patients. I. Variability and correlation with “casual” pressures. Circulation. 1964;30:882–892. [PubMed]


Hinman AT, Engel BT, Bickford AF. Portable blood pressure recorder. Accuracy and preliminary use in evaluating intradaily variations in pressure. Am Heart J. 1962;63:663–668. [PubMed]


Parati G, Lombardi C, Hedner J, et al. Recommendations for the management of patients with obstructive sleep apnoea and hypertension. Eur Respir J. 2013;41(3):523–538. [PubMed]


Hla KM, Young T, Finn L, Peppard PE, Szklo-Coxe M, Stubbs M. Longitudinal association of sleep-disordered breathing and nondipping of nocturnal blood pressure in the Wisconsin Sleep Cohort Study. Sleep. 2008;31(6):795–800. [PubMed Central][PubMed]


Mokhlesi B, Hagen EW, Finn LA, Hla KM, Carter JR, Peppard PE. Obstructive sleep apnoea during REM sleep and incident non-dipping of nocturnal blood pressure: a longitudinal analysis of the Wisconsin Sleep Cohort. Thorax. 2015;70(11):1062–1069. [PubMed]


Seif F, Patel SR, Walia HK, et al. Obstructive sleep apnea and diurnal nondipping hemodynamic indices in patients at increased cardiovascular risk. J Hypertens. 2014;32(2):267–275. [PubMed Central][PubMed]


Sarinc Ulasli S, Sarıaydın M, Gunay E, et al. Effects of nondipping pattern on systemic inflammation in obstructive sleep apnea. Sleep Breath. 2015;19(4):1185–1190. [PubMed]


Sasaki N, Ozono R, Edahiro Y, et al. Impact of non-dipping on cardiovascular outcomes in patients with obstructive sleep apnea syndrome. Clin Exp Hypertens. 2015;37(6):449–453. [PubMed]


Jenner R, Fatureto-Borges F, Costa-Hong V, et al. Association of obstructive sleep apnea with arterial stiffness and nondipping blood pressure in patients with hypertension. J Clin Hypertens (Greenwich). 2017;19(9):910–918


Epstein LJ, Kristo D, Strollo PJ Jr, et al. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med. 2009;5(3):263–276. [PubMed Central][PubMed]


Chobanian AV, Bakris GL, Black HR, et al. 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):2560–2571. [PubMed]


Murtagh G, Dawkins IR, O'Connell R, et al. Screening to prevent heart failure (STOP-HF): expanding the focus beyond asymptomatic left ventricular systolic dysfunction. Eur J Heart Fail. 2012;14(5):480–486. [PubMed]


Cano-Pumarega I, Barbé F, Esteban A, et al. Sleep apnea and hypertension: are there sex differences? The Vitoria Sleep Cohort. Chest. 2017;152(4):742–750. [PubMed]


Johns MW. A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep. 1991;14(6):540–545. [PubMed]


Berry RB, Budhiraja R, Gottlieb DJ, et al. Rules for scoring respiratory events in sleep: update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events. J Clin Sleep Med. 2012;8(5):597–619. [PubMed Central][PubMed]


Bloomfield D, Park A. Night time blood pressure dip. World J Cardiol. 2015;7(7):373–376. [PubMed Central][PubMed]


de la Sierra A, Gorostidi M, Banegas JR, Segura J, de la Cruz JJ, Ruilope LM. Nocturnal hypertension or nondipping: which is better associated with the cardiovascular risk profile? Am J Hypertens. 2014;27(5):680–687. [PubMed]


Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet. 2005;365(9464):1046–1053. [PubMed]


Portaluppi F, Provini F, Cortelli P, et al. Undiagnosed sleep-disordered breathing among male nondippers with essential hypertension. J Hypertens. 1997;15(11):1227–1233. [PubMed]


Crinion SJ, Ryan S, McNicholas WT. Obstructive sleep apnoea as a cause of nocturnal nondipping blood pressure: recent evidence regarding clinical importance and underlying mechanisms. Eur Respir J. 2017;49(1):1601818[PubMed]


Tkacova R, McNicholas WT, Javorsky M, et al. Nocturnal intermittent hypoxia predicts prevalent hypertension in the European Sleep Apnoea Database cohort study. Eur Respir J. 2014;44(4):931–941. [PubMed]


Min HJ, Cho YJ, Kim CH, et al. Clinical features of obstructive sleep apnea that determine its high prevalence in resistant hypertension. Yonsei Med J. 2015;56(5):1258–1265. [PubMed Central][PubMed]


Martinez-Garcia MA, Capote F, Campos-Rodriguez F, et al. Effect of CPAP on blood pressure in patients with obstructive sleep apnea and resistant hypertension: the HIPARCO randomized clinical trial. JAMA. 2013;310(22):2407–2415. [PubMed]


de la Sierra A, Redon J, Banegas JR, et al. Prevalence and factors associated with circadian blood pressure patterns in hypertensive patients. Hypertension. 2009;53(3):466–472. [PubMed]


Escourrou P, Grote L, Penzel T, et al. The diagnostic method has a strong influence on classification of obstructive sleep apnea. J Sleep Res. 2015;24(6):730–738. [PubMed]


Sarzani R, Spannella F, Giulietti F, Balietti P, Cocci G, Bordicchia M. Cardiac natriuretic peptides, hypertension and cardiovascular risk. High Blood Press Cardiovasc Prev. 2017;24(2):115–126. [PubMed Central][PubMed]


Ustun B, Westover MB, Rudin C, Bianchi MT. Clinical prediction models for sleep apnea: the importance of medical history over symptoms. J Clin Sleep Med. 2016;12(2):161–168. [PubMed Central][PubMed]


Chung F, Abdullah HR, Liao P. STOP-Bang questionnaire: a practical approach to screen for obstructive sleep apnea. Chest. 2016;149(3):631–638. [PubMed]


Bratton DJ, Gaisl T, Wons AM, Kohler M. CPAP vs mandibular advancement devices and blood pressure in patients with obstructive sleep apnea: a systematic review and meta-analysis. JAMA. 2015;314(21):2280–2293. [PubMed]


Pepin JL, Tamisier R, Barone-Rochette G, Launois SH, Levy P, Baguet JP. Comparison of continuous positive airway pressure and valsartan in hypertensive patients with sleep apnea. Am J Respir Crit Care Med. 2010;182(7):954–960. [PubMed]


Thunstrom E, Manhem K, Rosengren A, Peker Y. Blood pressure response to losartan and continuous positive airway pressure in hypertension and obstructive sleep apnea. Am J Respir Crit Care Med. 2016;193(3):310–320. [PubMed]