Full Terms & Conditions of access and use can be found athttp://www.tandfonline.com/action/journalInformation?journalCode=iceh20

Download by: [UC Santa Barbara Library] Date: 08 September 2017, At: 12:57

Clinical and Experimental Hypertension

ISSN: 1064-1963 (Print) 1525-6006 (Online) Journal homepage: http://www.tandfonline.com/loi/iceh20

Prevalence of sleep apnea and cardiovascularrisk factors in patients with hypertension in a dayhospital model

Eduardo Borsini , Magalí Blanco, Martín Bosio, Marcela Schrappe, GlendaErnst, Daniela Nosetto, Nazarena Gaggioli, Alejandro Salvado, OsvaldoManuale & Miguel Schiavone

To cite this article: Eduardo Borsini , Magalí Blanco, Martín Bosio, Marcela Schrappe, GlendaErnst, Daniela Nosetto, Nazarena Gaggioli, Alejandro Salvado, Osvaldo Manuale & MiguelSchiavone (2017): Prevalence of sleep apnea and cardiovascular risk factors in patientswith hypertension in a day hospital model, Clinical and Experimental Hypertension, DOI:10.1080/10641963.2017.1356841

To link to this article: http://dx.doi.org/10.1080/10641963.2017.1356841

Published online: 05 Sep 2017.

Submit your article to this journal

Article views: 4

View related articles

View Crossmark data

Prevalence of sleep apnea and cardiovascular risk factors in patients withhypertension in a day hospital modelEduardo Borsini a,b, Magalí Blancoa, Martín Bosioc, Marcela Schrappec, Glenda Ernsta,b, Daniela Nosettoc,Nazarena Gaggiolia, Alejandro Salvadoa, Osvaldo Manualec, and Miguel Schiavonec

aRespiratory Medicine Service, Hospital Británico, Buenos Aires, Argentina; bArgentine Research Group for Sleep Apnea (GAIAS), Buenos Aires,Argentina; cHypertension Section, Cardiology Service, Hospital Británico, Buenos Aires, Argentina

ABSTRACTIntroduction: To identify patients at risk for obstructive sleep apnea (OSA) syndrome at a specializedhypertension center, we administered questionnaires and used respiratory polygraphy (RP). Results: Westudied 168 patients (64.8% men and 35.2% women). Patients’ body mass index (BMI) was 34.7 ± 6.79and Epworth Sleepiness Scale (ESS) scores were 8.01 for male and 8.92 for women (p = 0.69). RPrecordings revealed AHI (Apnea-Hypopnea Index) of 18.03 ± 15.7, an ODI (Oxygen Desaturation Index)of 18.6 ± 15.2, and a time oxygen saturation <90% (%) of 20.8 ± 24.3. Around 44% of patients had an AHIof >15 events/h, and continuous positive airway pressure (CPAP) was recommended to 69 patients(41.07%). Pulse wave velocity (PWV) showed high values in AHI > 15/h (p = 0.050), and carotid intima-media thickness (IMT) did not correlate with AHI > 15; right IMT: 0.83 ± 1.3 versus 0.78 ± 0.13 mm(p = 0.41) and 0.82 ± 0.16 versus 0.78 ± 0.19 mm (p = 0.40). However, we find correlation with carotidplaque (p = 0.046). The ACC/AHA calculator revealed a gradual increase in the risk of cardiovascularevents: 8.7% with AHI < 5/h, and 30.3% in severe OSA. Conclusions: In hypertension (HT) patients, RPrevealed a high prevalence of OSA associated with carotid artery disease, high PWV, and increasedcardiovascular risk.

ARTICLE HISTORYReceived 12 March 2017Accepted 23 June 2017

KEYWORDSHypertension; respiratorypolygraphy; risk factor; sleepapnea; STOP–BANG

Introduction

Obstructive sleep apnea (OSA) syndrome represents a chal-lenge for the healthcare system due to its high prevalence inthe adult population1,2 (5–9% for men, and 3–5% forwomen)1 and associated morbi-mortality (e.g., traffic acci-dents and cardiovascular complications).

The highest level of epidemiologic evidence supports theassociation between OSA and high blood pressure (BP)3,4,though OSA has also been associated with other disorders,such as ischemic heart disease, arrhythmia, and pulmonaryhypertension. This cause–effect relationship has also beenreinforced by the identification of possible pathogenic path-ways and reports about the effects of continuous positiveairway pressure (CPAP) treatment on the cardiovascular sys-tem (2,5).

Hypertension (HT) affects approximately one-third of theadult Western population. It is now firmly established thatafter years of exposure, HT leads to cardiovascular disease,heart failure, and stroke. The underlying cause of HT isdetected in 10–15% of patients. Thus, OSA stands out as arelevant treatable factor associated with HT2,6,7.

Several studies have evidenced the role of OSA as anindependent risk factor for the development of HT6,6,8–10.The Wisconsin Sleep Cohort Study6,10 and the Sleep HeartHealth Study11 concluded that, in the general population,there is an association between OSA and HT which follows

a dose–response pattern based on the severity of Apnea-Hypopnea Index (AHI). Young et al.10 studied workers agedbetween 30 and 60 years and observed that the prevalence ofHT increased with AHI severity, regardless of age, sex, andBMI. Davies et al.5 described a non-dipping BP profile forsystolic blood pressure in OSA patients, who showed nodecline in nighttime BP.

In 2003, the JNC VII report7 on HT included OSA as thefirst identifiable cause of HT. Therefore, this factor shouldalways be considered in the differential diagnosis of resistantHT and newly diagnosed HT, particularly in obese patientsand patients without a decline in nighttime BP (non-dipping).

A large series of patients studied systematically for thediagnosis of secondary HT (São Paulo, Brazil, in 2011)showed that in 70% of the cases the underlying cause wasrelated to sleep-related breathing disorders12.

In addition to this, studies comparing CPAP versus placebohave shown that CPAP significantly reduces BP. This effect ismoremarked in patients with severe OSA13–17 and resistant HT18,and more modest in patients without daytime sleepiness19–22.

With the aim of identifying and describing symptomaticpatients or patients with an increased risk of sleep-relatedbreathing disorders in a real-life clinical setting, we objectivelyevaluated a consecutive series of HT patients referred to thehypertension center (HTC) of a local university hospital overa period of 1 year.

CONTACT Dr. Eduardo Borsini borsinieduardo@yahoo.com.ar Hospital Británico, Perdriel 74, Laboratorio Pulmonar, 1° piso, Buenos Aires CP1280AEB,Argentina.

CLINICAL AND EXPERIMENTAL HYPERTENSIONhttps://doi.org/10.1080/10641963.2017.1356841

© 2017 Taylor & Francis

Dow

nloa

ded

by [

UC

San

ta B

arba

ra L

ibra

ry]

at 1

2:57

08

Sept

embe

r 20

17

Objectives

● To obtain information about the prevalence of OSAfrom consultation at a specialized HTC.

● To study the usefulness of home respiratory polygraphy(RP) to identify OSA and the relationship between OSAand the cardiovascular risk of HT patients.

Study design

This is a single-center, prospective, observational, cross-sec-tional cohort study.

Materials and methods

Population

Inclusion criteriaWe included patients over 18 years old diagnosed with HTand referred for a complete medical examination through astratification protocol based on HTC recommendations for2016. Patients with frequent snoring defined as >3 nights/week and scores of >5 in STOP–BANG questionnaire or >10in the Epworth Sleepiness Scale (ESS) for assessing subjectivedaytime sleepiness were evaluated using self-administeredunmonitored RP.

Ethical approval. The protocol was approved by the ethicsand review committee at Hospital Británico de Buenos Aires.All procedures performed in this study involving humanparticipants were in accordance with the ethical standards ofthe institutional and/or national research committee and withthe 1964 Helsinki Declaration and its later amendments orcomparable ethical standards in accordance with the ethicalstandards of the Helsinki Declaration.

Exclusion criteriaPatients with symptomatic heart failure, neuromuscular dis-ease, known diagnosis of COPD, or use of CPAP or otherform of ventilatory support or supplemental oxygen wereexcluded.

Baseline measurements. We systematically measured anthro-pometric data, such as BMI, neck circumference, and waistcircumference using an inextensible tape measure and tookoximetry readings at rest and in sitting position (Nonin Onix,Nonin Inc. Minneapolis, USA). Three BP readings were taken atrest (>15 min) at 2 min intervals with an automatic pneumaticdevice (OMRON 7220, Omron Healthcare, Inc. Illinois, USA)

Questionnaires. Clinical data were gathered through cardiol-ogists’ questions who led clinical evaluations and supplemen-tary examinations according to recommendations in effect23.

Tools used

● The Berlin Questionnaire, which classifies patients intotwo groups (high-risk and low-risk patients) on the basis

of a combination of clinical parameters, BMI, or historyof HT24.

● STOP–BANG Questionnaire (yes/no questions)25,26.● A validated version of ESS translated into Spanish27.

Laboratory tests. A 5 ml sample of vein blood (morningfasting venipuncture) was processed under HTC protocol forblood tests and metabolic panel at the laboratory of HospitalBritánico on the same day of the clinical examination.

Respiratory polygraphy. We used Apnea Link Plus™ (ResMedInc. Sydney, Australia) with five channels and three basicsignals, pulse oximetry, respiratory flow nasal cannula, andthoracic effort (level III device)28. All patients received perso-nalized training in the use of the device, including a practicaldemonstration of how to set up the equipment. Trainingsessions were led by senior cardiology technicians29.

Recordings were made at patients’ homes during one nightand downloaded the following day using Apnea Link software(release 9.0). Unedited raw data together with clinical evalua-tion and questionnaires were sent by e-mail through theintranet to the sleep laboratory. All institutional data protec-tion standards were observed29. At the lab, expert pulmonol-ogists downloaded data and edited events manually.

Manual scoringRecordings were analyzed in 3–5 min epochs. When neces-sary, respiratory events were corrected manually30. Recordingsections with low-quality signals or transient disconnectionswere removed. We only accepted recordings with a valid totalrecording time (TRT; for manual analysis) of >240 min(>4 h). Apnea was defined as a >80% drop from baselineairflow for ≥10 s; and hypopnea as a 50% drop for ≥10 sassociated to ≥3% oxygen desaturation. The AHI was calcu-lated as the number of apneas/hypopneas per hour of validTRT. Patients were classified either as normal (AHI < 5/h),mild (AHI ≥ 5 and <15), moderate (AHI ≥ 15 and <30), orsevere (AHI ≥ 30). Pulmonologists based their recommenda-tions for the use of CPAP on local standards in effect31.

Ambulatory blood pressure monitoring. Twenty-four-hourambulatory blood pressure monitoring (ABPM) was per-formed using a 90217 Spacelabs Ultralite device (SpaceLabs,Redmond, WA, USA). BP measurements were taken every15 min during the day (8 AM–11 PM) and every 20 minduring the night (11 PM–8 AM). HTC physicians were incharge of final readings and reports. ABPM and RP wereperformed on consecutive nights (in random order).Controlled daytime and nocturnal BP was defined accordingto the following systolic and diastolic values: <135/85 and<120/80, respectively.

Pulse wave velocity. Baseline pulse wave velocity (PWV) wasmeasured with a pneumatic system (mobil-O-Graph; I.E.M.Stolberg, Deutschland). Four-minute measurements weretaken in upper limbs. Results were classified either as normalor high: >90th percentile adjusted for sex, age, weight, andheight32,33.

2 E. BORSINI ET AL.

Dow

nloa

ded

by [

UC

San

ta B

arba

ra L

ibra

ry]

at 1

2:57

08

Sept

embe

r 20

17

Other procedures. Associated cardiovascular risk wasassessed through 2D Echo Color-Doppler and ultrasound ofboth carotid arteries (HTC echocardiography laboratory) onthe same day of the clinical examination. Finally, we calcu-lated the risk of cardiovascular events over a 10-year periodusing the ACC/AHA score (2013), which includes variablessuch as race, age, sex, cholesterol level, blood pressure, dia-betes, and smoking.

Statistical analysis

Categorical variables were expressed as percentages, andnumerical variables as mean or standard deviation. Normallydistributed variables were expressed as mean or standarddeviation, and not-normally distributed variables as meanand percentiles (25–75%). Comparisons were made usingFisher’s exact test, Wilcoxon–Mann–Whitney, or χ2.Statistical analysis was conducted using STATA 12™ andGraph Pad Prism-5™ softwares.

Results

Population

We studied 168 patients over a 1-year period. Table 1 showsdemographic characteristics, baseline BP measurements, andoximetry at rest.

This study population was mostly made up of middle-agedsubjects with an increased risk of sleep apnea due to high BMI(34.7 ± 6.79) and enlarged neck circumference (43.74 ± 3.13 cmin men and 38.94 ± 3.66 cm in women) (see Table 2) whocomplained of mild subjective symptoms of excessive sleepiness(mean ESS score: 8.01 for men and 8.92 for women; p = 0.69).Only 19% had scores >10.

Due to pre-established selection criteria, almost 90% ofpatients were at high risk according to the Berlin question-naire, without differences between sexes. Four patients(2.38%) already had a diagnosis of OSA but were not receiv-ing any specific treatment.

The main reasons to perform RP were snoring (94.04%),age >50 years (68.3%), daytime tiredness (34.52%), and malegender. The STOP combination was identified in 22 patients(13.1%), and BANG in 11 (6.55%). Table 3 shows the fre-quency of each individual item in STOP–BANG. The fullcombination (STOP and BANG) was uncommon (2 patients;1.19%).

In blood tests, most frequently identified anomalies wererelated to glucose metabolism (diabetes, hyperglycemia, andhyperinsulinemia) (see Table 4). About 67.5% of HTpatients with OSA (54/80) had increased levels of seruminsulin (>12 µUI/ml), 14.8% presented anomalies in com-plete urinalysis, and 10 patients (6.41%) had above-normalTSH values.

Table 1. Study Population Characteristics

Variable Value

n 168Men 109 (64.88%)Age (years) 55 ± 12.75BMI (kg/m2) 34.7 ± 6.79ESS 8.03 ± 5.10ESS > 10 32 (19.04%)High risk by Berlin Q 153 (91.07%)Diastolic BPa 85 ± 11.35Systolic BPa 136.3 ± 18.48Arterial oxygen saturation at rest 96 ± 7.83Heart rate at rest 69 ± 11.65

±Standard deviation. BMI, body mass index; ESS, EpworthSleepiness Scale.

aBaseline day BP: mean of three readings.

Table 2. Comparison between genders

Variable Men Women Significance

N 109 59Age (years) 56.08 ± 16.47 52.97 ± 10.18 0.06BMI (kg/m2) 33.9 ± 0.5 36.2 ± 1.1 0.05ESS (0–24) 8.01 8.92 0.6High risk by Berlin 93 88 0.8Neck circumference (cm) 43.74 ± 3.13 38.94 ± 3.66 0.04Waist circumference (cm) 110.97 ± 15.98 109.17 ± 17.88 0.72

±Standard deviation. BMI, body mass index; ESS, Epworth Sleepiness Scale.

Table 3. Observations for each STOP-BANG component

Variables Frecquency %

S: Snore 158 94.04T: Tired 58 34.52O: Observed (observed apneas) 41 24.40P: Pressure (high blood pressure) 157 93.95Known or previously diagnosedB: BMI (body mass index) >35 35 20.83A: Age >50 years old 108 64.28N: Neck (neck circumference) >40 cm 55 32.74G: Gender (male) 109 64.88STOP 22 13.10BANG 11 6.55STOP–BANG 2 1.19>5 components 145 86.31

Table 4. Laboratory Results

Variable Mean valuea Medianb Unit

Hematocrit 42.4 ± 3.9 43 (40–45) %Hemoglobin 18.03 ± 15.7 14.4 (13.3–15.3) g/dlUricemia 5.9 ± 1.5 6 (5–6.7) mg/dlUremia 36 ± 12.2 35 (29–41) mg/dlGlycaemia 116 ± 58 101 (93–112) mg/dlGlycosylated hemoglobin (HbA1) 6.35 ± 4.6 5.6 (5.3–6) mg/dlTriglycerides 155 ± 88.6 133 (97–194) mg/dlTotal cholesterol 189 ± 37 189 (164–211) mg/dlLDL cholesterol 113 ± 34.1 115 (87–136) mg/dlHDL cholesterol 45 ± 11.5 43 (36–51) mg/dlMorning TSH 2.16 ± 1.97 1.78 (1.19–2.15) µUI/dlMorning baseline insulinaemia 21.8 ± 20.5 17 (10.5–27) µUI/mlHOMA index 5.86 ± 5.76 3.75 (2.4–8.1)Anomalies in complete urinalysis 14.88%

aValues expressed as mean ± standard deviation.bValues expressed as median (percentiles 25–75).

CLINICAL AND EXPERIMENTAL HYPERTENSION 3

Dow

nloa

ded

by [

UC

San

ta B

arba

ra L

ibra

ry]

at 1

2:57

08

Sept

embe

r 20

17

Respiratory polygraphy recordings

The mean delay between patient identification and RP reportswas 1.91 day (±1.78). About 4% of patients needed to repeatrecordings during a second night (due to disconnections or<4 h of valid TRT).

Over a mean valid TRT of 435.9 min (±101), the manualcount revealed an obstructive profile with a global AHI of18.03 ± 15.7, an ODI of 18.6 ± 15.2, and time with oxygensaturation <90% (in % of TRT) of 20.8 ± 24.3. Table 5 sum-marizes RP indicators.

Mild disturbances prevailed (40.5%), though 44% had anAHI > 15 events/h (Figure 1). CPAP therapy was recom-mended to 69 patients (41.07%).

Relationship between ABPM and RP indicators

The nighttime component of ABPM was the most markedlyaffected (34.4% for systolic BP and 14% for diastolic BP), ascompared with the daytime component (18%). The propor-tion of uncontrolled HT patients was 60.8% (AHI > 15/events≈ 62%). We did not find a statistical relationship between AHIand BP control through ABPM (p = 0.61).

Other indicators of cardiovascular risk and RP AHI

Left ventricular hypertrophy with concentric remodeling wasfound in 18.2% of patients, not related to AHI > 15/h (Fisher’sexact test; p = 0.55).

Ultrasound of neck vessels did not show statistical correla-tion between the intima-media thickness (IMT) and AHI >15or <15/events per hour; right IMT: 0.83 ± 1.3 versus0.78 ± 0.13 mm (p = 0.41) and 0.82 ± 0.16 versus0.78 ± 0.19 mm (p = 0.40). The presence of carotid plaque,however, had statistical significance (qualitative analysis)(n = 156; Fisher’s exact test; p = 0.046) (Table 6).

PWV revealed a larger proportion of patients with a highindex of arterial stiffness among patients with AHI > 15/h(55% vs. 49%; p = 0.050).

Finally, the ACC/AHA calculator revealed a gradualincrease in the risk of cardiovascular events (coronary eventor stroke) proportional to the increase in AHI severity cate-gories: 8.7% for patients with normal RP and; 19.7%, 27.8%,and 30.3% for patients with OSA, respectively (Figure 2).

Discussion

Our study evaluated HT patients with frequent snoring,excessive daytime sleepiness, or an increased risk of OSAaccording to STOP–BANG, a validated tool used in clinicalpractice29,31,34. Our results are relevant because 44% of HTpatients with these risk factors and referred to a specializedcenter presented moderate to severe sleep apneas and werecandidates to CPAP treatment.

This multidisciplinary network approach allowed for rapiddiagnosis (HTC) with simple tools, without the need to resortto sleep unit beds. Test repetition rate was low.

As it can be appreciated from baseline oximetry values, weexcluded patients with known breathing disorders, daytimehypoxemia, or respiratory comorbidity. By excluding patients

Table 5. Respiratory Polygraphy Indicators

Variable Value

TRT (m) 435.98 ± 101AHI 18.03 ± 15.7a

ODI 18.6 ± 15.2a

Time < 90 (% of TRT) 20.8 ± 24.3Central apneas (events) 1 (0.1–5)b

Obstructive apneas (events) 30 (2–36)b

Hypopneas (events) 59 (33–107)b

Mixed apneas (events) 0.1 (0–1.1)b

Recommendation for CPAP 69 (41.07%)

AHI, Apnea-Hypopnea Index (events recorded per hour); ODI: O2

Desaturation Index (threshold ≥ 3%). Time < 90, Time withSaO2 < 90%; TRT, total recording time valid for manual analysis.

aValues expressed as mean ± standard deviation.bValues expressed as median (percentiles 25–75).

Figure 1. Categorization by Apnea Hypopnea Index

Table 6. Presence of carotid plaques by US with regard to RP AHI value (n = 156)

Carotid plaques

AHI (events/h) No Yes Total

AHI < 15 69 17 86(80.2%) (19.8%) (100%)

AHI > 15 46 24 70(65.7%) (34.3%) (100%)

Total 115 41 153(73.7%) (26.3%) (100%)

Fisher’s exact test = 0.046.

Figure 2. Score of the American College of Cardiology/American HeartAssociation to estimate the risk of cardiovascular events over a period of 10years with regard to RP AHI value

4 E. BORSINI ET AL.

Dow

nloa

ded

by [

UC

San

ta B

arba

ra L

ibra

ry]

at 1

2:57

08

Sept

embe

r 20

17

with OSA and those using CPAP or other forms of positiveairway pressure, it is possible to rule out the potential effect ofthese therapies over recorded values.

Many causes may account for the high prevalence of OSAin our HT patients. First, both HT and OSA share commonrisk factors. The number of male patients and age of the studypopulation may also explain the large proportion of high AHIvalues1,6,8. Obesity is frequent in HT patients and is a well-established factor for the development of OSA6,8. In ourstudy, BMI was ≈34, being more evident in women(36.2 ± 1.1; p = 0.05), who had large waist circumferences(comparable with men).

According to available data, studies of poorly controlledHT patients show that the caudal-rostral flow has a patho-genic role in OSA35. Other mechanisms through which OSAmay contribute to poor HT control are increased sympatheticactivity, reduction in baroreflex sensitivity, disorders ofsodium metabolism and the distribution of extracellularwater, impaired endothelial function, hypoxia, and cyclic re-oxygenation, among others36,37.

Undoubtedly, the diagnosis of sleep-related breathing dis-orders in HT patients is especially relevant, since they arepotentially treatable. In spite of our better understanding ofOSA, it is estimated that most patients remain undiagnosed.In our series, only 2.38% had undergone previous polysom-nography (PSG) but were not receiving any specific treatment.The prevalence of OSA is consistently high across specializedhealthcare centers in our country, though it has not beenofficially reported. Developing countries or countries withlimited resources have a special need for simple and practicaldiagnostic methods that can be used by non-experts andinterpreted by sleep medicine experts remotely, allowing fora pragmatic evaluation of patients with risk factors forOSA29,31,34.

According to previous descriptions found in the literature,the low level of sleepiness in HT patients and their lowperception of daytime symptoms could result in fewer refer-rals to sleep laboratories. Consistently, our patients did notreport many symptoms by ESS scale (Table 1) and only one-third complained of frequent tiredness (Table 3).

Since we could not evaluate all HT patients at the HTC, weused a combined approach based on symptoms (snoring; ESSand STOP questionnaire) and anthropometric variables(BANG) during the clinical evaluation. Highly pathologicalAHI and cardiovascular relevant OSA were identified in 88%and in 44% of the study population, respectively.

The ESS > 10 criteria used during initial screening toidentify sleepy patients might underestimate the populationat risk. We discovered a surprising finding: 91% of patientsselected for RP obtained high scores in the Berlin question-naire and, even though this questionnaire was not used toexplore sleep-related breathing disorders, it clearly confirmsthe existence of a high-risk population.

We identified inadequate control of BP through ABPM (84patients: 85%) even when daytime baseline measurements wereacceptable. We also found an association between AHI and highPWV (p < 0.05), the latter being an expression of arterialstiffness or impaired endothelial function, which is consistentwith suggestions made by previous studies38. The physio-

pathological mechanisms through which OSA can impairendothelial function and increase arterial stiffness relate tointermittent hypoxemia, the production of reactive oxygen spe-cies, and oxidative stress39,40, which reduce nitric oxide41–43 andmay lead to accelerated atherosclerosis39,42,43. As a result of a re-oxygenation/hypoxia model, our HT patients presented highvalues of intermittent nighttime desaturation expressed throughODI per hour (Table 5). The impact on specific territories (e.g.,carotid arteries) may derive from OSA as a risk factor associatedwith HT, diabetes, obesity, and snoring as a direct damagemechanism44–47. In our experience, qualitative visual identifica-tion of atheroma plaques correlated better with a high AHI thanIMT, which is consistent with other publications44–47.

Finally, the ACC/AHA calculator (a widely used tool inspite of its potential for overestimating risks) revealed a gra-dual and progressive relationship (possibly related to a biolo-gical process) between AHI and the risk of events (stroke andmyocardial infarction)48,49. Strict criteria (>20% of events)revealed a prediction of 27.8% and 30.3% for patients withmoderate and severe OSA, respectively, which highlight thatthis population is at high risk.

Study limitations

This is a small study conducted on a selected sample of HTadults with suspicion of sleep apnea. Therefore, our findingscannot be extrapolated to all populations or populations seek-ing care at general hospitals. The main limitation of this studyis that our sample includes patients seen by HTC cardiologistswho, therefore, frequently received drugs for their known HTcondition and were subjected to changes in dose and type oftherapeutic drug regimen, which limits our conclusions.

The capacity of the polygraphy devices we used was lim-ited, though all of them included at least three basic signalsupon which manual readings were based. In addition to this,the use of home RP could lead to differences between ourresults and those of other studies using PSG in sleep labora-tories. As compared with conventional PSG, RP has an under-estimation rate of 10–15% for AHI29–31, a limitation inherentto the absence of neurophysiological signals. Used indexes(AHI) differ from those of PSG (AHI or RDI), since in PRthey result from the quotient between events and TRT28–31.

Conclusion

The use of questionnaires and home RP in a population of HTpatients revealed a high prevalence of OSA associated withcarotid artery disease, high PWV, and an increased risk ofcardiovascular events over the next 10 years.

Declaration of interest

The authors report no conflicts of interest and certify that they have noaffiliations with or involvement in any organization or entity with anyfinancial interest (such as honoraria; educational grants; participation inspeakers’ bureaus; membership, employment, consultancies, stock own-ership, or other equity interest; and expert testimony or patent-licensingarrangements), or non-financial interest (such as personal or professionalrelationships, affiliations, knowledge, or beliefs) in the subject matter or

CLINICAL AND EXPERIMENTAL HYPERTENSION 5

Dow

nloa

ded

by [

UC

San

ta B

arba

ra L

ibra

ry]

at 1

2:57

08

Sept

embe

r 20

17

materials discussed in this manuscript. The authors alone are responsiblefor the content and writing of the paper.

Funding

No funding was received for this research.

ORCID

Eduardo Borsini http://orcid.org/0000-0003-2930-6022

References

1. Durán J, Esnaola S, Ramón R, Iztueta A. Obstructive sleep apnea-hypopnea and related clinical features in a population-based sam-ple of subjects aged 30 to 70 years. Am J Respir Crit Care Med.2001;163:685–89.

2. Arias MA, García Río F. Disfunción ventricular en el síndrome deapnea-hipopnea obstructiva durante el sueño: en búsqueda de larelevancia clínica. Rev Esp Cardiol. 2007;60:569–72.

3. Worsnop CJ, Houston D, Finberg S, et al. Sleep apnea syndromeand essencial hypertension. Am J Cardiol. 1985;103:1019–22.

4. Tufik S, Santos-Silva R, Taddei JA, Bittencourt LR. Obstructivesleep apnea syndrome in the Sao Paulo Epidemiologic SleepStudy. Sleep Med. 2010 May;11(5):441–6.

5. Davies CWH, Crosby JH, Mullins RL, et al. Case-control study of24 hour ambulatory blood pressure in patients with obstructivesleep apnoea and normal matched control subjects. Thorax.2000;55:738–40.

6. Peppard PE, Young T, Palta M, Skatrud J. Prospective study of theassociation between sleep-disordered breathing and hypertension.N Engl J Med. 2000;342:1378–84.

7. Chobanian AV, Bakris GL, Black HR, et al. National high bloodpressure education program coordinating committee. The seventhreport of the joint national committee on prevention, detection,evaluation, and treatment of high blood pressure: the JNC 7report. JAMA. 2003;289:2560–72.

8. Newman AB, Nieto J, Guirdry U, Lind BK, Redline S, Sharar E,et al. Relation of sleep disordered breathing to cardiovascular riskfactors. The sleep heart health study. Am J Epidemiol.2001;154:50–59.

9. Lavie P, Herer P, Hoffstein V. Obstructive sleep apnea syndromeas a risk factor for hypertension: a population study. Brit Med J.2000;320:479–82.

10. Young T, Peppard P, Palta M, Mae K, Finn L, Morgan B, et al.Population-based study of sleep-disordered breathing as a riskfactor for hypertension. Arch Intern Med. 1997;157:1746–52.

11. O’Connor GT, Caffo B, Newman AB, Quan SF, Rapoport DM,Redline S, Resnick HE, Samet J, Shahar E. Prospective study ofsleep-disordered breathing and hypertension: the sleep hearthealth study. Am J Respir Crit Care Med. 2009;179:1159–64.

12. Pedrosa RP, Drager LF, Gonzaga CC, Sousa MG, De Paula LK,Amaro AC, Amodeo C, Bortolotto LA, Krieger EM, Bradley TD,et al. Obstructive sleep apnea: the most common secondary causeof hypertension associated with resistant hypertension.Hypertension. 2011;58(5):811–17.

13. Stradling JR, Partlett J, Davis RJ, Siegwart D, Tarassenko L. Effectof short term graded withdrawal of nasal continous positive air-way pressure on systemic blood pressure in patients with ostruc-tive sleep apnoea. Blood Press. 1996;5:234–40.

14. Pepperell J, Ramdassingh-Dow S, Crosthwaite N, Mullins R,Jenkinson C, Stradling J, Davies RJ. Ambulatory blood pressureafter therapeutic and subtherapeutic nasal continuous positiveairway pressure for obstructive sleep apnea: a randomised paralleltrial. Lancet. 2001;359:204–10.

15. Faccenda J, Mackay T, Boon N, Douglas N. Randomized placebo-controlled trial of continuous positive airway pressure on blood

pressure in the sleep apnea-hipopnea syndrome. Am J Respir CritCare Med. 2001;163:344–48.

16. Mooe T, Rabben T, Wiklund U, Franklin KA, Eriksson P. Sleepdisordered breathing in men with coronary artery disease. Chest.1996;109:659–63.

17. Durán-Cantolla J, Aizpuru F, Montserrat JM, Ballester E, Terán-Santos J, Aguirregomoscorta JI, Gonzalez M, Lloberes P, Masa JF,De La Peña M, et al., Spanish Sleep and Breathing Group.Continuous positive airway pressure as treatment for systemichypertension in people with obstructive sleep apnoea: randomisedcontrolled trial. Bmj. 2010;341.

18. Lozano L, Tovar JL, Sampol G, Romero O, Jurado MJ, Segarra A,Espinel E, Ríos J, Untoria MD, Lloberes P. Continuous positiveairway pressure treatment in sleep apnea patients with resistanthypertension: a randomized, controlled trial. J Hypertens. 2010Oct;28(10):2161–68.

19. Barbe F, Mayoralas LR, Duran J, Masa JF, Maimo A, MontserratJM, Monasterio C, Bosch M, Ladaria A, Rubio M, et al. Treatmentwith continuous positive airway pressure is not effective inpatients with sleep apnea but no daytime sleepiness. A rando-mized, controlled trial. Ann Intern Med. 2001;134:1015–23.

20. Hernández García C. Sleep apnea-hypopnea syndrome withoutexcessive daytime sleepiness. Arch Bronconeumol. 2009;45:240–44.

21. Barbé F, Durán-Cantolla J, Capote F, De La Peña M, Chiner E,Masa JF, Gonzalez M, Marín JM, Garcia-Rio F, De Atauri JD,et al. Long-term effect of continuous positive airway pressure inhypertensive patients with sleep apnea. Spanish sleep and breath-ing group. Am J Respir Crit Care Med. 2010;181:718–26.

22. Bratton DJ, Stradling JR, Barbé F, Kohler M. Effect of CPAP onblood pressure in patients with minimally symptomatic obstruc-tive sleep apnoea: a meta-analysis using individual patient datafrom four randomised controlled trials. Thorax. 2014 Dec;69(12):1128–35. 22.

23. Fleetham J, Ayas N, Bradley D, Fitzpatrick M, Oliver TK,Morrison D, Ryan F, Series F, Skomro R, Tsai W; CanadianThoracic Society Sleep Disordered Breathing Committee.Canadian Thoracic Society 2011 guideline update: diagnosis andtreatment of sleep disordered breathing. Can Respir J. 2011 Jan-Feb;18(1):25–47. Review.

24. Mancia G, Fagard R, Narkiewicz K, Redón J, Zanchetti A, BöhmM, Christiaens T, Cifkova R, De Backer G, Dominiczak A,Galderisi M, Grobbee DE, Jaarsma T, Kirchhof P, Kjeldsen SE,Laurent S, Manolis AJ, Nilsson PM, Ruilope LM, Schmieder RE,Sirnes PA, Sleight P, Viigimaa M, Waeber B, Zannad F; TaskForce Members. 2013 practice guidelines for the management ofarterial hypertension of the European Society of Hypertension(ESH) and the European Society of Cardiology (ESC): ESH/ESCtask force for the management of arterial hypertension. JHypertens. 2013 Oct;31(10):1925–38.

25. Chung F, Yegneswaran B, Liao P, Chung SA, Vairavanathan S,Islam S, Khajehdehi A, Shapiro CM. Validation of the Berlinquestionnaire and American society of anesthesiologists checklistas screening tools for obstructive sleep apnea in surgical patients.Anesthesiology. 2008 May;108(5):822–30.

26. Chung F, Yegneswaran B, Liao P, Chung SA, Vairavanathan S,Islam S, Khajehdehi A, Shapiro CM. STOP questionnaire: a toolto screen patients for obstructive sleep apnea. Anesthesiology.2008 May;108(5):812–21.

27. Chiner E, Arriero JM, Signes-Costa J, Marco J, Fuentes I.Validation of the Spanish version of the epworth sleepiness scalein patients with a sleep apnea síndrome. Arch Bronconeumol.1999;35:422–27.

28. Collop NA, Anderson WM, Boehlecke B, Claman D, Goldberg R,Gottlieb DJ, Hudgel D, Sateia M, Schwab R;Portable MonitoringTask Force of the American Academy of Sleep Medicine. Clinicalguidelines for the use of unattended portable monitors in thediagnosis of obstructive sleep apnea in adult patients. Portablemonitoring task force of the American academy of sleep medicine.J Clin Sleep Med. 2007;3:7.

6 E. BORSINI ET AL.

Dow

nloa

ded

by [

UC

San

ta B

arba

ra L

ibra

ry]

at 1

2:57

08

Sept

embe

r 20

17

29. Borsini E, Blanco M, Bosio M, Di Tullio F, Ernst G, Salvado A.“Diagnosis of sleep apnea in network” respiratory polygraphy as adecentralization strategy. Sleep Sci. 2016;9:244–48.

30. Berry, R. B., Budhiraja, R, Gottlieb, D.J., et al. Rules for scoringrespiratory events in sleep: update of the 2007 AASM manual forthe scoring of sleep and associated events. Deliberations of thesleep apnea definitions task force of the American academy ofsleep medicine. J Clin Sleep Med. 2012;8(5):597–619.

31. Nogueira F, Nigro C, Cambursano H, Borsini E, Silio J, Avila J.Practical guidelines for the diagnosis and treatment of obstructivesleep apnea syndrome. Medicina (B Aires). 2013;73(4):349–62.

32. Weiss W, Gohlisch C, Harsch-Gladisch C, Tölle M, Zidek W, vander Giet M. Oscillometric estimation of central blood pressure:validation of the mobil-o-graph in comparison with thesphygmoCor device. Blood Press Monit. 2012 Jun;17(3):128–31.

33. McEniery CM, Yasmin, Hall IR, Qasem A, Wilkinson IB,Cockcroft JR. Normal vascular aging: differential effects on wavereflection and aortic pulse wave velocity: the Anglo-CardiffCollaborative Trial (ACCT). J Am Coll Cardiol. 2005;46:1753–60.

34. Borsini E, Ernst G, Salvado A, Bosio M, Chertcoff J, Nogueira F,Nigro C. Utility of the STOP-BANG components to identify sleepapnea using home respiratory polygraphy. Sleep Breath. 2015;19(4):1327–33.

35. Friedman O, Bradley TD, Chan CT, Parkes R, Logan AG.Relationship between overnight rostral fluid shift and obstructivesleep apnea in drug-resistant hypertension. Hypertension.2010;56:1077–82.

36. Dempsey JA, Veasey SC, Morgan BJ, O’Donnell CP.Pathophysiology of sleep apnea. Physiol Rev. 2010;90:47–112.

37. Kohler M, Stradling JR. Mechanisms of vascular damage inobstructive sleep apnea. Nat Rev Cardiol. 2010;7:677–85.

38. Wang J, Yu W, Gao M, Zhang F, Gu C, Yu Y, Wei Y. Impact ofobstructive sleep apnea syndrome on endothelial function, arterialstiffening, and serum inflammatory markers: an updated meta-analysis and metaregression of 18 studies. J Am Heart Assoc. 2015Nov 13;4(11).

39. Lavie L, Lavie P. Molecular mechanisms of cardiovascular diseasein OSAHS: the oxidative stress link. Eur Respir J. 2009;33:1467–84.

40. Foster GE, Brugniaux JV, Pialoux V, Duggan CT, Hanly PJ,Ahmed SB, Poulin MJ. Cardiovascular and cerebrovascularresponses to acute hypoxia following exposure to intermittenthypoxia in healthy humans. J Physiol. 2009;587:3287–99.

41. Thomas SR, Chen K, Keaney JF Jr. Hydrogen peroxide activatesendothelial nitric-oxide synthase through coordinated phosphor-ylation and dephosphorylation via a phosphoinositide 3-kinase-dependent signaling pathway. J Biol Chem. 2002;277:6017–24.

42. Vasquez-Vivar J, Kalyanaraman B, Martasek P, Hogg N, MastersBS, Karoui H, Tordo P, Pritchard KA Jr. Superoxide generation byendothelial nitric oxide synthase: the influence of cofactors. ProcNatl Acad Sci USA. 1998;95:9220–25.

43. Lavie L. Oxidative stress–a unifying paradigm in obstructive sleepapnea and comorbidities. Prog Cardiovasc Dis. 2009;51:303–12.

44. Jelic S, Padeletti M, Kawut SM, Higgins C, Canfield SM, Onat D,Colombo PC, Basner RC, Factor P, LeJemtel TH. Inflammation,oxidative stress, and repair capacity of the vascular endotheliumin obstructive sleep apnea. Circulation. 2008;117:2270–78.

45. Liao LJ, Cho TY, Huang TW. Assessment of carotid artery intima-media thickness in patients with obstructive sleep apnea. ClinOtolaryngol. 2017 Jan 4. doi: 10.1111/coa.12823. [Epub ahead ofprint]

46. Nadeem R, Harvey M, Singh M, Khan AA, Albustani M, BaesslerA, Madbouly EM, Sajid H, Khan M, Navid N. Patients withobstructive sleep apnea display increased carotid intima media: ameta-analysis. Int J Vasc Med. 2013;2013:839582.

47. Gunnarsson SI, Peppard PE, Korcarz CE, Barnet JH, AeschlimannSE, Hagen EW, Young T, Hla KM, Stein JH. Obstructive sleepapnea is associated with future subclinical carotid artery disease:thirteen-year follow-up from the Wisconsin sleep cohort.Arterioscler Thromb Vasc Biol. 2014;34(10):2338–42.

48. DeFilippis AP, Young R, Carrubba CJ, McEvoy JW, Budoff MJ,Blumenthal RS, Kronmal RA, McClelland RL, Nasir K, Blaha MJ.An analysis of calibration and discrimination among multiplecardiovascular risk scores in a modern multiethnic cohort. AnnIntern Med. 2015;162:266–75.

49. Ridker PM, Cook NR. Comparing cardiovascular risk predictionscores. Ann Intern Med. 2015;162:313–15.

CLINICAL AND EXPERIMENTAL HYPERTENSION 7

Dow

nloa

ded

by [

UC

San

ta B

arba

ra L

ibra

ry]

at 1

2:57

08

Sept

embe

r 20

17

本文献由“学霸图书馆-文献云下载”收集自网络，仅供学习交流使用。

学霸图书馆（www.xuebalib.com）是一个“整合众多图书馆数据库资源，

提供一站式文献检索和下载服务”的24 小时在线不限IP

图书馆。

图书馆致力于便利、促进学习与科研，提供最强文献下载服务。

图书馆导航：

图书馆首页 文献云下载 图书馆入口 外文数据库大全 疑难文献辅助工具