Associations Between Obstructive Sleep Apnea and Measures of Arterial Stiffness
2019; American Academy of Sleep Medicine; Volume: 15; Issue: 02 Linguagem: Inglês
10.5664/jcsm.7616
ISSN1550-9397
AutoresJenny Theorell‐Haglöw, Camilla M. Hoyos, Craig L. Phillips, Brendon J. Yee, Kerri Melehan, Peter Y. Liu, Peter A. Cistulli, Ronald R. Grunstein,
Tópico(s)Cardiovascular and Diving-Related Complications
ResumoFree AccessObstructive Sleep Apnea - Women - Obesity - Diabetes - Hypertension - Cardiovascular Disease - Smoking - Scientific InvestigationsAssociations Between Obstructive Sleep Apnea and Measures of Arterial Stiffness Jenny Theorell-Haglöw, PhD, Camilla M. Hoyos, PhD, Craig L. Phillips, PhD, Brendon J. Yee, PhD, Kerri L. Melehan, PhD, Peter Y. Liu, PhD, Peter A. Cistulli, PhD, Ronald R. Grunstein, PhD Jenny Theorell-Haglöw, PhD Address correspondence to: Jenny Theorell-Haglöw, Department of Medical Sciences, Respiratory, Allergy and Sleep Research, Uppsala University, Sweden+46 18 6110242+46 18 6110228 E-mail Address: [email protected] Centre for Sleep and Chronobiology (CIRUS), Woolcock Institute of Medical Research, University of Sydney, New South Wales, Australia Uppsala University, Department of Medical Sciences, Respiratory, Allergy and Sleep Research, Uppsala, Sweden , Camilla M. Hoyos, PhD Centre for Sleep and Chronobiology (CIRUS), Woolcock Institute of Medical Research, University of Sydney, New South Wales, Australia School of Psychology, University of Sydney, New South Wales, Australia , Craig L. Phillips, PhD Centre for Sleep and Chronobiology (CIRUS), Woolcock Institute of Medical Research, University of Sydney, New South Wales, Australia Department of Respiratory and Sleep Medicine, Royal North Shore Hospital, New South Wales, Australia , Brendon J. Yee, PhD Centre for Sleep and Chronobiology (CIRUS), Woolcock Institute of Medical Research, University of Sydney, New South Wales, Australia Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia , Kerri L. Melehan, PhD Centre for Sleep and Chronobiology (CIRUS), Woolcock Institute of Medical Research, University of Sydney, New South Wales, Australia Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia , Peter Y. Liu, PhD Division of Endocrinology, Department of Medicine, David Geffen School of Medicine at UCLA, Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute, Los Angeles, California , Peter A. Cistulli, PhD Centre for Sleep and Chronobiology (CIRUS), Woolcock Institute of Medical Research, University of Sydney, New South Wales, Australia Department of Respiratory and Sleep Medicine, Royal North Shore Hospital, New South Wales, Australia Sleep Research Group, Charles Perkins Centre, University of Sydney, New South Wales, Australia , Ronald R. Grunstein, PhD Centre for Sleep and Chronobiology (CIRUS), Woolcock Institute of Medical Research, University of Sydney, New South Wales, Australia Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia Published Online:February 15, 2019https://doi.org/10.5664/jcsm.7616Cited by:1SectionsAbstractPDF ShareShare onFacebookTwitterLinkedInRedditEmail ToolsAdd to favoritesDownload CitationsTrack Citations AboutABSTRACTStudy Objectives:The aim of this study was to determine whether severity measures of obstructive sleep apnea (OSA) are associated with arterial stiffness and central blood pressure (two important cardiovascular risk factors) in a large group of patients with OSA.Methods:Baseline data from six studies on OSA in which arterial stiffness and central aortic blood pressure measures were determined using applanation tonometry were pooled. Associations between measures of arterial stiffness (heart rate corrected augmentation index [AI75]), central aortic blood pressure (central systolic pressure [CSP] and heart rate corrected central augmentation pressure [CAP75]) and measures of OSA severity were explored using stepwise regression modelling.Results:Data from 362 participants (M:F ratio 13:1) with mean (standard deviation) age 49.2 (11.0) years, body mass index 31.9 (5.3) kg/m2, apnea-hypopnea index (AHI) 35.7 (20.7) events/h were included in the analyses. The AHI, oxygen desaturation index (ODI3%), and sleep time with SpO2 < 90% (T90) were all associated with arterial stiffness (AI75), (AHI: adj. β = .069; P = .01; ODI3%: adj. β = .072; P = .01; T90: adj. β = .18; P < .0001) and CAP75 (AHI: adj. β = .030; P = .01; ODI3%: adj. β = .027; P = .02; T90: adj. β = .080; P < .0001). AHI was also associated with CSP (AHI: adj. β = .11; P = .002).Conclusion:OSA severity was significantly associated with augmentation index and CAP75 although the relationships were not strong.Citation:Theorell-Haglöw J, Hoyos CM, Phillips CL, Yee BJ, Melehan KL, Liu PY, Cistulli PA, Grunstein RR. Associations between obstructive sleep apnea and measures of arterial stiffness. J Clin Sleep Med. 2019;15(2):201–206.BRIEF SUMMARYCurrent Knowledge/Study Rationale: Obstructive sleep apnea is a risk factor for cardiovascular morbidity and mortality. Because recent large intervention trials have been negative, there is a need to focus on endpoints such as arterial stiffness to further explore the relationship. To our knowledge, no previous studies have explored the effect of different measures of sleep apnea severity on measures of arterial stiffness.Study Impact: In a large patient group, we show associations between measures of sleep apnea severity and several aspects of arterial stiffness. The results support a relationship between sleep apnea and cardiovascular disease beyond standard peripheral blood pressure measures. Further studies on the effect of sleep apnea on arterial stiffness are needed to clarify the mechanisms for increased vascular dysfunction.INTRODUCTIONObstructive sleep apnea (OSA) has been shown to be an independent risk factor for cardiovascular morbidity and mortality1,2 and in recent years, the strong association between OSA and cardiovascular disease has gained considerable interest.3–7 The intermittent hypoxia, arousals, and sympathetic activation that occur with apneas and hypopneas result in both temporary elevations in blood pressure during sleep as well as sustained daytime hypertension.6 However, hypertension does not develop in all patients with even severe OSA and there remains a need to better understand whether other nontraditional risk factors, such as arterial stiffness, may provide improved risk stratification.Arterial stiffness caused by structural changes in the vascular wall or sustained vascular smooth muscle contraction (vasoconstriction) is a composite marker of declining arterial health that is strongly associated with atherosclerosis8,9 and poorer cardiovascular outcomes including fatal and nonfatal cardiovascular events.10–14 Markers of arterial stiffness include pulse wave velocity and pulse wave analysis (PWA) derived variables such as aortic augmentation index and central aortic blood pressure. These markers provide prognostic information beyond standard risk factors including hypertension, diabetes, obesity, dyslipidemia, and smoking.10 In particular, central aortic blood pressure is a superior prognostic marker than conventional brachial blood pressure15 because it better correlates with target organ damage.16To our knowledge, no previous studies have explored the effect of different measures of OSA (apnea-hypopnea index [AHI], oxygen desaturation index [ODI3%] and arousal index) on several variables of PWA. The aim of this study was therefore to determine whether different measures of OSA severity were associated with arterial stiffness and central blood pressure in a large group of patients with OSA.METHODSParticipants and SettingThe patients included in this analysis were originally referred for investigation of OSA through sleep clinics at the Woolcock Institute of Medical Research and at Royal Prince Alfred and Royal North Shore Hospitals in Sydney, Australia. The analysis included pooled data from 6 studies in 362 patients (336 men and 26 women) where measures of arterial stiffness were made. All studies and study participants have been described in detail previously.7,17–21 In cases where a participant took part in more than one study, only data from their first study were included. Five of the six studies were randomized controlled trials with 121,7 60,17 56,18 33,19 and 4421 participants, respectively. The sixth study was an observational, open-label, intervention study and for the current study, data from 48 patients were included.21 Of the studies, only two included both men and women.7,19 In all the studies, only baseline data were included.OSA MeasurementsSleep and breathing variables in all participants were assessed using an attended overnight, in-laboratory polysomnography (PSG) device (Sandman Elite, V.9.2, Tyco Healthcare, Denver, Colorado, United States; E-Series, Compumedics, Melbourne, Australia, or Alice 5, Philips Respironics, Andover, Massachusetts, United States. For the current study, PSG data from baseline were used (standard diagnostic PSG, scored according to standard criteria22,23) and measures of OSA were as follows: AHI, ODI3%, nighttime oxygen saturation nadir, sleep time with oxygen saturation with < 90%. Additional details have been reported elsewhere.7,17–20Arterial Stiffness Measures Using PWAIn all of the six pooled studies, arterial stiffness was assessed by PWA using applanation tonometry of the radial artery (SphygmoCor, AtCor Medical, Inc., Australia). Apart from conduit arterial stiffness, PWA provides measures of central and peripheral blood pressure, pulse pressure amplification, and cardiac perfusion potential.10 Measures were rigorously performed with participants who had fasted for 5 hours and who were caffeine and smoke free. This therefore resulted in most measurements occurring in the morning or first half of the day. Because a diagnosis of OSA was an eligibility criterion for all source studies, most of the arterial stiffness measurements were performed on a different day after PSG. However, the measurements were conducted within 1 to 2 weeks of diagnosis.In all studies, the following measures of arterial stiffness were collected: central systolic pressure (CSP), central diastolic pressure (CDP), central pulse pressure (CPP), peripheral systolic pressure (PSP), peripheral diastolic pressure (PDP), peripheral pulse pressure (PPP), pulse pressure amplification (PPA), augmentation index corrected to a heart rate of 75 bpm (AI75), central augmentation pressure corrected to a heart rate of 75 bpm (CAP75), subendocardial viability ratio (SEVR; a measure of cardiac perfusion potential) and, time to reflection (TR; reflected component of the pulse pressure wave). In addition, the participants' age, sex, body mass index (BMI), smoking status, and comorbidities (diagnosis of diabetes, hypertension, or hyperlipidemia; or medication) were also included in the current dataset.StatisticsStatistical analyses were performed using Stata 13 (Stata Corporation, College Station, Texas, United States). Correlation analyses for OSA variables with PWA variables were conducted. The association between variables of OSA and measures of arterial stiffness were then assessed using a backward stepwise regression model approach for each of the measures of arterial stiffness and OSA variables. The threshold for exclusion of variables from the model was set at P ≥ .10. In all regression analyses age, sex, mean arterial pressure (MAP), smoking status, total cholesterol, height, weight, medical conditions (diabetes mellitus, hypertension, hyperlipidemia), and Epworth Sleepiness Scale were entered in the starting model and each of the OSA variables were entered separately. The results of the stepwise regression models are presented as adjusted β-coefficients with 95% confidence intervals (95% CI). A value of P < .05 was considered significant.Ethics StatementAll studies were in compliance with the Declaration of Helsinki, the Good Clinical Practice guidelines, and applicable regulatory requirements. All participants provided written informed consent to participate for the respective study, which was approved by the Central Ethics Committee (RPAH Zone) or the Human Research Ethics Committee at Sydney University. All except one of the included studies were registered with the Australia New Zealand Clinical Trials Registry ( http://www.anzctr.org.au).RESULTSTable 1 shows the baseline characteristics for the participants depicting a population with OSA and obesity who are middle aged. Of this population, 7.3% had a diagnosis of diabetes mellitus, 40.1% had hypertension, 22.2% had hyperlipidemia, and 5.9% were smokers. Table 2 shows that the participants had severe OSA with AHI and ODI3% ≥ 30 events/h and hypoxia variables showing a clear effect of OSA with mean saturation nadir of 80% and time with saturation < 90% of 7.4 minutes. Within the group, the total sleep time was 6 hours, with a range of 1.5 to 8.5 hours and the arousal index was on par with AHI and ODI3% (Table 2). Table 3 shows that most of the measures of arterial stiffness were within normal limits,24–29 although time to reflection was somewhat long (Table 3).Table 1 Characteristics of the study population (n = 362).Table 1 Characteristics of the study population (n = 362).Table 2 Measures of obstructive sleep apnea in the study population (n = 362).Table 2 Measures of obstructive sleep apnea in the study population (n = 362).Table 3 Measures of arterial stiffness in the study population (n = 362).Table 3 Measures of arterial stiffness in the study population (n = 362).Several of the OSA variables correlated with measures of arterial stiffness in the unadjusted analysis (Table 4). AHI and arousal index were primarily correlated with CDP, PSP, and PDP whereas the hypoxia variables seemed primarily correlated with SEVR, TR, and AI75. None of the OSA variables showed correlations with CPP and PPP (Table 4).Table 4 Correlations between OSA variables and measures of arterial stiffness.Table 4 Correlations between OSA variables and measures of arterial stiffness.From the stepwise regression models, only heart rate corrected CAP and augmentation index were associated with all of the OSA variables (Table 5). However, several of the OSA variables were associated with different measures of arterial stiffness as AHI was associated with CSP (adj. β = .11; P = .002), CDP (adj. β = .059; P = .03), CPP (adj. β = .071; P = .01), PSP (adj. β = .093; P = .01), AI75 (adj. β = .069; P = .01), and CAP75 (adj. β = .030; P = .01) and ODI3% was associated with AI75 (adj. β = .072; P = .01) and CAP75 (adj. β = .027; P = .02). In addition, arousal index was associated with CSP (adj. β = .079; P = .03), CPP (adj. β = .059; P = .05), PSP (adj. β = .077; P = .04), PPA (adj. β = −.00090; P = .04), AI75 (adj. β = .075; P = .02), and CAP75 (adj. β = .034; P = .01). Both measures of hypoxia showed associations with arterial stiffness with saturation nadir being associated with PPA (adj. β = .0030; P = .001), AI75 (adj. β = −.21; P = .001), and CAP75 (adj. β = −.071; P = .01) and T90 being associated with CPP (adj. β = .11; P = .02), PPA (adj. β = −.0022; P = .002), AI75 (adj. β = .18; P < .0001) and CAP75 (adj. β = .080; P < .0001).Table 5 Results from the stepwise regression model.Table 5 Results from the stepwise regression model.DISCUSSIONThe main finding of this study is that OSA is associated with measures of arterial stiffness and central blood pressure. Both OSA severity and hypoxia were correlated with measures of arterial stiffness but after adjusting for confounders, only CAP and the augmentation index were associated with all the OSA variables. Although the relationships were relatively weak, this suggests that OSA influences arterial stiffness and that further research into the relationship and its pathways is warranted.In the current study OSA severity, measured as either AHI, ODI3%, or arousal index was related to increased central pressure, peripheral pressure, CAP and/or the augmentation index. Several observational studies have shown relationships between OSA and arterial stiffness primarily using augmentation index as the measure of arterial stiffness and AHI as the measure of OSA severity.30–32 In addition, both randomized controlled trials and case-control studies have shown that treatment of OSA with continuous positive airway pressure may reduce arterial stiffness.11,33–36 Within the current study, the relationship between OSA and arterial stiffness was relatively weak whereas a case-control study Seetho et al. showed significantly stronger associations.36 This could possibly be explained by the fact that patients in the Seetho et al. study had more obesity. To our knowledge, no previous studies have explored the effect of different measures of OSA (AHI, ODI3% and arousal index) on other variables of PWA.Both hypoxia variables (ie, nighttime saturation nadir and time with saturation < 90%) were negatively associated with pulse pressure amplification but also central augmentation pressure and the augmentation index in the present study. Few previous studies have explored the effects of different hypoxia variables in patients with OSA on different variables of arterial stiffness. Nonetheless, within a group of patients with OSA Chung et al. showed that time with saturation < 90% was correlated with increased arterial stiffness measured using carotid-femoral pulse wave velocity,37 indicating that the relationship may at least in part be mediated though hypoxic pathways.Within the current study only CAP and the augmentation index were associated with all OSA variables after adjusting for potential confounders. However, as previous studies have mainly focused on AHI as the measure of OSA and augmentation index as the measure of arterial stiffness, the exact relationship between OSA and arterial stiffness is still not fully understood. Further studies on the effect of other OSA severity measures on arterial stiffness are needed to further clarify the mechanisms for increased vascular dysfunction in OSA.This study included a large clinical population pooled from several well-conducted clinical trials in patients with OSA. However, there are considerations when interpreting the results. Although all participants were patients with OSA and within the population age and BMI was representative, blood pressure levels were within the normal range as were measures of arterial stiffness. Furthermore, although hypertension was present in 40% of cases, blood pressure appeared to be well controlled. Overall, this may indicate that the group was relatively healthy. In addition, there were few women included in the current study as only two of the source studies included both sexes, making the results less generalizable and studies in a larger group of women are warranted. Finally, given the cross-sectional nature of the analysis and lack of a non-OSA control group, we cannot assume the relationship between OSA and arterial stiffness is causative. Causality can only be supported through findings from robustly designed randomized trials, which currently are scarce.18,19To conclude, the current study showed that after adjusting for confounders (including comorbidities), several measures of OSA severity were significantly associated with augmentation index and CAP. Although the associations were relatively weak, the results nevertheless indicate that OSA might influence vascular function. This may in turn play a role in the relationship between OSA and cardiovascular disease beyond standard peripheral blood pressure measures.DISCLOSURE STATEMENTInstitution where work was performed: Sleep and Circadian Research Group, NHMRC Centre for Integrated Research and Understanding of Sleep (CIRUS), Woolcock Institute of Medical Research, University of Sydney, Glebe, Australia. Funding from: Dr. Theorell-Haglöw's work was supported by the Swedish Heart-Lung Foundation and the Swedish Society for Medical Research. All authors have seen and approved the manuscript. Drs. Theorell-Haglöw, Hoyos, Phillips, Yee, and Grunstein report no conflicts of interest. Dr. Cistulli has an appointment to an endowed academic Chair at the University of Sydney, which was created from ResMed funding. He has received research support from ResMed, SomnoMed, and Zephyr Sleep Technologies. He is a consultant / adviser to Zephyr Sleep Technologies, NovoNordisk, Fisher & Paykel Healthcare, and Qantas Airways. He has a pecuniary interest in SomnoMed related to a previous role in R&D (2004). Dr. Liu was supported in part by K24HL138632. Dr. Melehan reports grants from the National Health and Medical Research Council, during the conduction of one of the studies. 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Volume 15 • Issue 02 • February 15, 2019ISSN (print): 1550-9389ISSN (online): 1550-9397Frequency: Monthly Metrics History Submitted for publicationMay 21, 2018Submitted in final revised formSeptember 3, 2018Accepted for publicationSeptember 25, 2018Published onlineFebruary 15, 2019 Information© 2019 American Academy of Sleep MedicineKeywordspatient cohortarterial stiffnessobstructive sleep apneaACKNOWLEDGMENTSDr. Theorell-Haglöw's work was supported by the Swedish Heart-Lung Foundation and the Swedish Society for Medical Research.PDF download
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