Association of obstructive sleep apnea with arterial stiffness and nondipping blood pressure in patients with hypertension.
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ABSTRACT:
SUBMITTER: Jenner R
PROVIDER: S-EPMC8030757 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Rationale: Maternal obstructive sleep apnea-hypopnea (OSAH) is associated with hypertensive disorders of pregnancy (HDP). Attenuation of the normal nocturnal blood pressure (BP) decline (non-dipping) is associated with adverse pregnancy outcomes. OSAH is associated with nocturnal non-dipping in the general population, but this has not been studied in pregnancy. We therefore analyzed baseline data from an ongoing RCT (NCT03309826) assessing the impact of OSAH treatment on HDP outcomes, to evaluate the relationship of OSAH to 24-h BP profile, in particular nocturnal BP dipping, and measures of arterial stiffness. Methods: Women with a singleton pregnancy and HDP underwent level II polysomnography. Patients with OSAH (apnea-hypopnea index (AHI) ≥ 5 events/h) then underwent 24-h ambulatory BP monitoring and arterial stiffness measurements (applanation tonometry, SphygmoCor). Positive dipping was defined as nocturnal systolic blood pressure (SBP) dip ≥ 10%. The relationships between measures of OSAH severity, measures of BP and arterial stiffness were evaluated using linear regression analyses. Results: We studied 51 HDP participants (36.5 ± 4.9 years, BMI 36.9 ± 8.6 kg/m2) with OSAH with mean AHI 27.7 ± 26.4 events/h at 25.0 ± 4.9 weeks' gestation. We found no significant relationships between AHI or other OSA severity measures and mean 24-h BP values, although BP was generally well-controlled. Most women were SBP non-dippers (78.4%). AHI showed a significant inverse correlation with % SBP dipping following adjustment for age, BMI, parity, gestational age, and BP medications (β = -0.11, p = 0.02). Significant inverse correlations were also observed between AHI and DBP (β = -0.16, p = 0.01) and MAP (β = -0.13, p = 0.02) % dipping. Oxygen desaturation index and sleep time below SaO2 90% were also inversely correlated with % dipping. Moreover, a significant positive correlation was observed between carotid-femoral pulse wave velocity (cfPWV) and REM AHI (β = 0.02, p = 0.04) in unadjusted but not adjusted analysis. Conclusion: Blood pressure non-dipping was observed in a majority of women with HDP and OSAH. There were significant inverse relationships between OSAH severity measures and nocturnal % dipping. Increased arterial stiffness was associated with increasing severity of OSAH during REM sleep in unadjusted although not adjusted analysis. These findings suggest that OSAH may represent a therapeutic target to improve BP profile and vascular risk in HDP.
| S-EPMC8558510 | biostudies-literature
Project description:Background Sleep characteristics and disorders are associated with higher blood pressure (BP) when measured in the clinic setting. Methods and Results We tested whether self-reported sleep characteristics and likelihood of obstructive sleep apnea (OSA) were associated with nocturnal hypertension and nondipping systolic BP (SBP) among participants in the CARDIA (Coronary Artery Risk Development in Young Adults) study who completed 24-hour ambulatory BP monitoring during the year 30 examination. Likelihood of OSA was determined using the STOP-Bang questionnaire. Global sleep quality, habitual sleep duration, sleep efficiency, and midsleep time were obtained from the Pittsburgh Sleep Quality Index. Nocturnal hypertension was defined as mean asleep SBP ≥120 mm Hg or diastolic BP ≥70 mm Hg. Nondipping SBP was defined as a decline in awake-to-asleep SBP <10%. Among 702 participants, the prevalence of nocturnal hypertension and nondipping SBP was 41.3% and 32.5%, respectively. After multivariable adjustment including cardiovascular risk factors, the prevalence ratios (PRs) for nocturnal hypertension and nondipping SBP associated with high versus low likelihood of OSA were 1.32 (95% CI, 1.00-1.75) and 1.31 (95% CI, 1.02-1.68), respectively. The association between likelihood of OSA and nocturnal hypertension was stronger for white participants (PR: 2.09; 95% CI, 1.23-3.48) compared with black participants (PR: 1.11; 95% CI, 0.79-1.56). The PR for nondipping SBP associated with a 1-hour later midsleep time was 0.92 (95% CI, 0.85-0.99). Global sleep quality, habitual sleep duration, and sleep efficiency were not associated with either nocturnal hypertension or nondipping SBP. Conclusions These findings suggest that addressing OSA risk and sleep timing in a clinical trial may improve BP during sleep.
| S-EPMC7428601 | biostudies-literature
Project description:Objective: Obstructive sleep apnea (OSA) results in increased carotid intima-media thickness (IMT) and arterial stiffness; however, the association between adipocytokines and IMT/arterial stiffness in OSA patients is unclear. Methods: We enrolled 95 normal weight and overweight, not obese, participants from May 2018 to December 2018 in this study. All subjects underwent a carotid artery ultrasound examination and polysomnography. Blood samples were used to determine serum chemerin, adiponectin, SFRP5, and apelin levels. Correlations between two quantitative variables were assessed using the Pearson or Spearman coefficient. Stepwise models of multiple linear regression analysis were performed to assess the independent relationships. Result: IMT in OSA patients was significantly higher than in the non-snorers. There were significant differences in the arterial stiffness parameters such as distensibility coefficient (DC), compliance coefficient (CC), and pulse wave velocity (PWV). SFRP5 level was lower in OSA patients than in non-snorers. Adiponectin correlated with CC, DC, and PWV among OSA patients; however, the relationship disappeared after a multivariable adjustment. Age was independently associated with all quantitative IMT and stiffness indices. AHI and minimum oxygen saturation (Mini SaO2) were independently related to arterial stiffness. Conclusion: The quantitative IMT and carotid arterial elasticity were significantly worse among OSA patients. Age was the main independent factor correlated with quantitative IMT and arterial stiffness, and AHI and mini SaO2 were associated factors. There were no relationships between aforementioned adipocytokines and quantitative IMT/carotid arterial stiffness.
| S-EPMC7142226 | biostudies-literature
Project description:Obstructive sleep apnoea (OSA) has been linked to cardiovascular risk factors, such as hypertension, and clinical cardiovascular endpoints. Our aim was to assess whether OSA is independently associated with atherosclerosis and vascular dysfunction as assessed by cardiovascular magnetic resonance (CMR).58 patients with OSA and 39 matched control subjects without OSA underwent CMR of the aorta and carotid arteries. Carotid and aortic wall thickness and aortic distensibility were measured. Multi-weighted, high resolution CMR imaging was used for carotid atheroma characterization according to the American Heart Association (AHA) atheroma classification, modified for CMR.Carotid [1.47±0.03 mm vs. 1.26±0.05 mm, (P<0.01)] and aortic wall thickness [2.95±0.09 mm vs. 2.05±0.07 mm, (P<0.001)] were increased in patients with OSA compared to controls. Aortic distensibility was decreased in patients with OSA [3.62±0.3 vs. 4.75±0.2 mmHg(-1)×10(-3), (P<0.05)]. Prevalence of carotid plaque, average carotid atheroma class, and prevalence of high risk features of carotid atheroma were increased in patients with OSA (P<0.005 for all). On multivariate analysis, Oxygen desaturation index (ODI) emerged as an independent predictor of carotid and aortic wall thickness, but not of aortic stiffness.OSA is associated with increased carotid and aortic atheroma burden and with advanced, high risk carotid atherosclerotic plaques, but not with aortic stiffening.
| S-EPMC4978311 | biostudies-literature
Project description:Hypertension in childhood may continue into adulthood and lead to adverse cardiovascular outcomes. Evidence suggests that adenotonsillectomy for childhood obstructive sleep apnea (OSA) may be associated with blood pressure (BP) improvement. However, how adenotonsillectomy is associated with BP in hypertensive and nonhypertensive children with OSA remains unclear.To investigate disparities in BP changes after adenotonsillectomy in hypertensive and nonhypertensive children with OSA.From January 1, 2010, to April 30, 2016, children (aged <18 years) with symptoms of OSA treated at National Taiwan University Hospital were enrolled in this retrospective case series study.Children underwent polysomnography for diagnosis of OSA (apnea-hypopnea index >1). All children with OSA underwent adenotonsillectomy.Preoperative and postoperative overnight polysomnographic data were obtained. Office BP was measured in a sleep center before (nocturnal BP) and after (morning) polysomnography.A total of 240 nonobese children (mean [SD] age, 7.3 [3.0] years; 160 [66.7%] male and 80 [33.3%] female) with OSA were recruited. Postoperatively, the apnea-hypopnea index decreased significantly from 12.1 to 1.7 events per hour (95% CI of difference, -12.3 to -8.4 events per hour). The whole cohort had a significant decrease in nocturnal diastolic BP (66.9 to 64.5 mm Hg; 95% CI of difference, -4.1 to -0.7 mm Hg) and morning diastolic BP (66.9 to 64.4 mm Hg; 95% CI of difference, -4.2 to -0.8 mm Hg). The number (percentage) of patients with diastolic BP in the greater than 95th percentile decreased significantly nocturnally (48 [20.0%] to 33 [13.8%]; 95% CI of difference, -12.1% to -0.4%) and in the morning (52 [21.7%] to 34 [14.2%]; 95% CI of difference, -13.6% to -1.4%). Postoperatively, hypertensive children had a significant decrease in all BP measures, including mean (SD) nocturnal and morning systolic BP (nocturnal: 107.5 [8.6] mm Hg; morning: 106.0 [9.4] mm Hg), systolic BP index (nocturnal: -4.3 [8.6]; morning: -5.7 [8.5]), diastolic BP (nocturnal: 65.1 [11.5] mm Hg; morning: 64.4 [10.1] mm Hg), and diastolic BP index (nocturnal: -10.7 [17.3]; morning: -11.6 [15.7]), whereas the nonhypertensive group had a slight increase in nocturnal systolic BP (103.8 to 105.9 mm Hg; 95% CI of difference, 0.4-3.9 mm Hg). A generalized estimating equation model for subgroup comparisons revealed that children with hypertension, compared with those without, had greater improvement in all BP measures.Hypertensive children with OSA had a significant improvement in BP after adenotonsillectomy. Hypertensive children with OSA should be screened and treated by adenotonsillectomy because proper treatment not only eases OSA symptoms but also potentially prevents future cardiovascular and end-organ disease.
| S-EPMC5876823 | biostudies-other
Project description:RationaleWe hypothesized that untreated severe obstructive sleep apnea (OSA) is associated with elevated ambulatory blood pressure (BP) in subjects with high cardiovascular disease (CVD) risk despite medical management.MethodsData from the baseline examination of the Heart Biomarker Evaluation in Apnea Treatment (HeartBEAT) study, a 4-site randomized controlled trial were analyzed. Individuals with moderate-severe OSA (apnea hypopnea index, AHI = 15-50) and cardiovascular risk were recruited from cardiology practices. Those with hypertension were included. Intensive antihypertensive regimen (IAR) was defined as ≥ 3 antihypertensives including a diuretic. Definitions were: controlled BP (BP < 130/80), uncontrolled elevated BP (BP ≥ 130/80 not on IAR) and resistant elevated BP (BP ≥ 130/80 mm Hg despite IAR). Associations of untreated severe OSA (AHI ≥ 30) and uncontrolled and resistant elevated BP were evaluated using logistic regression analyses adjusted for age, sex, race, body mass index, smoking status, diabetes, and CVD.ResultsAmong the 284 participants (mean age 63.1 ± 7.2 years, 23.6% with severe OSA), 61.6% had controlled BP, 28.5% had uncontrolled elevated BP, and 9.9% had resistant elevated BP. Among participants prescribed IAR, resistant elevated BP was more prevalent in those with severe compared to moderate OSA (58.3% vs. 28.6%, p = 0.01). Participants with severe OSA had a 4-fold higher adjusted odds of resistant elevated BP (OR 4.1, 95% CI: 1.7-10.2), a finding not reproduced in the absence of IAR use.ConclusionsAmong patients with increased cardiovascular risk and moderate to severe OSA, untreated severe compared to moderate OSA was associated with elevated BP despite IAR suggesting untreated severe OSA contributes to poor BP control despite aggressive medication use.CommentaryA commentary on this article appears in this issue on page 845.
| S-EPMC4106935 | biostudies-literature
Project description:STUDY OBJECTIVES:Obstructive sleep apnea (OSA) and hypertension are independent risk factors of cardiovascular morbidities. This study aims to investigate the relationship between OSA, blood pressure (BP) control, and myocardial injury in patients with difficult-to-control hypertension. METHODS:Patients with hypertension who required three or more medications were prospectively recruited at a tertiary referral center. In-laboratory polysomnography, followed by blood tests for fasting glucose, glycated hemoglobin, lipids, high-sensitivity troponin I (hsTnI), B-type natriuretic peptide (BNP), C-reactive protein, and advanced oxidation protein products were performed. After polysomnography, 24-hour ambulatory BP monitoring was arranged. RESULTS:A total of 98 participants were analyzed, with mean age 51 ± 9 years and body mass index 30 ± 5 kg/m2. Previously undiagnosed severe OSA (apneahypopnea index [AHI] ? 30 events/h) was present in 51 patients (52%). hsTnI was negatively correlated with nocturnal dip in systolic BP (r = -.205, P = .048). After controlling for confounders, including BP control, AHI and oxygen desaturation index (ODI) were positively correlated with hsTnI (r = .282, P = .009 and r = .279, P = .010, respectively) and C-reactive protein (r = .302, P = .005 and r = .285, P = .008, respectively), but not with BNP or advanced oxidation protein products. Age, ODI, and loss of nocturnal systolic BP dip were significant determinants of hsTnI level (? = .225, P = .022; ? = .293, P = .003; and ? = -.215, P = .029; R2 = .151). Age, female sex, 24-hour mean diastolic BP, and metabolic syndrome, but not indices of apnea severity, were predictors of BNP level. CONCLUSIONS:Unrecognized severe OSA was common in patients with difficult-to-control hypertension, and OSA severity was associated with myocardial injury, independent of BP control with medications. CLINICAL TRIAL REGISTRATION:Registry: ClinicalTrials.gov, Title: A Cross-sectional Study of the Occurrence and Effect of Obstructive Sleep Apnea in Subjects With Resistant Hypertension, Identifier: NCT00843583, URL: https://clinicaltrials.gov/ct2/show/NCT00843583.
| S-EPMC6223564 | biostudies-literature
Project description:BACKGROUND:Obstructive sleep apnea (OSA) is associated with cardiovascular co-morbidities and mortality. Arterial stiffness is an independent predictor of cardiovascular risk and mortality, and is influenced by the presence of OSA and related comorbidities. There is a paucity of data regarding long-term evolution of arterial stiffness in CPAP-treated OSA patients. We aimed to prospectively study long term PWV variations and determinants of PWV deterioration. METHODS:In a prospective obese OSA cohort, at time of diagnosis and after several years of follow-up we collected arterial stiffness measured by carotid-femoral pulse wave velocity (PWV), clinical and metabolic parameters, and CPAP adherence. Univariate and multivariate analyses were performed in order to determine contributing factors. RESULTS:Seventy two OSA patients (men: 52.8%, median age: 55.8 years and median BMI of 38.5 kg/m2) with a prevalence of hypertension: 58.3%, type 2 diabetes: 20.8%, hypercholesterolemia: 33.3%, current or past smoking: 59.7%, were evaluated after a median follow-up of 7.4 [5.8; 8.3] years. Over the period of follow-up, the median increase in PWV was 1.34 [0.10; 2.37] m/s. In multivariate analysis, the increase in PWV was associated with older age (10 extra years was associated with a 5.24 [1.35; 9.12] % increase in PWV) and hypertension (a significant increase in PWV of 8.24 [1.02; 15.57] %). No impact of CPAP adherence on PWV evolution was found. CONCLUSION:PWV progression in CPAP-treated OSA patients is mainly related to pre-existing cardio-metabolic comorbidities and not influenced by CPAP adherence. In this high cardiovascular risk population, it is crucial to associated weight management and exercise with CPAP treatment.
| S-EPMC7406029 | biostudies-literature
Project description:STUDY OBJECTIVES:The carbonic anhydrase inhibitor acetazolamide (AZT) modulates blood pressure at high altitude and reduces sleep-disordered breathing in patients with obstructive sleep apnea (OSA). We aimed to investigate the treatment effect of AZT and in combination with continuous positive airway pressure (CPAP) on blood pressure in patients with hypertension and OSA. METHODS:In a prospective, randomized, three-way crossover study, 13 male patients with hypertension and moderate to severe OSA (age 64 ± 7 years, body mass index 29 ± 4 kg/m2, and mean apnea-hypopnea index 37 ± 23 events/h) received AZT, CPAP, or AZT plus CPAP for 2-week periods. Antihypertensive medication was washed out. Office and 24-hour blood pressure, arterial stiffness, polygraphic sleep study data, and blood chemistry were compared. RESULTS:AZT alone and AZT plus CPAP, but not CPAP alone, reduced office mean arterial pressure compared to baseline (-7 [95% CI -11 to -4], -7 [95% CI -11 to -4] and -1 [95% CI -5 to 4] mmHg, respectively; repeated- measures analysis of variance (RM-ANOVA; P = .015). Aortic systolic pressure and augmentation index, assessed by radial artery oscillatory tonometry, were unaffected by CPAP but decreased after AZT and AZT plus CPAP (RM-ANOVA P = .030 and .031, respectively). The apnea-hypopnea index was significantly reduced in all three treatment arms, most prominently by AZT plus CPAP (RM-ANOVA P = .003). The reduction of venous bicarbonate concentration following AZT was correlated with the change of apnea-hypopnea index (r = 0.66, P = .013). CONCLUSIONS:AZT reduced blood pressure, vascular stiffness, and sleep-disordered breathing in patients with OSA and comorbid hypertension. Carbonic anhydrase inhibition may constitute a potential target for drug therapy in patients with sleep apnea and comorbid hypertension. CLINICAL TRIAL REGISTRATION:Registry: ClinicalTrials.gov; Identifier: NCT02220803; Title: A Short Term Open, Randomized Cross-over Trial Exploring the Effect of Carbonic Anhydrase Inhibition by Acetazolamide on Sleep Apnea Associated Hypertension and Vascular Dysfunction; URL: https://clinicaltrials.gov/ct2/show/NCT02220803 and Registry: EU Clinical Trials Register; EudraCT Number: 2013-004866-33; Title: A short term open, randomized cross over trial exploring the effect of carbonic anhydrase inhibition by acetazolamide on sleep apnea associated hypertension; URL: https://www.clinicaltrialsregister.eu/ctr-search/search?query=2013-004866-33.
| S-EPMC5837832 | biostudies-literature
Project description:We hypothesized increasing obstructive sleep apnea (OSA) severity would be associated with nondipping blood pressure (BP) in increased cardiovascular disease (CVD) risk.Baseline data from 298 cardiology patients recruited for a multicenter randomized controlled trial were examined. Dipping was defined as a sleep-related BP or heart rate (HR) reduction of at least 10%. Logistic regression models were fit, adjusting for age, sex, race, BMI, CVD risk factors, CVD, and study site.There was a statistically significant 4% increase in the odds of nondipping SBP per 1-unit increase in both apnea hypopnea index (AHI) and oxygen desaturation index (ODI). There was no significant relationship between AHI and nondipping mean arterial pressure (MAP); however, a 3% increase in the odds of nondipping MAP per 1-unit increase in ODI was observed [odds ratio (OR) = 1.03; 95% confidence interval (CI) 1.00-1.05]. At severe OSA levels, a 10 and 4% increase in odds of nondipping DBP per 1-unit increase in AHI and ODI were observed, respectively. A 6% [OR = 1.06; 95% CI (1.01-1.10)] increase in nondipping HR odds was observed with each increase in ODI until the upper quartile of ODI.In patients at cardiovascular risk and moderate-to-severe OSA, increasing AHI and/or ODI were associated with increased odds of nondipping SBP and nondipping MAP. More severe levels of AHI and ODI also were associated with nondipping DBP. These results support progressive BP burden associated with increased OSA severity even in patients managed by cardiology specialty care.
| S-EPMC4096765 | biostudies-literature