Association of Sleep-Disordered Breathing, Sleep Apnea, and Hypertension in a Large Community-Based Study

Nieto, F. Javier; Young, Terry; Lind, Bonnie K.; Shahar, Eyal; Samet, Jonathan M.; Redline, Susan; D’Agostino, Ralph B.; Newman, Anne B.; Lebowitz, Michael D.; Pickering, Thomas G.

doi:10.1001/jama.283.14.1829

Cited by 2,890 publications

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“…2e5 Systemic hypertension affects up to two-thirds of patients with OSA. 6,7 Some investigators have proposed that endothelial dysfunction is mechanistically implicated in a sustained increase in blood pressure 8,9 and is an early process in the development of atherosclerosis. 10,11 Patients with OSA have been shown to have endothelial dysfunction 12e15 and evidence for premature atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

Endothelial dysfunction and hypertension in obstructive sleep apnea – Is it due to intermittent hypoxia?

Jafari

Mohsenin

2013

Journal of Cardiovascular Disease Research

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a b s t r a c tBackground: Obstructive sleep apnea (OSA) is a prevalent disorder causing hypertension. Endothelial dysfunction appears to underlie development of hypertension. It is not known whether hypoxia during sleep is necessarily the prerequisite process for endothelial dysfunction and hypertension in OSA. We therefore examined the relationship between endothelial-dependent vasodilatory capacity, hypoxia and circulating angiogenesis inhibitors in OSA. Methods and results:We studies 95 subjects with and without OSA and hypertension. Endothelialdependent vasodilation was assessed using brachial artery flow-mediated vasodilation method (FMD). Plasma angiogenesis inhibitors, endoglin (sEng) and fms-like tyrosine kinase-1 (sFlt-1), were measured using ELISA. The apneaehypopnea indexes were 41 AE 5 and 48 AE 4 events/hr in normotensive OSA (N-OSA) and hypertensive OSA (H-OSA), respectively, indicating severe OSA. The sleep time spent with SaO 2 < 90% (T < 90%) were 34 AE 8 and 40 AE 9 min, respectively. FMD was markedly impaired in H-OSA (8.0% AE 0.5) compared to N-OSA (13.5% AE 0.5, P < 0.0001), H-non-OSA (10.5% AE 0.8, P < 0.01), and N-non-OSA (16.1% AE 1.0, P < 0.0001). There was no correlation between T < 90% and FMD. Both OSA groups had elevated levels of sFlt-1 (62.4 AE 5.9 and 63.9 AE 4.7 pg/ml) compared to N-non-OSA (32.1 AE 6.5, P ¼ 0.0008 and P ¼ 0.0004, respectively) and H-non-OSA (41.2 AE 7.0, P < 0.05 and P ¼ 0.03, respectively). In contrast, sEng was only elevated in H-OSA (4.20 AE 0.17 ng/ml) compared with N-OSA (3.64 AE 0.14, P ¼ 0.01) and N-non-OSA (3.48 AE 0.20, P ¼ 0.01). There was a modest but statistically significant inverse correlation between sEng and FMD in only H-OSA group (r ¼ À0.38, P < 0.05). Conclusion: These data show that patients with OSA and hypertension have marked impairment of FMD, independent of hypoxia exposure, which is associated with increased sEng.Copyright Ó 2013, SciBioIMed.Org, Published by Reed Elsevier India Pvt. Ltd. All rights reserved. Key MessagesObstructive sleep apnea is a highly prevalent disorder with associated high morbidity and mortality. Obstructive sleep apnea is now considered as one of the causes of systemic hypertension. No all patients with obstructive sleep apnea develop hypertension. There appears to be divergent responses to apnea-associated hypoxia. In this article a group of patients with severe obstructive sleep apnea and hypoxia exposure during sleep had normal blood pressure and relatively preserved endothelial-dependent vasodilatory capacity. A comparable group of patients with similar apnea severity and hypoxia exposure had marked impairment in endothelial-dependent vasodilatory capacity and hypertension. This group had significantly elevated circulating levels of soluble endoglin, an angiogenesis inhibitor, with known effect on endothelial function and development of hypertension. It is conceivable that inflammatory state of obstructive sleep apnea provokes release of angiogenesis inhibitors causing downstream perturbation of endothelial...

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Section: Introductionmentioning

confidence: 99%

Endothelial dysfunction and hypertension in obstructive sleep apnea – Is it due to intermittent hypoxia?

Jafari

Mohsenin

2013

Journal of Cardiovascular Disease Research

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“…While dietinduced weight loss is associated with a fall in blood pressure, 19 the effects from sibutramine are less clear. 20,21 Given that OSA is a risk factor for hypertension 22 and difficult to control blood pressure, 11 there may be specific concerns in using sibutramine in obese patients with OSA. It is possible that sibutramine may initially increase blood pressure in subjects with OSA at least in the early stages of use before weight loss occurs.…”

Section: Introductionmentioning

confidence: 99%

The effect of sibutramine-assisted weight loss in men with obstructive sleep apnoea

et al. 2006

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Objective: Obstructive sleep apnoea (OSA) occurs frequently in obese patients and may be reversible with weight loss. Obstructive sleep apnoea and obesity are both independent risk factors for hypertension and increased sympathetic activity. Sibutramine has been increasingly used in the management of obesity, but is relatively contraindicated in patients with hypertension. No studies have investigated the effect of sibutramine on OSA, blood pressure and heart rate. We aimed to assess the changes in OSA and cardiovascular parameters in obese men with OSA enrolled in a sibutramine-assisted weight loss programme (SIB-WL). Design: Open uncontrolled cohort study of obese male subjects with OSA in an SIB-WL. Subjects: Eighty-seven obese (body mass index ¼ 34.272.8 kg/m 2 ) middle-aged (46.379.3 years) male subjects with symptomatic OSA (Epworth score 13.473.6; respiratory disturbance index (RDI) 46.0723.1 events/h) completed the study. Results: At 6 months, there was significant weight loss (8.374.7 kg, Po0.0001), as well as a reduction in waist and neck circumference and sagittal height (all Po0.0001). These changes were accompanied by a reduction in OSA severity (RDI fell by 16.3719.4 events/h and Epworth score by 4.574.6), both Po0.0001). There was no significant change to systolic (P ¼ 0.07) or diastolic blood pressure (P ¼ 0.87); however, there was a mild rise in resting heart rate (Po0.0001). Conclusion: Moderate (B10%) weight loss with SIB-WL results in improvement in OSA severity without increase in blood pressure in closely monitored OSA subjects.

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“…Immediate consequences of OSAS are sleep fragmentation, arousal, poor school/job performance, irritability, intermittent hypercapnia and hypoxemia, nocturnal hypertension and marked changes in autonomic control of the cardiovascular system. 88 The long-term consequences of OSAS include sustained daytime and nocturnal hypertension, 89,90 cor pulmonale, left ventricular hypertrophy 91 and increased cardiovascular and cerebrovascular morbidity and mortality. 92 Indeed, cross-sectional results from the Sleep Heart Health Study showed a strong association between OSAS, heart failure and stroke.…”

Section: Cardiovascular Risksmentioning

confidence: 99%

Bariatric surgery for pediatric extreme obesity: now or later?

2006

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Obesity is a multifactorial disease of epidemic and global proportions that poses the most significant threat to the health of our younger generations. Those who are the most extremely affected bear the largest burden of health problems. In the US, extreme obesity affects approximately 9 million adults and 2 million children, and is associated with both immediate health problems and later health risk, including premature mortality. Present medical and behavioral interventions for extreme obesity in adults and children rarely result in the significant, durable weight loss necessary to improve health outcomes, prompting a search for more aggressive measures. Weight loss (bariatric) surgery has been advocated as an intervention for those with extreme obesity. In adults, bariatric surgery results in prolonged weight control and improvement in serious obesity comorbidities, namely type 2 diabetes, dyslipidemias, hypertension and obstructive sleep apnea syndrome. A surge in weight loss operations for adolescents has been observed recently, with a threefold increase in case volumes nationwide from 2000 to 2003. Current evidence suggests that after bariatric surgery, adolescents lose significant weight and serious obesity-related medical conditions and psychosocial status are improved. Thus it is reasonable to propose that bariatric surgery performed in the adolescent period may be more effective treatment for childhood-onset extreme obesity than delaying surgery for extremely obese youth until adulthood. This position has been echoed by a number of groups and an independent systematic review. Finally, it is conceivable that bariatric surgery performed in adulthood for childhood onset extreme obesity may not be as effective for comorbidity treatment as surgery performed earlier during adolescence. The purpose of this review is to examine the evidence, which supports early rather than later use of bariatric surgery in the treatment of extreme obesity, and to present this information in light of the medical and surgical risks of bariatric surgery.

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Association of Sleep-Disordered Breathing, Sleep Apnea, and Hypertension in a Large Community-Based Study

Abstract: Our findings from the largest cross-sectional study to date indicate that SDB is associated with systemic hypertension in middle-aged and older individuals of different sexes and ethnic backgrounds.

Cited by 2,890 publications

References 48 publications

Endothelial dysfunction and hypertension in obstructive sleep apnea – Is it due to intermittent hypoxia?

Endothelial dysfunction and hypertension in obstructive sleep apnea – Is it due to intermittent hypoxia?

The effect of sibutramine-assisted weight loss in men with obstructive sleep apnoea

Bariatric surgery for pediatric extreme obesity: now or later?

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