Epidemiology of Obstructive Sleep Apnea

Young, Terry; Peppard, Paul E.; Gottlieb, Daniel J.

doi:10.1164/rccm.2109080

Cited by 3,811 publications

(2,665 citation statements)

References 255 publications

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“…1 The high prevalence rates are disturbing considering that OSA patients have an increased risk of morbidity and mortality, particularly due to cardiovascular disease. [2][3][4][5][6][7] OSA patients are often excessively sleepy during the daytime causing traffic crashes and work injuries, and they commonly have an increased number and severity of cardiovascular risk factors, such as hypertension, obesity, atherosclerosis, insulin resistance, the presence of increased inflammatory markers and endothelial dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Increased arterial stiffness in obstructive sleep apnea: a systematic review

et al. 2010

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Obstructive sleep apnea is a prevalent disease that is associated with significant morbidity and mortality, particularly due to cardiovascular disease. An emerging cardiovascular risk factor, arterial stiffness, may also be involved in the cardiovascular complications of obstructive sleep apnea. The purpose of this review was to summarize the current literature regarding the effect of obstructive sleep apnea on arterial stiffness. We conducted a systematic literature review using PubMed, Embase and the Cochrane Library. We identified 24 studies that met search criteria investigating the effect of obstructive sleep apnea on arterial stiffness. Arterial stiffness was found to be increased in obstructive sleep apnea patients compared with controls or increased in severe compared with mild sleep apnea. In some studies, a positive correlation was identified between the degree of arterial stiffness and sleep apnea severity. In the two randomized, controlled trials and the two nonrandomized trials identified, treatment of obstructive sleep apnea with continuous positive airway pressure led to significant decreases in arterial stiffness. Obstructive sleep apnea appears to have an independent effect on arterial stiffness, which may be one of the mechanisms accounting for sleep apnea-associated cardiovascular risk.

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Section: Introductionmentioning

confidence: 99%

Increased arterial stiffness in obstructive sleep apnea: a systematic review

et al. 2010

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“…Despite the clear cause and effect association between OSA and hypertension, it is striking that the prevalence of hypertension among patients with OSA ranges from 35 to 70%. [15][16][17][18][19] Because these studies were based on populations referred to sleep laboratories, differences could be related to referral bias. However, in clinical practice, we frequently observe OSA patients, including severe OSA patients, without hypertension.…”

Section: Discussionmentioning

confidence: 99%

“…However, the reasons why the prevalence of hypertension among OSA patients varies widely (35-70%) are not clear. [15][16][17][18][19] Phenotypic factors could be associated with the presence or absence of hypertension among OSA patients with similar levels of disease severity.…”

Section: Discussionmentioning

confidence: 99%

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Phenotypic characteristics associated with hypertension in patients with obstructive sleep apnea

et al. 2006

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Obstructive sleep apnea (OSA) causes secondary hypertension. However, the reasons why the prevalence of hypertension among OSA patients varies widely (35-70%) are not clear. We sought to investigate the phenotypic characteristics of patients with and without hypertension among OSA patients who were matched for disease severity. We studied 152 OSA patients (76 normotensive and 76 hypertensive) diagnosed by polysomnography. Detailed phenotypic characteristics, including laboratorial analysis, were determined in all patients. Univariate analysis followed by multiple logistic regression analysis was used to identify variables that were independently associated with hypertension. The apnea-hypopnea index in normotensive and hypertensive patients was similar (48726 and 48726 events/ h, respectively) as well as minimum arterial oxygen saturation (76710 and 75710%, respectively) and total sleep time with oxyhaemoglobin saturation o90% (25725 and 28726%, respectively). Hypertensive patients were older (57711 vs 47712 years; Po0.001), had a higher body mass index (BMI; 3477 vs 3075 kg/m 2 ; Po0.001), had a higher frequency of women (37 vs 8%; Po0.001), had a higher incidence of diabetes (25 vs 6%; P ¼ 0.002) and a higher family history of hypertension (75 vs 42%; P ¼ 0.01) than did the normotensive patients. Multiple logistic regression analysis indicated that age (P ¼ 0.004), familial history of hypertension (P ¼ 0.004), BMI (P ¼ 0.04) and female sex (P ¼ 0.03) were the independent variables associated with hypertension. We concluded that increasing age and BMI, familial history of hypertension as well as female gender are phenotypic characteristics associated with hypertension among OSA patients with similar disease severity.

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“…Obstructive sleep apnea (OSA) is a common and serious breathing problem with significant clinical, social and economic consequences 1–3 . There is currently no pharmacotherapy for OSA.…”

Section: Introductionmentioning

confidence: 99%

A resource of potential drug targets and strategic decision‐making for obstructive sleep apnoea pharmacotherapy

2017

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There is currently no pharmacotherapy for OSA, but there is no principled a-priori reason why there shouldn’t be one. This review identifies a rational decision-making strategy with the necessary logical underpinnings that any reasonable approach would be expected to navigate to develop a viable pharmacotherapy for OSA. The process first involves phenotyping an individual to quantify and characterize the critical predisposing factor(s) to their OSA pathogenesis and identify, a-priori, if the patient is likely to benefit from a pharmacotherapy that targets those factors. We then identify rational strategies to manipulate those critical predisposing factor(s), and the barriers that have to be overcome for success of any OSA pharmacotherapy. A new analysis then identifies candidate drug targets to manipulate the upper airway motor circuitry for OSA pharmacotherapy. The first conclusion is that there are two general pharmacological approaches for OSA treatment that are of most potential benefit and are practically realistic, one being fairly intuitive but the second perhaps less so. The second conclusion is that after identifying the critical physiological obstacles to OSA pharmacotherapy, there are current therapeutic targets of high interest for future development. The final analysis provides a tabulated resource of “druggable” targets that are relatively restricted to the circuitry controlling the upper airway musculature, with these candidate targets being of high priority for screening and further study. We also emphasize that a pharmacotherapy may not cure OSA per se, but may still be a useful adjunct to improve the effectiveness of, and adherence to, other treatment mainstays.

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Epidemiology of Obstructive Sleep Apnea

Cited by 3,811 publications

References 255 publications

Increased arterial stiffness in obstructive sleep apnea: a systematic review

Increased arterial stiffness in obstructive sleep apnea: a systematic review

Phenotypic characteristics associated with hypertension in patients with obstructive sleep apnea

A resource of potential drug targets and strategic decision‐making for obstructive sleep apnoea pharmacotherapy

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