Endothelial Function and Circulating Endothelial Progenitor Cells in Patients with Sleep Apnea Syndrome

Peña, Mónica de la; Barceló, Antònia; Barbé, Ferrán; Piérola, Javier; Pons, J Pedro-Botet; Rimbau, Enric; Ayllón, O.; Agustí, Àlvar

doi:10.1159/000109643

Cited by 71 publications

(43 citation statements)

References 57 publications

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“…Conflicting results were also reported on the amounts of EPCs, which at low numbers are indicative of impaired vascular function. While one study described a reduced number of circulating EPCs in OSAHS [151], in another study no differences were noted between patients with OSAHS and controls [150]. Such conflicting results can stem from the very small numbers of apoptotic cells or EPCs in the circulation.…”

Section: Endothelial Cellsmentioning

confidence: 96%

Molecular mechanisms of cardiovascular disease in OSAHS: the oxidative stress link

Lavie¹,

Lavie²

2009

European Respiratory Journal

318

223

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Obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is a highly prevalent breathing disorder in sleep that is an independent risk factor for cardiovascular morbidity and mortality. A large body of evidence, including clinical studies and cell culture and animal models utilising intermittent hypoxia, delineates the central role of oxidative stress in OSAHS as well as in conditions and comorbidities that aggregate with it. Intermittent hypoxia, the hallmark of OSAHS, is implicated in promoting the formation of reactive oxygen species (ROS) and inducing oxidative stress. The ramifications of increased ROS formation are pivotal. ROS can damage biomolecules, alter cellular functions and function as signalling molecules in physiological as well as in pathophysiological conditions. Consequently, they promote inflammation, endothelial dysfunction and cardiovascular morbidity. Oxidative stress is also a crucial component in obesity, sympathetic activation and metabolic disorders such as hypertension, dyslipidaemia and type 2 diabetes/insulin resistance, which aggregate with OSAHS. These conditions and comorbidities could result directly from the oxidative stress that is characteristic of OSAHS or could develop independently. Hence, oxidative stress represents the common underlying link in OSAHS and the conditions and comorbidities that aggregate with it.

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Section: Endothelial Cellsmentioning

confidence: 96%

Molecular mechanisms of cardiovascular disease in OSAHS: the oxidative stress link

Lavie¹,

Lavie²

2009

European Respiratory Journal

318

223

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“…Nondipping nocturnal blood pressure is also associated with vascular endothelial dysfunction and reduced nitric oxide levels [36]. Furthermore, nocturnal nondippers demonstrate a reduced number of endothelial progenitor cells, which are responsible for repairing vascular damage and maintaining homeostasis [37], a finding also reported in patients with OSA [38].…”

mentioning

confidence: 89%

Obstructive sleep apnoea as a cause of nocturnal nondipping blood pressure: recent evidence regarding clinical importance and underlying mechanisms

2017

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Obstructive sleep apnoea (OSA) is highly prevalent, with recent general population studies indicating that up to 50% of males and 23% of females have moderate or severe sleep disordered breathing (SDB) based on an apnoea-hypopnoea index (AHI) of >15 events·h -1 [1, 2]. OSA is recognised as an independent risk factor for systemic hypertension [3] and a nondipping nocturnal blood pressure profile is particularly likely in patients with OSA [4], even in the absence of significant hypertension. Furthermore, hypertension is increasingly recognised as an important predictor of prevalent OSA and appears to be more predictive than excessive day-time sleepiness in some settings [5]. However, recent evidence also indicates that only moderate-severe OSA (AHI >20 events·h -1 ) constitutes a significant independent risk for hypertension [2] and cluster analysis of sleep clinic populations indicates that particular population subtypes are especially associated with hypertension [6].These recent reports regarding the very high general prevalence of SDB and factors that influence the relationship with hypertension prompt a reassessment of the clinical relevance regarding the association between OSA and hypertension, especially nocturnal hypertension, and the underlying mechanisms that may contribute to the development of a nondipping nocturnal blood pressure profile in OSA patients. This topic is important in the context of the recent SAVE (Sleep Apnea Cardiovascular Endpoints) trial report [7] involving 2717 patients with established cardiovascular disease and moderate or severe OSA associated with minimal sleepiness who were randomised to best usual care with or without added continuous positive airway pressure (CPAP) therapy and followed for up to 7 years. CPAP therapy was not associated with any improvement in cardiac or cerebrovascular outcome, although data on secondary and other end-points in the report indicated a small but significant reduction in diastolic blood pressure. This finding is particularly relevant in the context that the average compliance with CPAP was only 3.3 h and a recent meta-analysis indicates that beneficial effects of CPAP on blood pressure in OSA patients with minimal sleepiness are largely confined to patients using CPAP for >4 h per night [8].

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“…To assess the risk of atherosclerosis, arterial stiffness [5] or endothelial dysfunction [6,7] has been noninvasively measured by pulse wave velocity (PWV) [8] or flow-mediated dilatation (FMD) in the brachial artery [9], respectively. In predicting the risk of atherosclerosis of OSAS patients, arterial stiffness, compared to endothelial function, has been evaluated in only a few studies [10,11,12].…”

Section: Introductionmentioning

confidence: 99%

The Association of Nocturnal Hypoxemia with Arterial Stiffness and Endothelial Dysfunction in Male Patients with Obstructive Sleep Apnea Syndrome

et al. 2009

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Background: Obstructive sleep apnea syndrome (OSAS) is associated with cardiovascular complications, and atherosclerosis is considered to mediate this association. Arterial stiffness and endothelial dysfunction are widely accepted as early markers of atherosclerosis. Objectives: The purpose of this study was to investigate the influence of sleep apnea on arterial stiffness and endothelial dysfunction. Methods: We enrolled 83 OSAS patients including 39 with mild to moderate degree (apnea hypopnea index, AHI ≧5, AHI <30) and 44 with severe degree sleep apnea (AHI ≧30) and 29 normal control subjects (AHI <5). After finishing polysomnography, carotid-femoral pulse wave velocity (cfPWV) and flow-mediated dilation (FMD) were measured using noninvasive devices. Results: In patients with severe degree of OSAS, cfPWV was significantly higher than mild to moderate degree of OSAS or normal control subjects. Also, the severe OSAS group showed lower FMD than the normal control group (all p < 0.01). The cfPWV was significantly correlated with FMD (r = –0.26, p < 0.01). Age (β = 0.33, p < 0.01) and percentage of time below 90% O₂ saturation (β = 0.34, p < 0.01) were the significant variables to determine cfPWV (adjusted R² = 21%, p < 0.01) in multivariate analysis, and the lowest O₂ saturation was a significant determinant for FMD (β = 0.25, adjusted R² = 6%, p < 0.01). Conclusions: Nocturnal hypoxemia may alter arterial elasticity and endothelial function in OSAS patients, and those impairments could increase the risk of cardiovascular complications.

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Endothelial Function and Circulating Endothelial Progenitor Cells in Patients with Sleep Apnea Syndrome

Cited by 71 publications

References 57 publications

Molecular mechanisms of cardiovascular disease in OSAHS: the oxidative stress link

Molecular mechanisms of cardiovascular disease in OSAHS: the oxidative stress link

Obstructive sleep apnoea as a cause of nocturnal nondipping blood pressure: recent evidence regarding clinical importance and underlying mechanisms

The Association of Nocturnal Hypoxemia with Arterial Stiffness and Endothelial Dysfunction in Male Patients with Obstructive Sleep Apnea Syndrome

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