Endothelial Cell Apoptosis in Obstructive Sleep Apnea

Solh, Ali A. El; Akinnusi, Morohunfolu E.; Baddoura, Fadi H.; Mankowski, Corey R.

doi:10.1164/rccm.200611-1598oc

Cited by 140 publications

(103 citation statements)

References 41 publications

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“…In the current study, we did not characterize the state of activation or viability of the CECs or EPCs, Recently, El Solh et al [29] reported a significant increase in the number of CD146-positive and annexin V-positive cells in patients with OSA. The authors concluded that apoptotic CECs are increased in OSA.…”

Section: Discussionmentioning

confidence: 68%

Circulating Endothelial Cells and Endothelial Progenitor Cells in Obstructive Sleep Apnea

Martin

Stanchina

Kouttab

et al. 2008

Lung

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Increased circulating endothelial cells (CECs) have been observed in patients with vascular injury associated with acute myocardial infarction, pulmonary hypertension, and congestive heart failure. Decreased circulating endothelial progenitor cells (EPCs) have been observed in patients with risk factors for cardiovascular disease. Obstructive sleep apnea (OSA) is associated with increased risk of cardiovascular disease and endothelial dysfunction. Subjects were recruited from patients referred for overnight polysomnograms; 17 subjects had OSA and 10 control subjects did not have OSA. All subjects lacked vascular disease and risk factors for vascular disease. Peripheral blood was obtained from fasting subjects in the morning, following sleep studies. CECs and EPCs were quantified using magnetic bead separation with UV epifluorescence microscopy and flow

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Section: Discussionmentioning

confidence: 68%

Circulating Endothelial Cells and Endothelial Progenitor Cells in Obstructive Sleep Apnea

Martin

Stanchina

Kouttab

et al. 2008

Lung

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“…Numerous studies noted that flow-mediated dilation, measured locally in the brachial artery, was decreased in OSA patients compared with non-OSA controls, 2,53,[65][66][67] indicating that endothelial dysfunction occurs in OSA. However, here we discuss the available literature that furthers our understanding of the effect of OSA on arterial function, showing that not only local, but also global arterial function is impaired in OSA.…”

Section: Discussionmentioning

confidence: 99%

“…[2][3][4][5][6][7] Arterial stiffness is independently associated with cardiovascular risk [19][20][21][22][23][24]26,[28][29][30][31][75][76][77][78] and may therefore provide a potential explanation for the increased risk of cardiovascular events in OSA patients. Furthermore, a strong correlation between arterial stiffness and the development of atherosclerosis at various sites in the arteries has been noted.…”

Section: Therapeutic and Clinical Implicationsmentioning

confidence: 99%

“…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. 8 Although OSA patients commonly demonstrate one or more established cardiovascular risk factors, there is now a considerable body of evidence indicating that OSA itself is an independent cardiovascular risk factor.…”

Section: Introductionmentioning

confidence: 99%

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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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“…Several experimental and clinical studies have shown that nocturnal hypopnea induces increases in blood pressure levels 6,19 and the progression of arterial stiffness. 18,19 Endothelial dysfunction 4,[20][21][22] and disturbances of sympathetic activity 5,23 are recognized clinical features in OSA patients that increase vascular tone and accelerate the progression of arterial stiffness. 7 Chronic intermittent hypoxia causes dyslipidaemia and initiates the development of atherosclerosis, both of which contribute to arterial stiffness.…”

Section: Discussionmentioning

confidence: 99%

Effects of long-term treatment for obstructive sleep apnea on pulse wave velocity

Saito

Sugiyama

et al. 2010

Hypertens Res

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Continuous positive airway pressure (CPAP) treatment improves endothelial function and sympathetic activity in patients with obstructive sleep apnea (OSA). However, the long-term effects of CPAP on pulse wave velocity (PWV), which reflects arterial stiffness that is associated with cardiovascular events, have not been evaluated in OSA patients with or without hypertension (HT). In this study, 212 male OSA patients who had been receiving CPAP treatment for 2 years and were divided into two groups, those with HT (n¼114) and those without (n¼98), were studied. In both HT and normotensive (NT) patients, PWV decreased significantly over the first 6 months of treatment (P¼0.005 and 0.010, respectively), before increasing gradually from 6 to 24 months. Body mass index (BMI), body weight, heart rate (HR), systolic blood pressure (SBP) and diastolic blood pressure (DBP) levels decreased significantly in the HT group over the 2 years of CPAP treatment (Po0.001 for all). In contrast, only HR decreased significantly in the NT group over the 2 years of treatment (Po0.001). Multivariate regression analysis revealed that age (P¼0.008), decreases in DBP (Po0.001) and HR (Po0.001) and higher initial levels of serum high-density lipoprotein-cholesterol (P¼0.040) were independent factors related to changes in PWV over the 2 years of CPAP treatment in all patients. In conclusion, we found a significant decrease in PWV in both NT and HT patients after 6 months of CPAP treatment. In HT patients, long-term CPAP treatment significantly decreases blood pressure, which may contribute to explain the PWV improvement.

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Endothelial Cell Apoptosis in Obstructive Sleep Apnea

Cited by 140 publications

References 41 publications

Circulating Endothelial Cells and Endothelial Progenitor Cells in Obstructive Sleep Apnea

Circulating Endothelial Cells and Endothelial Progenitor Cells in Obstructive Sleep Apnea

Increased arterial stiffness in obstructive sleep apnea: a systematic review

Effects of long-term treatment for obstructive sleep apnea on pulse wave velocity

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