2007
DOI: 10.1164/rccm.200608-1141oc
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Silent Brain Infarction and Platelet Activation in Obstructive Sleep Apnea

Abstract: These results suggest that serum levels of sCD40L and sP-selectin are elevated and SBI is more common in patients with moderate to severe OSA, leading to elevated cerebrovascular morbidity. Moreover, nCPAP may be useful for decreasing risk in patients with moderate to severe OSA.

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Cited by 197 publications
(139 citation statements)
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“…84 Sleep deprivation also may trigger systemic inflammation. 85,86 The combination of repetitive hypoxemia and sleep deprivation in OSA patients may be associated with increased levels of plasma cytokines, adhesion molecules, 87,88 serum amyloid A, 89 and C-reactive protein. 88,90 -92 Although the increase in C-reactive protein in OSA appears to be independent of adiposity, 92 this question remains controversial.…”
Section: Inflammationmentioning
confidence: 99%
See 1 more Smart Citation
“…84 Sleep deprivation also may trigger systemic inflammation. 85,86 The combination of repetitive hypoxemia and sleep deprivation in OSA patients may be associated with increased levels of plasma cytokines, adhesion molecules, 87,88 serum amyloid A, 89 and C-reactive protein. 88,90 -92 Although the increase in C-reactive protein in OSA appears to be independent of adiposity, 92 this question remains controversial.…”
Section: Inflammationmentioning
confidence: 99%
“…In a cross-sectional study of Japanese men, brain magnetic resonance imaging revealed silent brain infarction in 25% of patients with moderate to severe OSA but in only 8% of patients with mild OSA and in 6% of control subjects, suggesting that OSA may elicit early and asymptomatic cerebrovascular damage. 88 Available data often are limited by the use of oximetry rather than complete polysomnographic studies and by the relatively small numbers of subjects studied. Furthermore, the broad spectrum of comorbidities and pharmacological intervention in poststroke patients constrains identification of any independent premorbid etiologic role of sleep apnea.…”
Section: Osa and The Origin And Progression Of Strokementioning
confidence: 99%
“…But the mechanisms of Plt activation in patients with OSAS may be the chronic intermittent hypoxia and high levels of catecholamines which is a result of sympathetic activity [30][31][32]. Minogluchi et al [33] reported that the levels of sCD40L and sPselectin which were known as Plt activation markers increased in patients with moderate and severe OSAS. Hui at al.…”
Section: Discussionmentioning
confidence: 99%
“…Carotid artery IMT was assessed by B-mode ultrasound scanning with a 7.5-MHz linear phase array transducer (Prosoundα10, Hitachi- Repeated hypoxia during sleep in patients with OSA may induce systemic inflammation and oxidative stress [22,23] and as a result, contribute to the development of endothelial dysfunction [17]. Endothelial dysfunction promotes the development and clinical manifestation of atherosclerosis.…”
Section: Carotid Imtmentioning
confidence: 99%