Silent Brain Infarction and Platelet Activation in Obstructive Sleep Apnea

ArticleinAmerican Journal of Respiratory and Critical Care Medicine 175(6):612-7 · March 2007with5 Reads
DOI: 10.1164/rccm.200608-1141OC · Source: PubMed
Silent brain infarction (SBI) and increased levels of soluble CD40 ligand (sCD40L) and soluble P-selectin (sP-selectin) are associated with an increased risk of cerebrovascular disease. The aim of this study was to evaluate whether SBI and serum levels of sCD40L and sP-selectin are increased in patients with obstructive sleep apnea (OSA). SBI was studied by brain magnetic resonance images in 50 male patients with OSA and 15 obese male control subjects who were free of comorbidities. In addition, the effects of 3 months of treatment with nasal continuous positive airway pressure (nCPAP) on serum parameters were studied in 24 patients with moderate to severe OSA. The percentage of SBI in patients with moderate to severe OSA (25.0%) was higher than that of obese control subjects (6.7%) or patients with mild OSA (7.7%). Serum levels of sCD40L and sP-selectin were significantly higher in patients with moderate to severe OSA than in obese control subjects (p < 0.05) or patients with mild OSA (p < 0.05). In addition, nCPAP significantly decreased serum levels of sCD40L (p < 0.03) and sP-selectin (p < 0.01) in patients with moderate to severe OSA. 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.
    • "Hypertension. There were five articles based on 4 longitudinal studies (17, 87–90) and 18 cross-sectional studies (8, 14, 16, 29, 38, 45, 46, 50, 51, 66, 91–98) that addressed the impact of mild OSA on hypertension. Three of the longitudinal studies evaluated population-based cohorts (17, 87, 89). "
    [Show abstract] [Hide abstract] ABSTRACT: Background: Mild obstructive sleep apnea (OSA) is a highly prevalent disorder in adults; however, whether mild OSA has significant neurocognitive and cardiovascular complications is uncertain. Objectives: The specific goals of this Research Statement are to appraise the evidence regarding whether long-term adverse neurocognitive and cardiovascular outcomes are attributable to mild OSA in adults, evaluate whether or not treatment of mild OSA is effective at preventing or reducing these adverse neurocognitive and cardiovascular outcomes, delineate the key research gaps, and provide direction for future research agendas. Methods: Literature searches from multiple reference databases were performed using medical subject headings and text words for OSA in adults as well as by hand searches. Pragmatic systematic reviews of the relevant body of evidence were performed. Results: Studies were incongruent in their definitions of "mild" OSA. Data were inconsistent regarding the relationship between mild OSA and daytime sleepiness. However, treatment of mild OSA may improve sleepiness in patients who are sleepy at baseline and improve quality of life. There is limited or inconsistent evidence pertaining to the impact of therapy of mild OSA on neurocognition, mood, vehicle accidents, cardiovascular events, stroke, and arrhythmias. Conclusions: There is evidence that treatment of mild OSA in individuals who demonstrate subjective sleepiness may be beneficial. Treatment may also improve quality of life. Future research agendas should focus on clarifying the effect of mild OSA and impact of effective treatment on other neurocognitive and cardiovascular endpoints as detailed in the document.
    Article · May 2016
    • "Recent evidence has indicated that OSA patients exhibited elevated platelet activity, fibrinogen levels, plasminogen activator inhibitor-1 levels, erythrocyte adhesiveness, and aggregation [7] [8] [9]. All of these conditions may cause OSA patients to develop a hypercoagulopathy status and predispose them to venous thromboembolism (VTE), which consist of deep vein thrombosis (DVT) and pulmonary embolism (PE). "
    [Show abstract] [Hide abstract] ABSTRACT: Background: Obstructive sleep apnea (OSA) is a major contributor to cardiovascular disease, and may cause severe morbidity and mortality. Recent studies have indicated that OSA patients exhibited elevated platelet activity, fibrinogen levels, and platelet aggregation. Objectives: We investigated the risk of deep vein thrombosis (DVT) and pulmonary embolism (PE) in patients diagnosed with OSA compared with age-and sex-matched unaffected people. Patients/Methods: This longitudinal, nationwide, population-based cohort study was conducted using data from Taiwan National Health Insurance Research Database (NHIRD) recorded between January 2000 and December 2011. The study consisted of 3511 patients with OSA and 35110 matched comparison individuals. A Cox proportional hazard regression was used to compute the risk of DVT and PE in patients with OSA compared with those without OSA. Results: The DVT and PE risks were 3.50- and 3.97-fold higher (95% CI = 1.83-6.69 and 1.85-8.51) respectively, in the OSA cohort than in the reference cohort after we adjusted for age, sex, and comorbidities. Conclusion: This nationwide population-based cohort study indicates that patients with OSA exhibit a higher risk of subsequent DVT and PE.
    Full-text · Article · Jun 2014
    • "In addition, there is evolving evidence that OSA may contribute to insulin resistance and other components of the metabolic syndrome such as obesity and increased elevated leptin levels, a hormone produced by the adipocytes strongly associated with obesity. Mounting evidence suggest that OSA is related to subclinical brain infarcts and white matter hyperintensities by MRI707172. In a study of Japanese men, 25 % of patients with moderate to severe OSA had silent brain infarcts when compared to 6 % of controls. "
    [Show abstract] [Hide abstract] ABSTRACT: The purpose of this review is to highlight existing literature on the epidemiology, pathophysiology, and novel risk factors for vascular dementia. We further examine the evidence linking chronic brain hypoperfusion induced by a variety of cardiovascular diseases to the development of vascular dementia. In the elderly, in whom cerebral perfusion is diminished by the aging process, additional reduction in cerebral blood flow stemming from exposure to potentially modifiable vascular risk factors increases the probability of developing vascular dementia. Finally, we discuss the association between obstructive sleep apnea, an underrecognized risk factor for stroke, and vascular dementia. Obstructive sleep apnea is linked to cerebrovascular disease through many intermediary vascular risk factors and may directly cause cerebrovascular damage through microvacular disease. Insight into how cardiovascular risk factors induce vascular dementia offers an enhanced understanding of the multifactorial pathophysiology by this disorder and ways of preventing and managing the cerebrovascular precursors of vascular dementia. Many vital questions about the relation of obstructive sleep apnea with stroke and vascular dementia are still unanswered and await future well-designed studies.
    Full-text · Article · Sep 2013
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