Article

Silent Brain Infarction and Platelet Activation in Obstructive Sleep Apnea

First Department of Internal Medicine, Showa University, School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8666, Japan.
American Journal of Respiratory and Critical Care Medicine (Impact Factor: 13). 03/2007; 175(6):612-7. DOI: 10.1164/rccm.200608-1141OC
Source: PubMed

ABSTRACT

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.

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    • "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). "
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    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 · Thrombosis Research
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    • "The aim of our study was to investigate OSA as an independent risk factor for the onset and progression of SCI based on stroke subtypes and brain regions in both the general population and in a non-obese population. Several previous studies have attempted to examine the relationship between these two conditions, but there is a lack of epidemiological data that could determine the relationship between OSA and silent stroke in a low-risk, populationbased sample (Davies et al., 2001; Eguchi et al., 2005; Minoguchi et al., 2007; Nishibayashi et al., 2008). Moreover, very few studies have investigated the relationship between OSA and stroke subtypes, such as lacunar infarction and particularly cerebral regions (Alchanatis et al., 2004; Bassetti et al., 2006; Bonnin-Vilaplana et al., 2009; Jackson and Sudlow, 2005). "
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    ABSTRACT: Previous studies have suggested that obstructive sleep apnoea (OSA) may be a risk factor for stroke. In this study, we assessed that OSA is an independent risk factor of silent cerebral infarction (SCI) in the general population, and in a non-obese population. This study recruited a total of 746 participants (252 men and 494 women) aged 50-79 years as part of the Korean Genome and Epidemiology Study (KoGES); they underwent polysomnography, brain magnetic resonance imaging and health screening examinations. SCI was assessed by subtypes and brain regions, and lacunar infarction represented lesions <15 mm in size in the penetrating arteries. Moderate-severe OSA was determined by apnoea-hypopnoea index ≥15. The results indicated that 12.06% had moderate-severe OSA, 7.64% of participants had SCI and 4.96% had lacunar infarction. Moderate-severe OSA was associated positively with SCI [odds ratio (OR): 2.44, 95% confidence interval (CI): 1.03-5.80] and lacunar infarction (OR: 3.48, 95% CI: 1.31-9.23) in the age ≥65-year group compared with those with non-OSA. Additionally, in the basal ganglia, OSA was associated with an increase in the odds for SCI and lacunar infarction in all age groups, and especially in the ≥65-year age group. In the non-obese participants, OSA was also associated positively with SCI in the ≥65-year age group, lacunar infarction in all age groups, and especially in the ≥65-year age group. There was also a positive association with the basal ganglia. Moderate-severe OSA was associated positively with SCI and lacunar infarction in elderly participants. Treatment of OSA may reduce new first-time cerebrovascular events and recurrences.
    Full-text · Article · Feb 2013 · Journal of Sleep Research
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    • "There is a strong association between OSA and AF [28]. Platelet activation [16] and silent brain infarction were also more common in patients with moderate to severe OSA than in controls [29]. OSA may accelerate atherosclerosis through the effect of hypertension and other mechanisms such as insulin resistance, diabetes, and dyslipidemia. "
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    ABSTRACT: To examine the long-term effect of CPAP on carotid artery intima-media thickness (IMT) in patients with Obstructive sleep apnea syndrome(OSAS). A prospective observational study over 12 months at a teaching hospital on 50 patients newly diagnosed with OSAS who received CPAP or conservative treatment (CT). Carotid IMT was assessed with B-mode Doppler ultrasound from both carotid arteries using images of the far wall of the distal 10 mm of the common carotid arteries at baseline, 6 months and 12 months. MEASUREMENTS AND RESULTS [MEAN (SE)]: Altogether 28 and 22 patients received CPAP and CT respectively without significant differences in age 48.8(1.8) vs 50.5(2.0)yrs, BMI 28.2(0.7) vs 28.0(1.2)kg/m2, ESS 13.1(0.7) vs 12.7(0.6), AHI 38(3) vs 39(3)/hr, arousal index 29(2) vs 29(2)/hr, minimum SaO2 75(2) vs 77(2)% and existing co-morbidities. CPAP usage was 4.6(0.3) and 4.7(0.4)hrs/night over 6 months and 1 year respectively. Carotid artery IMT at baseline, 6 months, and 12 months were 758(30), 721(20), and 705(20)micron for the CPAP group versus 760(30), 770(30), and 778(30)micron respectively for the CT group, p = 0.002. Among those free of cardiovascular disease(n = 24), the carotid artery IMT at baseline, 6 months and 12 months were 722(40), 691(40), and 659(30)micron for the CPAP group (n = 12) with usage 4.5(0.7) and 4.7(0.7) hrs/night over 6 months and 12 months whereas the IMT data for the CT group(n = 12) were 660(20), 685(10), and 690(20)micron respectively, p = 0.006. Reduction of carotid artery IMT occurred mostly in the first 6 months and was sustained at 12 months in patients with reasonable CPAP compliance.
    Full-text · Article · Mar 2012 · Respiratory research
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