Key result
Sleep apnea (AHI ≥10/h), present in 48.7% of acute ischemic stroke patients, was associated with significantly higher levels of sTNF-R1 and sTNF-R2 compared to those without sleep apnea.
Why the study?
Are plasma concentrations of inflammatory and endothelial dysfunction biomarkers increased in acute ischemic stroke patients with sleep apnea compared to those without?
Cross-Sectional (n=76)
Are plasma concentrations of inflammatory and endothelial dysfunction biomarkers increased in acute ischemic stroke patients with sleep apnea compared to those without?
Sleep apnea in acute ischemic stroke is associated with elevated levels of sTNF-R1 and sTNF-R2, suggesting a potential inflammatory pathophysiological link.
SA-associated biomarker elevations may implicate inflammation in stroke risk; hypothesis-generating and should not yet change practice.
OBJECTIVE: Although sleep apnea (SA) is a risk factor for ischemic stroke and an important prognostic factor in affected patients, the exact pathophysiological link between SA and stroke is unknown. We investigated whether the plasma concentration of biomarkers of inflammation and endothelial dysfunction, including soluble tumor necrosis factor receptor-1 and -2 (sTNF-R1 and sTNF-R2), tumor necrosis factor-β (TNF-β), soluble intercellular cell adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) are increased in patients with acute stroke and SA compared with stroke patients without SA. DESIGN/METHODS: In total, 76 patients with ischemic stroke admitted to the stroke unit were included in this study. Plasma concentrations of biomarkers were determined after CT scans on admission. All patients received cardiorespiratory polygraphy within the first 72 h after admission. In all patients, demographic data, National Institutes of Health Stroke Scale scores and cerebrovascular risk factors were assessed. RESULTS: An apnea-hypopnea index (AHI) ≥10/h was found in 37 of our patients (48.7%). In these patients with SA, sTNF-R1 and sTNF-R2 levels were significantly higher than in patients with an AHI lower than 10/h. TNF-β, however, showed no significant difference between both groups, just like the soluble intercellular and vascular cell adhesion molecules sICAM-1 and sVCAM-1. CONCLUSIONS/RELEVANCE: SA is associated with raised levels of sTNF-R1 and sTNF-R2 in patients with acute ischemic stroke. Taking into account the established impact of these two markers on the causation and course of cerebrovascular disease, these proteins may be part of the pathophysiological pathway linking SA to stroke.
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Kunz et al. (2012) conducted a cross-sectional in Ischemic stroke (n=76). Sleep apnea (AHI ≥10/h) vs. No sleep apnea (AHI <10/h) was evaluated on Plasma concentrations of sTNF-R1, sTNF-R2, TNF-β, sICAM-1, and sVCAM-1. Sleep apnea (AHI ≥10/h), present in 48.7% of acute ischemic stroke patients, was associated with significantly higher levels of sTNF-R1 and sTNF-R2 compared to those without sleep apnea.
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