C-Reactive Protein and Fibrinogen in Acute Stroke Patients with and without Sleep Apnea

Background and Purpose: Although sleep apnea (SA) is a risk factor for ischemic stroke and an important prognosticator in affected patients, the exact pathophysiological link between SA and stroke remains to be established. We investigated whether levels of C-reactive protein (CRP) and fibrinogen ar...

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Veröffentlicht in:Cerebrovascular diseases (Basel, Switzerland) Switzerland), 2007-01, Vol.24 (5), p.412-417
Hauptverfasser: Dziewas, Rainer, Ritter, Martin, Krüger, Linn, Berger, Stefanie, Langer, Claus, Kraus, Jörg, Dittrich, Ralf, Schäbitz, Wolf R., Ringelstein, E. Bernd, Young, Peter
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Sprache:eng
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Zusammenfassung:Background and Purpose: Although sleep apnea (SA) is a risk factor for ischemic stroke and an important prognosticator in affected patients, the exact pathophysiological link between SA and stroke remains to be established. We investigated whether levels of C-reactive protein (CRP) and fibrinogen are increased in patients with acute stroke and SA compared with stroke patients without SA. Patients and Methods: 117 consecutive patients with ischemic stroke admitted to our stroke unit within 12 h after stroke onset were included in this study. On admission, CRP and fibrinogen levels were determined. All patients received cardiorespiratory polygraphy during the first 72 h of their hospital stay. In all patients, demographic data, National Institutes of Health Stroke Scale score and cerebrovascular risk factors were assessed. Results: SA defined by an apnea-hypopnea index (AHI) of ≧10/h was found in 64 (55%) patients. Elevated CRP and fibrinogen levels were seen twice as often in patients with SA than in patients without (CRP: 52 vs. 26%; fibrinogen: 72 vs. 37%). After multivariate logistic regression analysis, an AHI of ≧10/h was independently correlated with raised levels of both of these parameters. Conclusion: SA is independently associated with raised levels of CRP and fibrinogen in patients with acute ischemic stroke. We assume that both proteins are part of the pathophysiological pathway linking SA to stroke.
ISSN:1015-9770
1421-9786
DOI:10.1159/000108430