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Erschienen in:
20.08.2020 | Original Work
TNF-R1 Correlates with Cerebral Perfusion and Acute Ischemia Following Subarachnoid Hemorrhage
Erschienen in: Neurocritical Care | Ausgabe 3/2020
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Background
Early cerebral hypoperfusion and ischemia occur after subarachnoid hemorrhage (SAH) and influence clinical prognosis. Pathophysiological mechanisms possibly involve inflammatory mediators. TNF-α has been associated with complications and prognosis after SAH. We investigated the relation of perfusion parameters and ischemic lesions, with levels of TNF-α main receptor, TNF-R1, after SAH, and their association with prognosis.
Methods
We included consecutive SAH patients admitted within the first 72 h of SAH onset. Blood samples were simultaneously collected from a peripheral vein and from the parent artery of the aneurysm. Levels of TNF-R1 were measured using ELISA (R&D Systems Inc., USA). CT perfusion and MRI studies were performed in the first 72 h. Correlation and logistic regression analysis were used to identify outcome predictors.
Results
We analyzed 41 patients. Increased levels of TNF-R1 correlated with increased Tmax (arterial: r = −0.37, p = 0.01) and prolonged MTT (arterial: r = 0.355, p = 0.012; venous: r = 0.306, p = 0.026). Increased levels of both arterial and venous TNF-R1 were associated with increased number of lesions on DWI (p = 0.006). In multivariate analysis, venous TNFR1 levels > 1742.2 pg/mL (OR 1.78; 95%CI 1.18–2.67; p = 0.006) and DWI lesions (OR 14.01; 95%CI 1.19–165.3; p = 0.036) were both independent predictors of poor outcome (mRS ≥ 3) at 6 months.
Conclusion
Increased levels of TNF-R1 in arterial and venous blood correlate with worse cerebral perfusion and with increased burden of acute ischemic lesions in the first 72 h after SAH. Venous levels of TNF-R1 and DWI lesions were associated with poor outcome at 6 months. These results highlight the pathophysiological role of TNF-α pathways in SAH and suggest a possible role of combined imaging and laboratorial markers in determining prognosis in acute SAH.