Exploring the Relationship Between Cerebrospinal Fluid Interleukin-6 and Cerebral Autoregulation After Subarachnoid Hemorrhage
Madelynne Olexa1, Yelyzaveta Begunova1, Emily Gilmore2, Jennifer Kim2, Alison Herman3, Rachel Beekman4, Jessica Magid-Bernstein5, Charles Matouk1, Kevin Sheth6, Eliza Miller7, Santiago Ortega Gutierrez8, Adam De Havenon3, Lauren Sansing1, Nils Petersen3
1Yale School of Medicine, 2Yale University School of Medicine, 3Yale University, 4Yale New Haven Medical Center, 5Yale New Haven Health, 6Yale UniversityDivision of Neuro and Critical Care, 7Columbia University Dept of Neurology, 8University of Iowa
Objective:
This research assesses serial CSF IL-6 levels' relationship with cerebral autoregulation in aSAH patients.
Background:
Elevated levels of Interleukin-6 (IL-6) levels in cerebrospinal fluid (CSF) have been correlated with delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH). However, the role of neuroinflammation in SAH pathophysiology remains incompletely understood. In a pig stroke model, IL-6 antagonist prevented hypotension-induced pial artery impairment, suggesting a role in post-stroke vascular derangement.
Design/Methods:
We prospectively enrolled aSAH patients at Yale-New Haven Hospital. Autoregulatory function was measured by interrogating changes in near-infrared spectroscopy-derived tissue oxygenation response to changes in mean arterial pressure (MAP). The resulting autoregulatory index was used to trend the MAP range at which autoregulation was most preserved. Percent time that MAP exceeded the upper limit of autoregulation or decreased below the lower limit of autoregulation was calculated for each patient. IL-6 levels were assessed through serial CSF samples and correlated with hemodynamic parameters.
Results:
We calculated limits of autoregulation for twenty-two patients (mean age 60 ± 9 years, mean Hunt Hess score 3.4 ± 1.2, mean modified Fisher score 3.7 ± 0.58, average monitoring time 10.1 ± 7.3 hours). Optimal MAP and limits were calculated an average of 74% ± 20% of monitoring time. Our study provides preliminary support for a potential association between IL-6 levels and percent time that MAP was within limits of autoregulation (b = -0.31, p=0.009, Fig. 1A). Additionally, there was a significant correlation between IL-6 levels and the extent to which MAP deviated from computed optimal MAP (r= 0.636, p=0.009, Fig. 1B).
Conclusions:
IL-6 may contribute to impaired autoregulation post aSAH. Further studies are needed to validate findings and refine MAP management for improved outcomes in aSAH patients.