Abstract T P396: Endothelial Inflammation Correlates with Severity of Bleed and Outcome in SAH Patients
Introduction: Subarachnoid hemorrhage (SAH) is a devastating disease that portends a high rate of morbidity and early mortality in its patients. Although brain injury that is assumed in the early phases of SAH is an important prognosticator of functional outcome, the underlying mechanism behind the acute phase of the disease is still poorly understood. The aim of this study is to investigate endothelial inflammation in the early phases of SAH, and to determine its association with severity of bleed, mortality risk, and functional outcome.
Hypothesis: We hypothesize that endothelial inflammation will be higher in SAH patients with severe bleed and poor functional outcome.
Methods: Patients (n=15) admitted to our neurosurgical intensive care unit within 24 hours of bleed onset (day 1) and angiographic evidence of aneurysmal SAH were identified. Endothelial inflammation was studied as intracellular adhesion marker-1 (ICAM-1) levels in blood samples drawn at admission and on days 3 and 7 post-SAH (ICAM-1 ELISA; R&D Systems). Severity of bleed and patient status at admission was studied via Hunt Hess (HH) (1-5) grade and modified Fisher (mF) score (0-4), and 7-day outcome was assessed via Rankin functional and NIHSS score. ANOVA and Pearson correlation analyses (SAS) were used to assess the data.
Results: ELISA analysis demonstrated that levels of ICAM-1/CD54 were significantly greater in high grade (grade 4) mF score (p=0.025, ANOVA), and correlated to higher Rankin score (p=0.0097, Pearson). HH scores when grouped as 1,2 vs 3 vs 4,5 showed a positive trend in relation to increased ICAM-1/CD54 (p=0.087, ANOVA). No correlation between ICAM-1 level and NIHSS score was found.
Conclusion: Endothelial inflammation (ICAM-1/CD54 levels) associates with severity of bleed and poor 7 day outcome, and hence may serve as a useful biomarker for assessment of clinical severity of bleed in SAH patients.
Author Disclosures: J. Lee: None. E.L. Gordon: None. J.B. Bederson: None. S. Sobotka: None. S.A. Mayer: None. F.A. Sehba: None.
This research has received full or partial funding support from the American Heart Association, Founders - Connecticut, Maine, Massachusetts, New Hampshire, New Jersey, New York, Rhode Island, Vermont.
- © 2015 by American Heart Association, Inc.