Abstract DP118: Systemic Inflammation and Cardiac Dysfunction After Non-Traumatic Subarachnoid Hemorrhage

Non-traumatic subarachnoid hemorrhage (SAH) is frequently complicated by systemic inflammation and cardiac dysfunction, which contribute significantly to its high morbidity and mortality. This study aimed to characterize immune cell subpopulations and their relationship to cardiac abnormalities in patients with SAH. In this single site prospective observational study, adult patients with SAH requiring external ventricular drain (EVD) placement were enrolled between January 8, 2018 to August 7, 2023. Peripheral blood (PB) samples were collected on post-bleed days (PBDs) 1, 3, 5, 7, and 10. Flow cytometric analysis was used to quantify immune cell subpopulations and cell-surface biomarkers. Clinical data was obtained via chart review. Patients were classified as having cardiac dysfunction based on a composite scoring system based on QTc prolongation on EKG, elevated troponin, abnormal echocardiogram. Neutrophil-secreted factors including lipocalin-2 and myeloperoxidase were measured in platelet-free plasma using ELISA. We evaluated the association of immune subpopulations, cardiac dysfunction, and outcomes. Sixty patients were enrolled; 65% were female, with median age of 58 (IQR 51-68). Half (51.7%, n=31) had a Hunt Hess grade of 4-5. All patients had EVDs; 78% were intubated, and 87% underwent aneurysm repair via coiling or clipping. Common complications included vasospasm (77%), cardiac dysfunction (50%), and shock (6.7%). Average ICU and hospital lengths of stay was 18.5 (IQR 12.2-22) and 23 (IQR 18.2-33.8) days, respectively. In-hospital mortality was 11.8%, with 6-month mortality reaching 25%. Discharge dispositions included home (40%), skilled nursing facility (45%), and hospice (3.3%). Cardiac dysfunction after SAH was associated with elevated circulating neutrophils, predominantly CD10- immature subsets, and systemic degranulation indicated by increased plasma lipocalin-2 (LPN) and myeloperoxidase (MPO). These immune changes correlated with higher Hunt-Hess scores and prolonged ICU and hospital stays. A trend toward elevated pro-brain natriuretic peptide levels was also noted in affected patients. Severe SAH induces a systemic inflammatory response, dominated by immature neutrophils that contribute to increased levels of pro-inflammatory LPN2 and MPO. This inflammatory milieu is linked to cardiac dysfunction and adverse clinical outcomes, highlighting the potential role of targeted immunomodulation in improving prognosis after SAH.