Abstract 52: Inflammatory Biomarkers Correlate With Etiology in Childhood Arterial Ischemic Stroke

Abstract

Introduction: Etiologies of childhood arterial ischemic stroke (AIS) are heterogeneous, yet most cases fall into one of three subtypes: arteriopathic, cardioembolic, or idiopathic. Circulating inflammatory mediators could play a role in the pathogenesis of each subtype, whether through inflammatory injury to arterial or cardiac endothelium, or by promoting thrombosis. Hypothesis: Patterns of post-stroke serum inflammation in children will differ by etiologic subtype. Methods: From the “Vascular effects of Infection in Pediatric Stoke” (VIPS) study cohort (355 cases of AIS, ages 29 days through 18 years), we selected cases centrally classified as arteriopathic (N=119), spontaneous cardioembolic (N=58; excluding peri-procedural cardioembolic AIS), or idiopathic (N=82). We used Luminex assays to measure serum concentrations (pg/mL) of 20 inflammatory biomarkers selected for their correlation with adult AIS or arteriopathy in other settings. We compared analyte concentrations across the three etiologic subtypes in unadjusted and adjusted analyses. Results: Serum samples were collected at a median of 5.5 days post-stroke (IQR 3, 10 days). Compared to children with idiopathic AIS, those with cardioembolic AIS had higher levels of four analytes (IL-6, IL-8, IL-10, IP-10), even after adjustment for age, sex, infarct volume, and other potential confounders (Table). Children with arteriopathic AIS, on the other hand, had higher levels of two analytes (IL-10, IP-10), and lower levels of another two (fractalkine, MCP-1). Conclusion: Patterns of post-AIS serum inflammation differ by stroke subtype in children, and may provide clues to stroke pathogenesis. We will perform network analyses using unsupervised machine learning approaches to elucidate these patterns further.