Abstract 122: Cortical Superficial Siderosis is a Predictor of Early Recurrent Intracerebral Hemorrhage in Cerebral Amyloid Angiopathy

Abstract

Background and Purpose: Cerebral amyloid angiopathy (CAA) is a major cause of lobar intracerebral hemorrhage (ICH). A subgroup of patients with CAA experience multiple, recurrent ICHs over a short period of time. In this study, we investigated predictors of early lobar ICH recurrence (defined as ICH within six month after index event) in order to better understand the mechanisms for early recurrence in CAA-related ICH. Methods: Subjects were consecutive survivors (age≥55) of spontaneous symptomatic CAA-related lobar ICH according to the Boston criteria drawn from an ongoing longitudinal cohort study. All subjects had brain computed tomography (CT) scan and magnetic resonance imaging (MRI) at presentation. Baseline clinical, imaging and laboratory data were collected. Neuroimaging markers including focal (≤3 sulci) or disseminated (>3 sulci) cortical superficial siderosis (cSS), acute convexity subarachanoid hemorrhage (cSAH), cerebral microbleeds (CMBs), white matter hyperintensities and baseline ICH volume, on CT and/or MRI were evaluated. Subjects were followed prospectively for future recurrent symptomatic ICH. Cox proportional hazard models were used to identify predictors of early recurrent ICH adjusting for potential confounders. Results: A total of 296 patients with probable or possible CAA were enrolled. In univariable analysis, the presence of disseminated cSS, cSAH, and number of CMBs were predictors of early recurrent ICH (p<0.05 for all comparisons). After adjusting for age and previous symptomatic ICH history, disseminated cSS on MRI and cSAH on CT were independent predictors of early recurrent ICH (HR 3.79, 95% CI 1.46-9.84, p=0.006, HR 3.16, 95% CI 1.05-9.51, p=0.041, respectively). Conclusions: Disseminated cSS on MRI and cSAH on CT are independent imaging markers of increased risk for early recurrent ICH. These markers may provide additional insights into the mechanisms of ICH recurrence in patients with CAA.