Primary Intracerebral Hemorrhage: A Closer Look at Hypertension and Cerebral Amyloid Angiopathy.
Academic Article
Overview
abstract
BACKGROUND/PURPOSE: Primary intracerebral hemorrhage (ICH) studies often use hematoma location rather than ICH etiologies when assessing outcome. Characterizing ICH using hematoma location is effective/reproducible, but may miss heterogeneity among these ICH locations, particularly lobar ICH where competing primary ICH etiologies are possible. We subsequently investigated baseline characteristics/outcome differences of spontaneous, primary ICH by their etiologies: cerebral amyloid angiopathy (CAA) and hypertension. METHODS: Primary ICH clinical/outcomes data were prospectively collected between 2009 and 2015. Modified Boston criteria were used to identify "probable/definite" and "possible" CAA-ICH, which were evaluated separately. SMASH-U criteria were used to identify hypertension ICH. Medication and systemic disease coagulopathy ICH were excluded. Baseline characteristics/outcomes among "probable/definite" CAA-ICH, "possible" CAA-ICH, and hypertension ICH were compared using logistic regression. Mortality models using ICH etiologies compared to hematoma location as predictor variables were assessed. RESULTS: Two hundred and four hypertension ICHs, 55 "probable/definite" CAA-ICHs, and 46 "possible" CAA-ICHs were identified. Despite older age and larger ICH volumes, lower hospital mortality was seen in "probable/definite" CAA-ICH versus hypertension ICH (OR 0.2; 95% CI 0.05-0.8; p = 0.02) after adjusting for female gender, components of ICH score, and EVD placement. There were no mortality differences between "possible" CAA-ICH and hypertension ICH. However, lower hospital mortality was seen in "probable/definite" versus "possible" CAA-ICH (OR 0.2; 95% CI 0.04-0.7; p = 0.02). When using ICH etiology rather than hematoma location, hospital mortality models significantly improved (χ2: [df = 2, N = 305] = 6.2; p = 0.01). CONCLUSIONS: Further investigation is required to confirm the mortality heterogeneity seen within our primary ICH cohort. Hematoma location may play a role for these findings, but the mortality differences seen among lobar ICH using CAA-ICH subtypes and a failure to identify mortality differences between "possible" CAA-ICH and hypertension ICH suggest the limitations of accounting for hematoma location alone.
