Published in:
01-08-2018 | Original Article
Primary Intracerebral Hemorrhage: A Closer Look at Hypertension and Cerebral Amyloid Angiopathy
Published in: Neurocritical Care | Issue 1/2018
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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.