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Genetic and environmental risk factors for intracerebral hemorrhage: preliminary results of a population-based study
Daniel Woo1, Laura R Sauerbeck, Brett M Kissela
1Department of Neurology, University of Cincinnati, Cincinnati, Ohio 45267-0525, USA. Daniel.woo@uc.edu
Insights
Genetic and environmental factors influence intracerebral hemorrhage (ICH) risk differently based on location. Apolipoprotein E alleles are linked to lobar ICH, while hypertension is key for nonlobar ICH.
Area of Science:
- Neurology
- Epidemiology
- Genetics
Background:
- Intracerebral hemorrhage (ICH) presents a high mortality rate (40-50%) with limited treatment options.
- This study investigates genetic and environmental risk factors for ICH.
Purpose of the Study:
- To identify significant independent risk factors for lobar and nonlobar intracerebral hemorrhage.
- To determine the attributable risk of identified factors for different ICH subtypes.
Main Methods:
- Population-based case-control study involving 188 ICH cases and 366 controls.
- Prospective identification of stroke cases across 16 hospitals.
- Multivariable logistic regression analysis to identify independent risk factors.
Main Results:
- Lobar ICH risk factors: apolipoprotein E2/E4 allele, alcohol use, prior stroke, family history.
- Nonlobar ICH risk factors: hypertension, prior stroke, family history.
- Increased education correlated with decreased nonlobar ICH risk.
Conclusions:
- Pathophysiology of ICH differs significantly by location.
- Apolipoprotein E alleles account for 29% of lobar ICH; hypertension accounts for 54% of nonlobar ICH.
Background And Purpose:
Intracerebral hemorrhage (ICH) has a 30-day mortality rate of 40% to 50% and lacks a proven treatment. We report a preplanned, midpoint analysis of the first population-based, case-control study that examines both genetic and environmental risk factors of ICH.
Methods:
We prospectively identified cases of hemorrhagic stroke at all 16 hospitals in the Greater Cincinnati/Northern Kentucky region. All cases underwent medical record and neuroimaging review. Cases enrolled in the direct interview and genetic sampling arm of the study were matched to population-based control subjects by age, race, and sex. Multivariable logistic regression was performed to identify significant independent risk factors.
Results:
We enrolled 188 cases of ICH (67 lobar, 121 nonlobar) and 366 control subjects in the direct interview arm of the study. Significant independent risk factors for lobar ICH included the presence of an apolipoprotein E2 or E4 allele, frequent alcohol use, prior stroke, and first-degree relative with ICH. Significant independent risk factors for nonlobar ICH were hypertension, prior stroke, and first-degree relative with ICH. An increasing level of education was associated with a decreased risk of nonlobar ICH. The attributable risk of apolipoprotein E2 or E4 for lobar ICH was 29%, and the attributable risk of hypertension for nonlobar ICH was 54%.
Conclusions:
There is significant epidemiological evidence that the pathophysiology of ICH varies by location. We estimate that a third of all cases of lobar ICH are attributable to possession of an apolipoprotein E4 or E2 allele and that half of all cases of nonlobar ICH are attributable to hypertension.
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