Cerebrospinal Fluid Apolipoprotein E, Calcium and Cerebral Vasospasm after Subarachnoid Hemorrhage

Intracellular calcium (Ca ++ ) regulation of cerebral vessels is impaired after subarachnoid hemorrhage (SAH), making secondary pathways, such as that involving apolipoprotein E, potentially more influential. To evaluate cerebrospinal fluid (CSF) apolipoprotein E and Ca ++ levels as biomarkers of cerebral vasospasm, we examined changes in levels over time and apolipoprotein E (APOE) ε4 allele presence after SAH in individuals with and without vasospasm. We hypothesized that individuals with low apolipoprotein E levels, increased Ca ++ levels and/or at least one copy of the APOE ε4 allele would have vasospasm. Daily samples from 50 participants, aged 18—75, with SAH were used to quantify apolipoprotein E and Ca ++ levels. Vasospasm was verified using cerebral angiogram and/or elevated transcranial Dopplers in combination with clinical neurologic deterioration. Overall apolipoprotein E levels were higher in individuals with the APOE ε4 allele (p = .02) or angiographic vasospasm (p = .01), but there were no differences between individuals with and without symptomatic vasospasm. There were no significant changes in apolipoprotein E levels over time. Individuals with the ε4 allele had lower Ca ++ levels (p = .02) with trends suggesting a different pattern of change over time (p = .07). CSF Ca ++ levels were lower in individuals with symptomatic vasospasm (p < .01). Change in apolipoprotein E and Ca ++ levels (p = .006) correlated over time regardless of genotype or vasospasm status. These findings suggest that apolipoprotein E and Ca ++ may be interacting after SAH, but this interaction does not appear to influence vasospasm.