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Cerebrospinal Fluid Apolipoprotein E, Calcium and Cerebral Vasospasm after Subarachnoid Hemorrhage
Sheila A. Alexander, RN, PhD
School of Nursing, University of Pittsburgh, Pennsylvania, salexand{at}pitt.edu
Mary E. Kerr, RN, PhD
National Institute of Nursing Research, National Institutes of Health, Bethesda, Maryland
Jeffrey Balzer, PhD
Department of Neurologic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
Michael Horowitz, MD
Department of Neurologic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
Amin Kassam, MD
Department of Neurologic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania
Yookyung Kim, PhD
School of Nursing, University of Pittsburgh, Pennsylvania
Leslie Hoffman, RN, PhD
School of Nursing, University of Pittsburgh, Pennsylvania
Yvette P. Conley, PhD
School of Nursing, University of Pittsburgh, Pennsylvania
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) 4 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 4 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 4 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 4 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.
Key Words: subarachnoid hemorrhage cerebral vasospasm apolipoprotein E calcium cerebrospinal fluid
Biological Research For Nursing, Vol. 10, No. 2,
102-112 (2008)
DOI: 10.1177/1099800408321722

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