Apolipoprotein E genotype and outcome after aneurysmal subarachnoid hemorrhage.
OBJECTIVE
After aneurysmal subarachnoid hemorrhage (SAH), conflicting results concerning an association between the APOE genotype and impaired outcome have been reported. The authors tested prospectively whether APOE epsilon2 or epsilon4 allele-containing genotypes (epsilon2+ and epsilon4+) affect outcome after SAH.


METHODS
Previous disease histories and clinical and radiological variables were recorded for 105 patients who were admitted within 48 hours after SAH. Fifteen patients (14%) had the epsilon2+ genotype and 31 (30%) [corrected] had epsilon4+ genotypes. Factors predicting poor outcome according to the Glasgow Outcome Scale and cerebral infarction visible on CT scans obtained at 3 months after SAH were tested with multiple logistic regression analyses.


RESULTS
Apolipoprotein E epsilon2 or epsilon4-containing genotypes were not associated with outcome, occurrence of cerebral infarction, or with any of their predictors, either in univariate or multivariate analysis. Poor outcome was predicted independently by the occurrence of intraventricular bleeding and intracerebral hematoma as well as by elevated levels of both plasma glucose and D-dimer, and delayed cerebral ischemia (p < 0.05 for each factor), and in univariate analysis only by clinical condition on admission and patient age. Cerebral infarction was predicted independently according to clinical condition on admission (p < 0.05), amount of subarachnoid blood (p < 0.01), duration of intraoperative parent artery clipping (p < 0.01), and body mass index (p < 0.05). In the univariate analysis only cerebral infarction was also predicted by patient age, intracerebral hematoma, and delayed cerebral ischemia.


CONCLUSIONS
Severity of bleeding for the most part predicts outcome after SAH; APOE polymorphisms seem to have no prognostic value for outcome after SAH. This result was in accordance with the findings from the largest ischemic stroke studies.
Juvela
Seppo
S
Department of Neurosurgery, Helsinki University Central Hospital, Helsinki, Turku, Finland. seppo.juvela@helsinki.fi
Siironen
Jari
J
Lappalainen
Jaakko
J
D000483:Alleles; D053329:Apolipoprotein E2 / Q000235:genetics*; D053327:Apolipoprotein E4 / Q000235:genetics*; D002545:Brain Ischemia / Q000209:etiology; D002544:Cerebral Infarction / Q000209:etiology; D005260:Female; D005838:Genotype; D006801:Humans; D002532:Intracranial Aneurysm / Q000150:complications*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D011446:Prospective Studies; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000235:genetics
D053329:Apolipoprotein E2; D053327:Apolipoprotein E4