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Elevated BNP is Associated with Vasospasm-Independent Cerebral Infarction Following Aneurysmal Subarachnoid Hemorrhage
Journal article   Peer reviewed

Elevated BNP is Associated with Vasospasm-Independent Cerebral Infarction Following Aneurysmal Subarachnoid Hemorrhage

Pam R. Taub, Jeremy D. Fields, Alan H. B. Wu, Jacob C. Miss, Michael T. Lawton, Wade S. Smith, William L. Young, Jonathan G. Zaroff and Nerissa U. Ko
Neurocritical care, Vol.15(1), pp.13-18
08/01/2011
PMID: 21479679

Abstract

Clinical Neurology Critical Care Medicine General & Internal Medicine Life Sciences & Biomedicine Neurosciences & Neurology Science & Technology
Elevated levels of B-type natriuretic peptide (BNP) have been associated with cardiac dysfunction and adverse neurological outcomes after subarachnoid hemorrhage (SAH). We sought to determine whether elevated levels of BNP are independently associated with radiographic cerebral infarction after SAH. Plasma BNP levels were measured after admission, a mean of 5.5 +/- A 3.0 days after SAH onset. Cerebral infarction was determined by retrospective review of computerized tomography (CT) scans. Cerebral vasospasm was confirmed by the presence of vascular narrowing on cerebral angiogram. The association between BNP and cerebral infarction was quantified using multivariable logistic regression and reverse stepwise elimination of clinical covariates. A stratified analysis was performed to quantify the association between BNP levels and infarction in patients with and without angiographic vasospasm. BNP levels were measured from 119 subjects. The median BNP level was 105 pg/ml (interquartile range 37-275 pg/ml). In our multivariable model, the top quartile of BNP levels (a parts per thousand yen276 pg/ml) were associated with an increased odds of cerebral infarction (OR 4.2, P = 0.009). The stratified analysis showed that the association between BNP and infarction was strongest in patients without angiographic vasospasm (OR 7.8, P = 0.006). Elevated levels of BNP are strongly and independently associated with cerebral infarction, and the association is most pronounced in patients without angiographic vasospasm. These results provide further evidence that other mechanisms can contribute to infarction, and BNP may be a useful biomarker in detecting patients at risk for adverse outcomes without large vessel vasospasm.

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