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- Christoph J Griessenauer, Michelle H Chua, Khalid A Hanafy, Yaw Tachie Baffour, Ruiya Chen, Robert H LeBlanc, Apar S Patel, Mohamed Salem, S Ananth Karumanchi, Dihua Xu, Ravi Thadhani, Christopher S Ogilvy, and Ajith J Thomas.
- Neurosurgical Service, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. Electronic address: christoph.griessenauer@gmail.com.
- World Neurosurg. 2017 Dec 1; 108: 84-89.
BackgroundThe molecular mechanisms underlying cerebral vasospasm and delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH) are incompletely understood. We hypothesized that circulating antiangiogenic factors, such as soluble Fms-like tyrosine kinase 1 (sFlt-1) and soluble transforming growth factor β coreceptor, soluble endoglin (sEng), are important markers of their pathophysiology.MethodsWe performed a prospective study in patients with aSAH and measured cerebrospinal fluid and serum levels of sFlt-1 and sEng on postbleed day 1 and 6 and correlated levels with incidence and severity of cerebral vasospasm and DCI.ResultsTwenty-seven patients with aSAH were enrolled in the study. Severe angiographic vasospasm was present in 14.8% of patients and DCI occurred in 33.3%. Serum sFlt1 levels were increased on postbleed day 6 in patients who developed vasospasm. However, on postbleed day 1, there were no differences in patients who developed vasospasm. Increased serum sFlt-1 levels on postbleed day 1 were found to predict the development of severe angiographic vasospasm with an area under the curve of 0.818 with an optimal cutoff value of 95 pg/mL. Alterations in sFlt1 were not associated with DCI. Serum and cerebrospinal fluid sEng levels did not correlate with vasospasm or DCI.ConclusionsSerum levels of sFlt-1 are increased in patients with aSAH who are at risk for severe vasospasm. Further studies with larger sample sizes are needed to evaluate whether sFlt-1 levels may predict onset of severe vasospasm and DCI.Copyright © 2017 Elsevier Inc. All rights reserved.
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