Modeling Intracerebral Hemorrhage Growth and Response to Anticoagulation

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Modeling Intracerebral Hemorrhage Growth and Response to Anticoagulation

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Title: Modeling Intracerebral Hemorrhage Growth and Response to Anticoagulation
Author: Greenberg, Charles H.; Frosch, Matthew P.; Goldstein, Joshua Norkin; Rosand, Jonathan; Greenberg, Steven Mark

Note: Order does not necessarily reflect citation order of authors.

Citation: Greenberg, Charles H., Matthew P. Frosch, Joshua N. Goldstein, Jonathan Rosand, and Steven M. Greenberg. 2012. Modeling intracerebral hemorrhage growth and response to anticoagulation. PLoS ONE 7(10): e48458.
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Abstract: The mechanism for hemorrhage enlargement in the brain, a key determinant of patient outcome following hemorrhagic stroke, is unknown. We performed computer-based stochastic simulation of one proposed mechanism, in which hemorrhages grow in “domino” fashion via secondary shearing of neighboring vessel segments. Hemorrhages were simulated by creating an initial site of primary bleeding and an associated risk of secondary rupture at adjacent sites that decayed over time. Under particular combinations of parameters for likelihood of secondary rupture and time-dependent decay, a subset of lesions expanded, creating a bimodal distribution of microbleeds and macrobleeds. Systematic variation of the model to simulate anticoagulation yielded increases in both macrobleed occurrence (26.9%, 53.2%, and 70.0% of all hemorrhagic events under conditions simulating no, low-level, and high-level anticoagulation) and final hemorrhage size (median volumes 111, 276, and 412 under the same three conditions), consistent with data from patients with anticoagulant-related brain hemorrhages. Reversal from simulated high-level anticoagulation to normal coagulation was able to reduce final hemorrhage size only if applied relatively early in the course of hemorrhage expansion. These findings suggest that a model based on a secondary shearing mechanism can account for some of the clinically observed properties of intracerebral hemorrhage, including the bimodal distribution of volumes and the enhanced hemorrhage growth seen with anticoagulation. Future iterations of this model may be useful for elucidating the effects of hemorrhage growth of factors related to secondary shearing (such as small vessel pathology) or time-dependent decay (such as hemostatic agents).
Published Version: doi:10.1371/journal.pone.0048458
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3484132/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:10579549
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