Abstract
BackgroundCerebral hyperperfusion syndrome develops in a small subset of patients following carotid artery surgery (CAS) performed to treat severe carotid artery stenosis. This syndrome has been found to have a close correlation with cerebral hyperperfusion occurring after CAS. The purpose of this study is to investigate whether and how the anatomy of the Circle of Willis (CoW) of the cerebral circulation influences post-CAS cerebral hyperperfusion.MethodsA computational model of the cerebral circulation coupled with the global cardiovascular system has been developed to investigate hemodynamic events associated with CAS. Nine topological structures of the CoW were investigated in combination with various distribution patterns of stenosis in the feeding arteries of the cerebral circulation.ResultsThe occurrence of post-CAS cerebral hyperperfusion was predicted for the CoW structures that have poor collateral pathways between the stenosed cerebral feeding arteries and the remaining normal feeding arteries. The risk and the localization of post-CAS hyperperfusion were determined jointly by the anatomy of the CoW and the distribution pattern of stenosis in the cerebral feeding arteries. The presence of basilar artery stenosis or contralateral ICA stenosis increased the risk of post-CAS hyperperfusion and enlarged the cerebral region affected by hyperperfusion. For a certain CoW structure, the diameters of the cerebral communicating arteries and the severity of carotid artery stenosis both had a significant influence on the computed post-CAS cerebral hyperperfusion rates. Moreover, post-CAS cerebral hyperperfusion was predicted to be accompanied with an excessively high capillary transmural pressure.ConclusionsThis study demonstrated the importance of considering the anatomy of the CoW in assessing the risk of post-CAS cerebral hyperperfusion. Particularly, since the anatomy of the CoW and the distribution pattern of stenosis in the cerebral feeding arteries jointly determine the risk and localization of post-CAS cerebral hyperperfusion, a patient-specific hemodynamic analysis aimed to help physicians identify patients at high risk of cerebral hyperperfusion should account for the combined effect of the anatomy of cerebral arteries and cerebral feeding artery stenoses on cerebral hemodynamics.
Highlights
Cerebral hyperperfusion syndrome develops in a small subset of patients following carotid artery surgery (CAS) performed to treat severe carotid artery stenosis
Post-CAS hyperperfusion has been observed in 9-14% of patients in clinical studies [2,4] and suggested to be an important hemodynamic factor underlying cerebral hyperperfusion syndrome (CHS), for instance, the risk of developing CHS is 10 times higher in patients with hyperperfusion than those without [2], and intracranial hemorrhage (ICH) develops in 3.3% of patients with hyperperfusion vs. only 0.24% of those without [4]
We have developed a novel computational model of the cerebral circulation which is capable of describing cerebral hemodynamics under various physiological/pathological conditions
Summary
Cerebral hyperperfusion syndrome develops in a small subset of patients following carotid artery surgery (CAS) performed to treat severe carotid artery stenosis. This syndrome has been found to have a close correlation with cerebral hyperperfusion occurring after CAS. A potential risky problem with CAS is that cerebral hyperperfusion syndrome (CHS) (characterized by ipsilateral headache, seizure or intracranial hemorrhage (ICH)) develops in a small subset (0.75-3%) of patients following successful CAS [2]. Post-CAS hyperperfusion has been observed in 9-14% of patients in clinical studies [2,4] and suggested to be an important hemodynamic factor underlying CHS, for instance, the risk of developing CHS is 10 times higher in patients with hyperperfusion than those without [2], and ICH develops in 3.3% of patients with hyperperfusion vs only 0.24% of those without [4]. There is evidence that identifying patients at high risk of hyperperfusion and treating them early help to reduce the incidence of ICH and lead to better prognosis [5,6]
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