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A comprehensive analysis of the relationship between ACA velocities and ACA infarction following aneurysmal subarachnoid hemorrhage.
Journal of the Neurological Sciences 2017 May 16
PURPOSE: To evaluate the relationship between anterior cerebral artery (ACA) velocities (and ancillary parameters) and ACA infarction following aneurysmal subarachnoid hemorrhage (aSAH), and to examine the factors that influence velocities.
METHODS: Retrospective investigation of 500 consecutive aSAH patients. ACA mean velocities (Vm) were evaluated by daily transcranial ultrasound during the early (days 1-4) and late (days 5-20) periods posthemorrhage. Presence and timing of acute ACA infarctions were identified by serial retrospective review of cerebral computerized tomography (CT) scans. Predictors of ACA velocities were identified and compared to predictors of vasospasm and infarction from the literature.
RESULTS: Decreased velocities on the day of infarction were observed in infarct-positive vessels when compared to infarct-negative vessels. ACA velocity increases, ipsilateral/contralateral ACA velocity ratios, and ACA velocity ranges, were inaccurate in anticipating infarction. Decreased ACA index velocities were moderately accurate in anticipating ACA infarction during the early [Vm<60cms/s], late [Vm<70cms/s] and overall [Vm<70cms/s] time periods. Decreased index velocities also independently predicted infarction during all time periods. ACA velocities were most consistently predicted by age, race, hemorrhage quantity on CT, and ACA/ACom (anterior communicating artery) aneurysm location.
CONCLUSIONS: ACA velocity increases and ancillary parameters do not relate to the development of infarction, whereas velocity decreases are moderately accurate in anticipating infarction. Predictors of velocity increases generally coincide with those of vasospasm, whereas predictors of velocity decreases coincide more with those of infarction following aSAH.
METHODS: Retrospective investigation of 500 consecutive aSAH patients. ACA mean velocities (Vm) were evaluated by daily transcranial ultrasound during the early (days 1-4) and late (days 5-20) periods posthemorrhage. Presence and timing of acute ACA infarctions were identified by serial retrospective review of cerebral computerized tomography (CT) scans. Predictors of ACA velocities were identified and compared to predictors of vasospasm and infarction from the literature.
RESULTS: Decreased velocities on the day of infarction were observed in infarct-positive vessels when compared to infarct-negative vessels. ACA velocity increases, ipsilateral/contralateral ACA velocity ratios, and ACA velocity ranges, were inaccurate in anticipating infarction. Decreased ACA index velocities were moderately accurate in anticipating ACA infarction during the early [Vm<60cms/s], late [Vm<70cms/s] and overall [Vm<70cms/s] time periods. Decreased index velocities also independently predicted infarction during all time periods. ACA velocities were most consistently predicted by age, race, hemorrhage quantity on CT, and ACA/ACom (anterior communicating artery) aneurysm location.
CONCLUSIONS: ACA velocity increases and ancillary parameters do not relate to the development of infarction, whereas velocity decreases are moderately accurate in anticipating infarction. Predictors of velocity increases generally coincide with those of vasospasm, whereas predictors of velocity decreases coincide more with those of infarction following aSAH.
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