Does Preoperative Measurement of Cerebral Blood Flow with Acetazolamide Challenge in Addition to Preoperative Measurement of Cerebral Blood Flow at the Resting State Increase the Predictive Accuracy of Development of Cerebral Hyperperfusion after Carotid Endarterectomy? Results from 500 Cases with Brain Perfusion Single-photon Emission Computed Tomography Study

Abstract

The purpose of the present study was to determine whether preoperative measurement of cerebral blood flow (CBF) with acetazolamide in addition to preoperative measurement of CBF at the resting state increases the predictive accuracy of development of cerebral hyperperfusion after carotid endarterectomy (CEA). CBF at the resting state and cerebrovascular reactivity (CVR) to acetazolamide were quantitatively assessed using N-isopropyl-p-[ 123 I]-iodoamphetamine (IMP)-autoradiography method with single-photon emission computed tomography (SPECT) before CEA in 500 patients with ipsilateral internal carotid artery stenosis (≥ 70%). CBF measurement using 123 I-IMP SPECT was also performed immediately and 3 days after CEA. A region of interest (ROI) was automatically placed in the middle cerebral artery territory in the affected cerebral hemisphere using a three-dimensional stereotactic ROI template. Preoperative decreases in CBF at the resting state [95% confidence intervals (CIs), 0.855 to 0.967; P = 0.0023] and preoperative decreases in CVR to acetazolamide (95% CIs, 0.844 to 0.912; P < 0.0001) were significant independent predictors of post-CEA hyperperfusion. The area under the receiver operating characteristic curve for prediction of the development of post-CEA hyperperfusion was significantly greater for CVR to acetazolamide than for CBF at the resting state (difference between areas, 0.173; P < 0.0001). Sensitivity, specificity, and positive-and negative-predictive values for the prediction of the development of post-CEA hyperperfusion were significantly greater for CVR to acetazolamide than for CBF at the resting state (P < 0.05, respectively). The present study demonstrated that preoperative measurement of CBF with acetazolamide in addition to preoperative measurement of CBF at the resting state increases the predictive accuracy of the development of post-CEA hyperperfusion.

Preoperative Cerebral Oxygen Extraction Fraction Imaging Generated from 7T MR Quantitative Susceptibility Mapping Predicts Development of Cerebral Hyperperfusion following Carotid Endarterectomy

“…1,2 Cerebral hyperperfusion syndrome after CEA is a complication of cerebral hyperperfusion; 3 its characteristic features include unilateral headache, pain in the face or eyes, seizures, and focal symptoms secondary to intracerebral hemorrhage or cerebral edema. [1][2][3][4] Intracerebral hemorrhage has a low incidence (1%), but patients with this condition have a poor prognosis.…”

“…[1][2][3][4] Intracerebral hemorrhage has a low incidence (1%), but patients with this condition have a poor prognosis. 5 Moreover, several studies have found that post-CEA hyperperfusion, even when asymptomatic, causes slight but diffuse damage to the ipsilateral cerebral cortex and white matter.…”

“…5 Moreover, several studies have found that post-CEA hyperperfusion, even when asymptomatic, causes slight but diffuse damage to the ipsilateral cerebral cortex and white matter. 3,6,7 This damage that occurs after CEA hyperperfusion is a principal cause of the postoperative cognitive impairment observed in 10% of patients following CEA. 3,6,7 Cerebrovascular autoregulatory mechanisms operate through dilation of precapillary resistance vessels that maintain CBF when reductions in cerebral perfusion pressure occur, and this is referred to as stage 1 ischemia.…”

“…3,6,7 This damage that occurs after CEA hyperperfusion is a principal cause of the postoperative cognitive impairment observed in 10% of patients following CEA. 3,6,7 Cerebrovascular autoregulatory mechanisms operate through dilation of precapillary resistance vessels that maintain CBF when reductions in cerebral perfusion pressure occur, and this is referred to as stage 1 ischemia. 3,[8][9][10] However, the autoregulatory mechanism provides insufficient compensation for severe decreases in cerebral perfusion pressure, which then leads to decreased CBF, referred to as misery perfusion or stage 2 ischemia.…”

“…3,6,7 Cerebrovascular autoregulatory mechanisms operate through dilation of precapillary resistance vessels that maintain CBF when reductions in cerebral perfusion pressure occur, and this is referred to as stage 1 ischemia. 3,[8][9][10] However, the autoregulatory mechanism provides insufficient compensation for severe decreases in cerebral perfusion pressure, which then leads to decreased CBF, referred to as misery perfusion or stage 2 ischemia. 3,[8][9][10] Thus, misery perfusion, which is defined as marginally sufficient cerebral blood supply relative to cerebral metabolic demand, is a situation with severely impaired cerebral hemodynamics.…”