Quantitative perfusion computed tomography measurements of cerebral hemodynamics: Correlation with digital subtraction angiography identified primary and secondary cerebral collaterals in internal carotid artery occlusive disease

摘要

Background: The aim of the present study was to assess hemodynamic variations in symptomatic unilateral internal carotid artery occlusion (ICAO) patients with primary collateral flow via circle of Willis or secondary collateral flow via ophthalmic artery and/or leptomeningeal collaterals. Methods: Thirty-eight patients with a symptomatic unilateral ICAO were enrolled in the study. Based on digital subtraction angiography (DSA) findings, patients were classified into 2 groups: primary collateral (n = 14) and secondary collateral (n = 24) groups. Collateral flow hemodynamics were investigated with perfusion computed tomography (PCT) by measuring the cerebral blood flow (CBF), cerebral blood volume (CBV) and time to peak (TTP) in the hemispheres ipsilateral and contralateral to ICAO. Based on the measurements, the ipsilateral to contralateral ratio for each parameter was calculated and compared. Results: Irrespective of the collateral patterns, ipsilateral CBF was not significantly different from that of the contralateral hemisphere (P = 0.285); ipsilateral CBV and TTP was significantly increased compared with those of the contralateral hemisphere (P = 0.000 and P = 0.000 for CBV and TTP, respectively). Furthermore, patients with secondary collaterals had significantly larger ipsilateral-to-contralateral ratios for both CBV (rCBV, P = 0.0197) and TTP (rTTP, P = 0.000) than those of patients with only primary collaterals. These two groups showed no difference in ipsilateral-to- contralateral ratio for CBF (rCBF, P = 0.312). Conclusion: Patients with symptomatic unilateral ICAO in our study were in an autoregulatory vasodilatation status. Moreover, secondary collaterals in ICAO patients were correlated with ipsilateral CBV and delayed TTP that suggested severe hemodynamic impairment, presumably increasing the risk of ischemic events.