Association of local collateral formation on TOF-MRA with plaque characteristics and ischemic stroke in intracranial atherosclerotic stenosis
摘要
To investigate the features of local collateral vessel formation at the site of intracranial atherosclerotic stenosis (ICAS) and its relationship with cerebral infarction events.
MethodsRetrospectively analyzed patients diagnosed with ICAS or moyamoya disease (MMD) who underwent three-dimensional T1-weighted turbo-spin-echo (3D T1W-TSE), 3D time-of-flight magnetic resonance angiography (TOF-MRA), and DSA between June 2018 and March 2025. Key imaging features, including ICAS with local collateral vessels (ICAS-lcv), hyperintense vessel sign score, degree and location of M1-MCA stenosis, plaque enhancement grade, and posterior cerebral artery (PCA) diameter, were independently quantified by two neuroradiologists blinded to clinical data. Subgroup and logistic-regression analyses were then performed.
ResultsA total of 149 cases with atherosclerotic stenosis in the middle cerebral artery (MCA) and 41 cases with MMD were enrolled. Among them, 29 cases with ICAS-lcv, and 59 MMD lesions exhibited moyamoya vessels. More ICAS-lcv cases were observed in individuals with severe stenosis or occlusion. Multivariable logistic regression identified the degree of stenosis as an independent risk factor for collateral formation in non-infarcted ICAS. Inter-group and subgroup analyses revealed that the infarct group had a lower incidence of ICAS-lcv than the non-infarct group. After adjustment for confounders, multivariable logistic regression showed that the presence of ICAS-lcv (OR, 0.24; 95%CI [0.08–0.70]; p = 0.009) was independently associated with infarction. Moreover, the diameter of the PCA distinguished ICAS-lcv from MMD with an area under the curve (AUC) of 0.87.
ConclusionThe evidence of local collateral vessels on TOF-MRA contributes to managing the risk of cerebral infarction in ICAS, whereas the caliber of the PCA serves as a potential imaging marker to differentiate ICAS-lcv from MMD.