The study was a prospective and registry study, had been approved by ethics committee of our hospital. Written informed consent was obtained from the patients or their legally relatives.
Enrollment of Patients
Patients suspected to symptomatic intracranial atherosclerotic stenosis (ICAS) at admission were enrolled. All patients received thorough evaluations to determine the cause of ischemic events including transit ischemic attack (TIA) or ischemic stroke, including carotid duplex, transcranial Doppler, echocardiography, electrocardiogram, computer tomography (CT), magnetic resonance imaging (MRI), CT angiography (CTA), magnetic resonance angiography (MRA) and digital subtract angiography (DSA). Patients were enrolled in this study according to the following criteria: 1) age≥18 years; 2) ischemic stroke or TIA in the target territories posterior circulation within 90 days; 3)basilar artery stenosis ≥70%, and without coexistent≥50% ipsilateral extracranial vertebral artery stenosis; 4) Without potential sources of cardioaortic embolism based on the modified Trial of ORG 10 172 in Acute Stroke Treatment (TOAST) classification , 5) one or more atherosclerotic risk factors; 6) all the patients received DSA examination. Risk factors were recorded including hypertension, dyslipidemia, diabetes, smoking and obesity.
Patients with the following conditions were excluded: 1) nonatherosclerotic vasculopathy such as vasculitis and arterial dissection, diagnosed by comprehensive laboratory examinations (such as erythrocyte sedimentation rate or C-reactive protein elevations, antinuclear antibody, or antiphospholipid antibody positivity), vascular imaging, and clinical evaluation. 2) contraindication to MR examination, medical instability precluding MR examination.
HRMRI acquisition and analysis
All HRMRI studies were performed on a 3T GE DISCOVERY MR 750 (GE Healthcare, Waukesha, WI, USA) or a 3T Siemens Trio MR scanner (Siemens Healthcare, Ehrlangen, Germany). The details were presented in study protocol (see the supplemental etable 1). Image reconstruction were conducted by Reformate tool in AW 4.5 workstation (GE Healthcare) and 3D multiple planer reconstruction tool in Siemens workstation. MR images were then processed for all identified plaques using commercially available software (Vessel Mass; Leiden University Medical Center, Leiden, The Netherlands).
A culprit plaque was defined as the single lesion at the supplying artery for the infarct zone or the most severe stenotic lesion when multiple plaques were present at the supplying artery [15-16].
Arterial remodeling index (RI) was calculated as the ratio of outer wall area (OWA) at the site of maximal lumen narrowing to that at the reference site (RI=OWA lesion/OWA reference) . The reference site was selected based on the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) trial method . There are three remodeling categories as previously described, following RI ≥1.05 as positive remodeling, 0.95 <RI< 1.05 as intermediate remodeling, RI≤0.95 as negative remodeling. Plaque distributions were dichotomized into diffuse and non-diffuse patterns at culprit lesion. The anatomical location of the plaque was recorded as ventral, dorsal, left, and right quadrants . Plaques spreading across four quadrants were defined as diffuse and that involving ≤3 quadrants were defined as non-diffuse. Intraplaque hemorrhage (IPH) was defined as a signal intensity greater than 150% of T1 signal of adjacent muscle . As to plaque enhancement, non-enhancement was defined as similar to or less than that of normal intracranial arterial walls nearby, while enhancement meant signal intensity was greater than non-enhancement, and less than or greater than that of the pituitary infundibulum .
We adopted the same principal when interpreting HRMRI vessel wall imaging over arterial remodeling and vessel wall features as we have published before with small intrao-bserver and inter-observer variability [10,17,21]. The intra- and inter-observer variability of the two scanners and vessel wall features of HRMRI were good to excellent (weighted k =0.82, 95% CI: 0.46, 1.00 and 0.83, 95% CI: 0.41-1.00, respectively).
Definition of configurations of BA
Configurations of BA were divided as complete and incomplete configuration. (see figure 1) The patients with normal bilateral vertebral arteries and posterior cerebral arteries were categorized as complete configuration. If the patients had one VA dysplasia and (or) fPCA were defined as incomplete configuration on DSA and(or) CTA, MRA. The presence of posterior communicating arteries was also recorded. The presence of hypoplastic VA was defined as with a diameter <2 mm, ended in the posterior inferior cerebellar artery, or lumen diameter more than 50% difference [4-5]. The fPCA was defined as the blood flow of posterior cerebral artery from internal carotid artery, and without P1 segment of PCA or dysplasia of P1 segment of PCA [6-7]. Two neurologists (Z.Q.X. and N.M) reviewed the DSA images independently and discrepancies were resolved by consensus.
Continuous variables were presented as means ± SD or median with interquartile range. Categorical variables were presented as percentages. All baseline characteristics, plaque enhancement, intraplaque hemorrhage, arterial remodeling patterns and plaque distribution were compared with χ2 test for categorical variables and 1-way analysis of variance or the Kruskal-Wallis test for continuous variables between complete and incomplete configurations group. The analyses were performed using SPSS 23.0 statistical software (IBM, Chicago, IL, USA). A two-tailed P value less than 0.05 was considered statistically significant.