| Objective: With the development of high-resolution MRI,the imaging sequence of intracranial vessel wall is gradually maturing and studies on intracranial vessel wall are gradually increasing,the morphology and enhancement of the vessel wall in the intracranial vascular disease such as intracranial atherosclerotic plaque,vasculitis,moyamoya disease and other vascular related diseases has been further developed and improved.Our goal was to suing HR-MRI to explore the difference of enhancement and remodeling pattern between culprit and non-culprit plaque,then to assess whether plaque enhancement and remodeling pattern can be used as a radiographic marker for plaque vulnerability.Subjects and Methods: Patients suspected of atherosclerosis who underwent head and neck MRA were performed the additional 3D-T1-SPACE(three dimensional-T1 weighted imaging Sampling Perfection with Application optimized Contrast using different angle Evolutions)sequence before and after contrast.44 patients(33men,mean age: 61.5)met our standards(acute stroke,n=21;TIA,n=8;asymptomatic patients,n=15).All patients met the following standards: older than 50 years old;have at least two high risk factors of atherosclerosis(diabetes mellitus,hyperlipidemia and hypertension).The color Doppler,MRA,CTA examination showed a certain narrow or plaque in the carotid artery or intracranial artery.The exclusion criteria for the symptomatic patients were as follows: internal carotid artery stenosis(>50%)on MRA or/and cardiac embolism.Symptomatic patients were considered for inclusion if the patients were admitted with infarction involving MCA or BA territory on the diffusion-weighted image and had the corresponding clinical manifestations within seven days or had transient ischemic attacks(TIA)recently.All subjects recruited in our study underwent head MRI、head and neck MRA,pre and post 3D T1WI-SPACE.A culprit plaque was defined as the plaque in the proximal vessels that supplied the ischemic lesion referring to arterial territories of the human brain.A non-culprit plaque was defined as either a plaque occurring in a contralateral artery of a symptomatic patient or one in asymptomatic patient reference.Then lumen area(LA),outer wall area(OWA),and wall area(WA)were measured both at the lesion and reference.Plaque burden was counted as WA divided by OWA.The arterial remodeling ratio(RR)was counted as OWA at the lesion site divided by OWA at the reference site.Arterial remodeling pattern was classified as positive if RR>1.05,intermediate if 0.95≤RR≤1.05,and negative if RR<0.95.Results: A total of 47 plaques(culprit,n=21;non-culprit,n=26)were identified in 44 patients.Forty-four plaques were found in 44 patients,21 culprit plaques and 26 non-culprit plaques.A total of 30 plaques were found in 21 patients with acute cerebral infarction,including 21 culprit plaques and 5 non-culprit plaques;4 non-culprit plaques were found in 8 TIA patients;17 non-culprit plaques were found in 15 asymptomatic patients.Plaques.All culprit plaques and 23 of 26 non-culprit had contrast enhancement.There was no significantly statistical difference in presence of contrast enhanced plaques between the two types(χ2>0.05),but culprit plaques had greater degree of contrast enhancement than did non-culprit plaques(0.88±0.33 VS 0.46±0.23,P<0.001).5 culprit and 7 non-culprit plaques demonstrated the positive remodeling.All plaques lead to eccentric wall thickening.In addition,all the patients in our study showed that the wall of intracranial internal carotid artery(i-ICA)and intracranial bilateral vertebral artery(i-VA)in the scan range had uniform circular contrast enhancement almost at the same level.Conclusions: All plaques lead to eccentric wall thickening.Plaque enhancement may be a common feature in both culprit and non-culprit plaques,but the degree of enhancement is different.This suggests only the presence of contrast enhancement is not characteristics of vulnerable plaque and the great degree of enhancement is associated with plaque vulnerability. |
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