Characteristics And Transformation In Patients With Intracranial Atherosclerotic Vulnerable Plaque Assessed By High-resolution Vessal Wall Magnetic Resonance Imaging

Background:Intracranial atherosclerotic disease(ICAD)is one of the common reasons of acute ischemic stroke.More and more studies on atherosclerotic diseases have shown that lumen stenosis is not a reliable indicator of the severity of plaques,and the vulnerability of plaque is more significance.Vulnerable plaques in intracranial arteries have a higher risk of cerebrovascular events.Assessing the vulnerability of intracranial plaques can help predict the risk of cerebrovascular events in the future.High-resolution vascular wall imaging(HR-MRI)has become the best non-invasive assessment method for vulnerable plaques in intracranial atherosclerosis.It can clearly present fibrous caps,lipid cores,intramural hematomas and lumen stenosis of atherosclerotic plaques.Also it has been widely used in the etiology diagnosis,efficacy evaluation and prognosis of cerebral infarction.Statins are a kind of reductase inhibitors.Long-term and regular use of statins can slow and stabilize the progression of atherosclerosis,and even reverse the plaques.Our topic closely follows the current hot spot of clinical research.By comparing the different features of different plaques in patients with acute ischemic stroke,this study investigates the application value of HR-MRI in atherosclerotic vulnerable plaques.Objective:This study is aim to explore the differences in enhancement degree,stenosis degree,thickening pattern and remodeling of culprit lesions,probably culprit lesions and non culprit lesions by using HR-MRI.Meanwhile we want to find the imaging signs of plaque vulnerability,improve finding the cause of stroke,guide the time of taking statins,and formulate precise secondary prevention strategies through this study.Materials and Methods:Between January 2018 and July 2020,patients were enrolled in this study if they had been admitted to the Second Hospital of Dalian Medical University for the treatment of acute ischemic stroke within 7 days of symptom onset.All patients were collected baseline data on the day of admission,including gender,age,and atherosclerotic disease related risk factors(hypertension,diabetes,hyperlipidemia,coronary heart disease,smoking and drinking history).On the second day of admission and 6 months after regular medical treatment,fasting venous blood will be drawn and the following indicators were collected:fasting blood glucose,glycosylated hemoglobin,blood lipids(total cholesterol,triglycerides,high density lipoprotein and low density lipoprotein),erythrocyte sedimentation rate(ESR),Hypersensitive C-reactive protein(hs-CRP)and homocysteine(HCY).According to the possibility of each plaque causing this acute cerebral infarction,each plaque is divided into culprit lesions,probably culprit lesions and nonculprit lesions.All patients completed routine MRI scan,magnetic resonance angiography and HR-MRI within 7 days of onset,took atorvastatin regularly after discharge,and completed the above-mentioned examinations again 6 months later.We measured the signal intensity of the vulnerable plaque and pituitary gland within7 days and 6 months after the onset,the lumen diameter and area of the blood vessel at the vulnerable plaque,the lumen diameter,area of the reference blood vessel,and calculated the degree of vascular stenosis[(1-lumen diameter at stenosis/reference vessel lumen diameter)*100%],plaque load[(vascular area-lumen area)/vascular area],remodeling index(vascular outer edge area at stenosis/reference outside vessel margin area)and the degree of plaque enhancement.Use SPSS 23.0(IBM SPSS statistics 23,Chicago,USA)to process data,and all tests were conducted with bilateral test.The difference was statistically significant(P<0.05).Results:A total of 21 patients were included in this study,including 13 males and 8females,with an average age of 56.7 years.They all took antiplatelet drugs and statins as directed by doctors.There was no significant difference in high density lipoprotein,triglyceride,fasting blood glucose and glycosylated hemoglobin between 1 weeks and 6months after treatment(P>0.05).There were significant differences in total cholesterol,low density lipoprotein,HCY,hs-CRP and ESR(P<0.001).A total of 56 atherosclerotic vulnerable plaques were collected,including 21 culprit lesions,7 probably culprit lesions,and 28 nonculprit lesions.There were significant differences among the three types of plaques in enhancement grade(χ~2=17.209,P<0.001),but there were no significant differences in plaque size,plaque burden,wall area,remodeling index,remodeling mode,thickening mode and degree of stenosis(P>0.05).No difference was found in plaque size,plaque burden,degree of enhancement,thickening mode,enhancement mode,remodeling index and degree of stenosis in all 56 intracranial atherosclerotic vulnerable plaques(P>0.05).Conclusions:1.Plaque enhancement may be a common feature of the plaques of culprit lesions,probably culprit lesions,and nonculprit lesions,but there are significant differences among the three.The enhancement degree of the plaques of culprit lesions is significantly higher than that of probably culprit lesions and nonculprit lesions.2.Plaque enhancement mainly occurred in neovascularization area and active inflammation area.There were significant differences in inflammatory indicators(CRP,ESR)within 1 weeks and 6 months after the onset,but no significant changes in the degree of enhancement,which may indicate neovascularization forming in the plaque.3.There is no significant change in the degree of enhancement of the same plaque within 1 weeks and 6 months after onset.It shows that in the short term(at least 6 months)taking statins do not reverse plaques,but may be stable plaques.How long it can last is still inconclusive,so for patients diagnosed with ischemic stroke,it illustrates the importance of long-term use of statins.