Academic official account of national Wei Jian Committee on stroke prevention and control committee
As doctors, they can never catch up with this era without reading. For young people who come to Xuanwu for training, they have smart minds and good basic education. Cramming theory teaching + devil type technical training is no longer the whole thing, and the main learning of the latest foreign literature has become an important link. Therefore, on the morning of Monday, Wednesday and Thursday every week, eight minutes after the early shift handover, is the time for further study doctors to interpret the literature. We will select some of them every month to read for xuan5.
——Joule group
Reported by: Cheng Kaili
Daqing people's Hospital, attending physician
Undergraduate, the 39th student of Xuanwu Hospital
This is an article on the reasons for the enhancement of contrast agents in the middle cerebral artery plaque through silica gel model, published by Korean scholar Sol-Ki Kim and others in Neuroradiology in July 2019.
At present, the pathophysiological mechanism of middle cerebral artery plaque enhancement is not clear, and its histological and imaging manifestations are not clear. The aim of the study was to assess the enhanced association between patients with MCA stenosis or occlusion and a silica gel model of MCA stenosis.
In this paper, we retrospectively analyzed black blood (BB) enhanced T1 weighted imaging (ce-t1w) in patients with acute stroke between January 2017 and January 2018. The subjects were divided into groups according to whether the results of cerebral angiography indicated stenosis or occlusion. The center collected 215 patients with acute ischemic stroke within 24 hours. All the patients had MRI and the symptoms of stroke were detected by nervous system. MR imaging was performed immediately after exclusion of intracranial hemorrhage. The imaging sequence includes:
(a) Diffusion weighted imaging (DWI);
(b) 3D-TOF MRA of intracranial artery;
(c) SWI;
(d) 3D BB ce-t1w imaging.
BB ce-t1w imaging was performed about 5 minutes after injection of contrast medium.
Model group: four kinds of MCA stenosis models were made (stenosis area: 0.8 mm, 1.0 mm, 1.2 mm and 1.4 mm), and the original lumen was 3 mm.
MCA silica gel stenosis model: MR examination
The silica gel model is connected to a flow rate of 5 L / min. The velocity in the narrow region of MCA silica gel model was measured by Doppler ultrasound. The control flow rate was similar to the blood flow rate, and then the silica gel model was immersed in normal saline for MR examination.
MR imaging analysis
Adopt the 4-point system (1 poor; 2 sufficient; 3 good; 4 excellent). Images with a score of 1 were excluded. Compared with the normal part of blood vessels in BB ce-t1 MRI, patients were also divided into BB enhancement positive or negative (excluding slight enhancement of blood vessel wall) according to the presence of intra-arterial enhancement.
Patients with positive BB enhancement on MR angiography were divided into stenosis group and occlusion group. The signal intensity (SI) of plaque enhancement was obtained on the sagittal images of BB ce-t1w. The signal intensity ratio (SIR) of the enhanced area of stenosis / occlusion in MCA was calculated as follows: the enhanced area Si / the normal lumen area Si. We analyzed the correlation between the degree of MCA stenosis and the contrast stagnation / enhancement in MR examination of the silicone tube stenosis model. At the same time, the near end / narrow region Sir of the stenosis model was calculated.
Statistical analysis and results:
In 215 consecutive patients, 44 (29 males; median age 69 years, range 48-89) showed stenosis and occlusion on BB ce-t1w. 41 patients were included in this study, 3 of whom were excluded due to poor imaging quality. Of the 41 patients, 19 had complete MCA occlusion and 22 had MCA stenosis. The SIR of CE in MCA occlusion group was significantly higher than that in MCA stenosis group (27.6 ± 19.6 vs. 22.7 ± 9.8, P = 0.005).
The diameter of carotid artery (proximal) was 5.8-6.0mm, the wall thickness was 0.45-0.65mm; the diameter of MCA (distal) was 3.2-3.5mm, the wall thickness was 0.22-0.41mm. The mean velocity of 0.8 mm MCA and 1.0 mm MCA were 70 cm / s and 55 cm / s, respectively. The average velocity of 1.2 mm and 1.4 mm silica gel models was 45 cm / s. The CE values of the vascular wall in the silicone tube stenosis model were 0.8 mm and 1.0 mm, respectively (& gt; 70% stenosis). The SIR of vascular wall and lumen CE was 31.0 ± 11.2. The SIR of MCA model with silicone tube stenosis was similar to that of MCA group with occlusion.
Discussion: in this study, we found that the SIR of stenosis MCA silica gel model on BB ce-t1w image was similar to that of MCA occlusion, and the SIR of MCA occlusion was significantly higher than that of MCA stenosis.
Vwi of carotid artery can be compared between the histology of carotid endarterectomy specimen and high-resolution MR imaging of carotid plaque, while vwi of intracranial artery can not be compared with the histology of living body. Therefore, we can only speculate the mechanism of the enhancement of middle cerebral artery atherosclerotic plaque.
In addition to lumen stenosis, plaque components such as lipid, IPH, hemorrhage, neovascularization and thrombus may be the cause of cerebral infarction. Is the mechanism of MCA plaque enhancement related to the above components?
One
IPH is more common in responsible plaques than in non responsible plaques. However, in the study report, the lower prevalence of IPH involves the intracranial artery: only one lesion in 205 intracranial artery segments is accompanied by IPH, which is inconsistent with the occurrence rate of MCA plaque enhancement.
Two
Inflammatory cell infiltration: macrophage infiltration is the main factor of plaque vulnerability. Chen et al. Found that the infiltration of macrophages and lymphocytes in infarct related atherosclerotic plaques was greater than that in non infarct related plaques. However, Ritz et al. Reported a lower degree of infiltration of macrophages in the brain than in the coronary artery. Therefore, it is difficult to explain the enhancement of vwi as the inflammation of intracranial plaque.
Three
Histology of plaque: the current understanding of the pathophysiology of intracranial atherosclerosis comes from the literature of carotid plaque. The enhancement of carotid plaque has been proved to be related to histology. The main components of the carotid endarterectomy specimens were fibrous tissue and lRNC. The BB ce-t1w imaging of vwi showed that there was an enhanced fibrous cap in the outer layer of the plaque and an unreinforced lipid necrosis core (lRNC) in the center. The vwi of BB ce-t1w did not show lamellar plaque in the necrotic core of MCA plaque, but only enhanced plaque in MCA.
CE of MCA patients was enhanced in the proximal and distal part of the occluded segment and the thrombus in BB CE-T1W. This finding suggests that the enhancement is related to the slow flow or stagnation of the occlusive phase contrast medium. Compared with the intracranial occlusion group, the CE in the intracranial stenosis group showed weak strength, linear or eccentric shape.
Based on the above analysis, a silica gel tube stenosis model with similar diameter and wall thickness to MCA was established. Through the above research methods, it was found that the SIR of silica gel tube stenosis group was similar to that of MCA occlusion group. These results suggest that the wall enhancement of MCA may be caused by the stagnation of contrast medium in the stenosis area. In this study, SIRS of silica gel stenosis model was higher than that of MCA stenosis group. Considering that the silicone stenosis model can not express the irregularity or stenosis length of plaque surface.
In conclusion, the study showed that the degree of CE in silicon model with severe MCA stenosis (0.8 mm and 1.0 mm) was similar to that in MCA occlusion group. The SIR of MCA occlusion group was significantly higher than that of MCA stenosis group. These findings may be related to the stagnation of contrast media, but not to inflammation or plaque instability.
Self comment:
This study has some limitations. First of all, MR examination was performed on the model of silicone tube stenosis with normal saline. Due to the presence of brain tissue, the internal and external boundaries of vwi in patients with MCA stenosis are not clear. However, the use of saline instead of brain tissue reduces the signal-to-noise ratio of the background. Secondly, different MR machines are used for imaging. This may result in different measurements.
Comments by Yang Bin:
This study was unable to reproduce various conditions of patients, such as the nature of plaque, blood viscosity, blood pressure, age, etc. Compared with the data of transcranial Doppler ultrasound in patients with MCA stenosis, the average blood flow velocity of silica gel model is lower. However, the low flow rate may be the reason for the stagnation of contrast medium in the narrow area.
In addition, it is mentioned in the article that the layered plaque displayed by bb ce-t1w imaging of carotid vwi is not likely to be related to the small plaque and limited imaging analysis of middle cerebral artery. This article only explains the reason for the enhancement of middle cerebral artery plaque, which has no practical guiding significance for the current clinical work.
Wu Fang comments:
Intracranial artery stenosis can lead to the decrease of blood turbulence and wall shear force. When gadolinium contrast agent is injected for MR angiography, the retention of local contrast agent can produce the effect of shortening T1, so as to show the enhancement of the wall. For example, occlusive lesions will show the enhancement of the wall of the long segment, suggesting that we should not exaggerate the significance of the enhancement when interpreting the image.
This study explored the correlation between contrast retention and enhancement of stenosis / occlusion in MCA using silica gel model with similar size and degree of stenosis in patients with stroke. It was concluded that "these findings may be related to stagnation of contrast medium, but not to inflammation or plaque instability", but the enhancement of stenosis / occlusion in intracranial artery may be enlarged and enhanced due to retention of contrast medium However, whether there is inflammatory reaction or neovascularization or not should be confirmed by pathological study.
Reviewer: Yang Bin
Xuanwu Hospital of Capital Medical University
Attending neurologist
Professor Ling Feng, a postdoctor, left Xuanwu Hospital to work in neurosurgery, taking into account the operation and interventional treatment of ischemic cerebrovascular disease.
Reviewer: Wu Fang
Xuanwu Hospital of Capital Medical University
Radiologist
He is a young member of the medical imaging technology branch of the Chinese society of biomedical engineering. He is mainly engaged in the diagnosis and research of cerebrovascular diseases and the research of high-resolution MRI of intracranial vessels. He has published 5 SCI papers of the first author in the Journal of stroke, jaha, European Radiology, etc
Previous review:
The relationship between rnf213 variation and plaque characteristics, vascular remodeling and hemodynamics in patients with ICAS
Case sharing, column participation, manuscript review and submission,
Business cooperation and other matters,
Please send an email to:
strokesj@163.com