From the Russell H. Morgan Department of Radiology and Radiological Sciences (Y.Q., S.M., B.A.W.) and Department of Neurology (S.R.Z., R.L., V.U., R.W.), Johns Hopkins Hospital, Johns Hopkins University School of Medicine, 367 East Park Building, 600 N Wolfe St, Baltimore, MD 21287.
Radiology. 2014 May;271(2):534-42. doi: 10.1148/radiol.13122812. Epub 2014 Jan 16.
To characterize intracranial plaque inflammation in vivo by using three-dimensional (3D) high-spatial-resolution contrast material-enhanced black-blood (BB) magnetic resonance (MR) imaging and to investigate the relationship between intracranial plaque inflammation and cerebrovascular ischemic events.
The study was approved by the institutional review board and was HIPAA compliant. Twenty-seven patients (19 men; mean age, 56.8 years ± 12.4 [standard deviation]) with cerebrovascular ischemic events (acute stroke, n = 20; subacute stroke, n = 2; chronic stroke, n = 3; transient ischemic attack, n = 2) underwent 3D time-of-flight MR angiography and contrast-enhanced BB 3-T MR imaging for intracranial atherosclerotic disease. Each identified plaque was classified as either culprit (the only or most stenotic lesion upstream from a stroke), probably culprit (not the most stenotic lesion upstream from a stroke), or nonculprit (not within the vascular territory of a stroke). Plaque contrast enhancement was categorized on BB MR images (grade 0, enhancement less than or equal to that of normal arterial walls seen elsewhere; grade 1, enhancement greater than grade 0 but less than that of the pituitary infundibulum; grade 2, enhancement greater than or equal to that of the pituitary infundibulum), and degree of contrast enhancement was calculated. Associations of the likelihood of being a culprit lesion with both plaque contrast enhancement and plaque thickness were estimated with ordinal logistic regression.
Seventy-eight plaques were identified in 20 patients with acute stroke (21 [27%] culprit, 12 [15%] probably culprit, and 45 [58%] nonculprit plaques). In these patients, grade 2 contrast enhancement was associated with culprit plaques (odds ratio 34.6; 95% confidence interval: 4.5, 266.5 compared with grade 0) when adjusted for plaque thickness. Grade 0 was observed in only nonculprit plaques. Culprit plaques had a higher degree of contrast enhancement than did nonculprit plaques (25.9% ± 13.4 vs 13.6% ± 12.3, P = .003).
Contrast enhancement of intracranial atherosclerotic plaque is associated with its likelihood to have caused a recent ischemic event and may serve as a marker of its stability, thereby providing important insight into stroke risk.
通过使用三维(3D)高空间分辨率对比增强黑血(BB)磁共振成像(MR)来描述颅内斑块炎症,并探讨颅内斑块炎症与脑血管缺血事件之间的关系。
该研究得到了机构审查委员会的批准,并符合 HIPAA 规定。27 例(19 名男性;平均年龄 56.8 岁±12.4[标准差])有脑血管缺血事件(急性脑卒中 20 例;亚急性脑卒中 2 例;慢性脑卒中 3 例;短暂性脑缺血发作 2 例)的患者进行了 3D 时间飞跃 MR 血管造影和对比增强 3T BB MR 成像,以评估颅内动脉粥样硬化性疾病。每个确定的斑块均分为罪魁祸首(脑卒中上游唯一或最狭窄的病变)、可能的罪魁祸首(脑卒中上游不是最狭窄的病变)或非罪魁祸首(不在脑卒中的血管区域内)。在 BB MR 图像上对斑块的增强程度进行分类(0 级,增强程度与其他部位正常动脉壁相等;1 级,增强程度大于 0 级但小于垂体柄;2 级,增强程度等于或大于垂体柄),并计算增强程度。使用有序逻辑回归估计斑块增强程度和斑块厚度与成为罪魁祸首病变的可能性之间的关联。
20 例急性脑卒中患者中发现了 78 个斑块(21 个[27%]为罪魁祸首斑块,12 个[15%]为可能的罪魁祸首斑块,45 个[58%]为非罪魁祸首斑块)。在这些患者中,当调整斑块厚度时,2 级增强与罪魁祸首斑块相关(优势比 34.6;95%置信区间:4.5,266.5 与 0 级相比)。仅在非罪魁祸首斑块中观察到 0 级增强。罪魁祸首斑块的增强程度高于非罪魁祸首斑块(25.9%±13.4%与 13.6%±12.3%,P=0.003)。
颅内动脉粥样硬化斑块的增强与近期缺血事件发生的可能性相关,可能是其稳定性的标志物,从而为卒中风险提供了重要的见解。