Intracranial Plaque Enhancement in Patients with Cerebrovascular Events on High-Spatial-Resolution MR Images

被引:304
|
作者
Qiao, Ye [1 ]
Zeiler, Steven R. [2 ]
Mirbagheri, Saeedeh [1 ]
Leigh, Richard [2 ]
Urrutia, Victor [2 ]
Wityk, Robert [2 ]
Wasserman, Bruce A. [1 ]
机构
[1] Johns Hopkins Univ, Sch Med, Russell H Morgan Dept Radiol & Radiol Sci, Johns Hopkins Hosp, Baltimore, MD 21287 USA
[2] Johns Hopkins Univ, Sch Med, Dept Neurol, Johns Hopkins Hosp, Baltimore, MD 21287 USA
关键词
BLACK BLOOD MRI; ATHEROSCLEROTIC PLAQUE; ARTERY ATHEROSCLEROSIS; CEREBRAL ATHEROSCLEROSIS; CAROTID PLAQUE; WALL; STENOSIS; STROKE; NEOVASCULARIZATION; INFLAMMATION;
D O I
10.1148/radiol.13122812
中图分类号
R8 [特种医学]; R445 [影像诊断学];
学科分类号
1002 ; 100207 ; 1009 ;
摘要
Purpose: 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. Materials and Methods: 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. Results: 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). Conclusion: 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.
引用
收藏
页码:534 / 542
页数:9
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