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

Abstract

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.

Differential Features of Culprit Intracranial Atherosclerotic Lesions: A Whole‐Brain Vessel Wall Imaging Study in Patients With Acute Ischemic Stroke

“…In addition, mean SI was quantified in each of plaques at their most thickened cross sections and also in their adjacent reference normal vessel wall, brain parenchyma, and the pituitary infundibulum on both precontrast and postcontrast images. Contrast enhancement ratio (ER), calculated as SI postcontrast /SI precontrast ×100%, was determined for the plaque, reference wall, and pituitary infundibulum, where SI precontrast and SI postcontrast were the specific tissue's SI normalized by the SI of adjacent brain parenchyma on precontrast and postcontrast images, respectively 15. The degree of lesion enhancement was graded as follows: grade 0, plaque ER ≤ reference wall ER; grade 1, reference wall ER < plaque ER < pituitary infundibulum ER; grade 2, plaque ER ≥ pituitary infundibulum ER.…”

“…), but had no access to VWI data to avoid influence of their decision by postcontrast wall enhancement. A culprit lesion was defined as the following: (1) the only lesion within the vascular territory of the stroke or (2) the most stenotic lesion when multiple plaques were present within the same vascular territory of the stroke 15. A lesion was considered probably a culprit plaque if it was within the same vascular territory of the stroke but was not the most stenotic lesion 15.…”

“…A culprit lesion was defined as the following: (1) the only lesion within the vascular territory of the stroke or (2) the most stenotic lesion when multiple plaques were present within the same vascular territory of the stroke 15. A lesion was considered probably a culprit plaque if it was within the same vascular territory of the stroke but was not the most stenotic lesion 15. A lesion was deemed a nonculprit plaque when it was not within the vascular territory of the stroke 15.…”

“…A lesion was considered probably a culprit plaque if it was within the same vascular territory of the stroke but was not the most stenotic lesion 15. A lesion was deemed a nonculprit plaque when it was not within the vascular territory of the stroke 15. Any disagreements between the 2 reviewers were resolved with discussion and consensus.…”

“…The advent of 3‐dimensional VWI techniques in the past few years also makes it possible to simultaneously assess atherosclerotic plaques presenting in multiple arterial segments 11, 12. Using VWI, several plaque features have been intimately associated with symptomatic or asymptomatic lesions, such as high signal on T1‐weighted images (HST1), wall thickening pattern, and postcontrast enhancement 7, 13, 14, 15, 16, 17, 18. However, most of previous studies were limited to one feature only, a local arterial segment, or a cohort with heterogeneous time periods after symptom onset.…”