Carotid Artery Wall Imaging: Perspective and Guidelines from the ASNR Vessel Wall Imaging Study Group and Expert Consensus Recommendations of the American Society of Neuroradiology

Abstract

Identification of carotid artery atherosclerosis is conventionally based on measurements of luminal stenosis and surface irregularities using in vivo imaging techniques including sonography, CT and MR angiography, and digital subtraction angiography. However, histopathologic studies demonstrate considerable differences between plaques with identical degrees of stenosis and indicate that certain plaque features are associated with increased risk for ischemic events. The ability to look beyond the lumen using highly developed vessel wall imaging methods to identify plaque vulnerable to disruption has prompted an active debate as to whether a paradigm shift is needed to move away from relying on measurements of luminal stenosis for gauging the risk of ischemic injury. Further evaluation in randomized clinical trials will help to better define the exact role of plaque imaging in clinical decision-making. However, current carotid vessel wall imaging techniques can be informative. The goal of this article is to present the perspective of the ASNR Vessel Wall Imaging Study Group as it relates to the current status of arterial wall imaging in carotid artery disease.

Fig 1.

Plaque volume analysis in a 75-year-old man with a TIA. In the volume-rendered image, the carotid is traced (A), and in the curved-planar-reconstructed postprocessed image (CTA module, Aquarius iNtuition Edition, Version 44121382907; TeraRecon, San Mateo, California) (B), the plaque is identified based on the green contours (white arrows). The volume analysis with automated boundary detection and tissue segmentation is shown in panels C, D, and E (corresponding to the 3 arrows, proximal-to-distal) with contours delineating the lumen (red contour), outer wall (blue contour), and shading of calcium (blue), mixed tissue (green), and lipid component (red).

Fig 2.

Ulcerated carotid artery plaques detected with CT and MR imaging. In the first case, the CTA of a 74-year-old man with a TIA demonstrates an ulcerated carotid artery plaque (white arrows) in the left internal carotid artery (white arrow) in the MIP (A) and axial source (B) images. In the second case, an MR imaging analysis of a 63-year-old man with a TIA shows a tiny ulceration (white arrows) in the right internal carotid artery visible in the axial (C) and paracoronal (D) planes.

Fig 3.

Carotid atherosclerotic plaque MR imaging and a specimen from a 73-year-old man with stenosis of the carotid bulb measuring 69% by the NASCET criteria demonstrated on a contrast-enhanced MRA (A). The precontrast (mask) image from the contrast-enhanced MRA demonstrates bright signal indicative of intraplaque hemorrhage, specifically subacute blood, or methemoglobin (B, arrow). Subacute blood is also identified as bright signal on the precontrast T1-weighted black-blood image (C, arrow). A rim of hemosiderin is identified as hypointense signal on the postcontrast black-blood image (D) and a hemosiderin-sensitive sequence (E) and is confirmed on the endarterectomy specimen (F and G). The fibrous cap is also delineated (green arrow, D and F). Black-blood imaging was achieved by using 2D cardiac-gated double inversion recovery turbo spin-echo. ECA indicates external carotid artery; CCA, common carotid artery; TFE, turbo field echo.

Fig 4.

Carotid atherosclerotic plaque MR imaging and a specimen from a 76-year-old woman with transient ischemic attacks ipsilateral to carotid bulb stenosis, measuring 47% by the NASCET criteria demonstrated on a contrast-enhanced MRA. A, Narrowing is caused by the plaque characterized by 2D cardiac-gated double inversion recovery black-blood MR imaging (B). Regional enhancement (green arrow) within the lipid core (yellow arrow) suggests focal inflammation with neovascularity as confirmed on the endarterectomy specimen (C, green circle). Contrast enhancement is also useful for delineating the fibrous cap (B and C, orange arrowheads). Calcification is identified as areas of hypointensity (B, red arrows, and C, red circle).

Fig 5.

Smooth left internal carotid artery stenosis with intraplaque hemorrhage. All images were acquired with a 16-channel neurovascular coil at 3T. The CE-MRA demonstrates a smooth, nonulcerated stenosis in the bulbous and postbulbous parts of the left internal carotid artery (white arrowhead, A). Oblique reformat of a coronally acquired MPRAGE image shows extensive intraplaque hemorrhage, which appears hyperintense (white arrow, B). The IPH is hyperintense on the nonenhanced T1 fat-saturated spin-echo image (C) and isointense on the gadolinium-enhanced T1 fat-saturated spin-echo image (D). On the TOF MRA source data, the IPH also appears hyperintense but to a lesser degree than the intraluminal flow signal (E).

Fig 6.

Matched cross-sectional images of a carotid plaque with high signal intensity (white arrows), consistent with the presence of intraplaque hemorrhage on MPRAGE (A) and SNAP MR imaging (B). Note the greater conspicuity of the carotid lumen (L) on SNAP compared with the MPRAGE image. There is a penetrating ulcer (asterisk) that is more easily detected on SNAP compared with the TOF MRA image (C).

Fig 7.

In a 68-year-old male patient, coexistent plaque components, fresh intraplaque hemorrhage (arrows), and superficial calcifications (arrowheads) are detected by MATCH (first row) and the conventional multicontrast protocol (second row). Compared with T1-weighted TSE and TOF, MATCH provides more conspicuous depiction of intraplque hemorrhage on the hyper-T1-weighted image and calcification on the gray blood image. Notice that the calcification is also visible on the MATCH T2-weighted image but not on the T2-weighted TSE image.

Fig 8.

A, Contrast-enhanced MRA of the extracranial carotid bifurcation indicating the level of 2D-FSE images obtained with 1.5T. B, T1-weighted double inversion recovery black-blood FSE image shows an eccentric plaque (arrow) in the internal carotid artery. C, T2-weighted double inversion recovery black-blood FSE image at the same level shows a crescentic, hypointense signal from the necrotic core, which is separated by a higher intensity fibrous cap from the flow lumen.

Fig 9.

Volume transfer constant (K^trans) map of a patient with carotid plaque. Maps were generated using pharmacokinetic modeling of dynamic contrast-enhanced MR images. The parametric map is overlaid on the anatomic MR image, and voxel K^trans values (Patlak model) are color-coded. The necrotic core exhibits low K^trans values at the center of the plaque, while the highly vascularized adventitia at the outer rim exhibits high K^trans values. There is another region of higher K^trans values near the inner rim of the plaque.

Fig 10.

[¹⁸F] fluorocholine positron-emission tomography CT (¹⁸F-FCH PET CT) image of a symptomatic (arrow) and contralateral asymptomatic (arrowhead) carotid plaque of a patient who experienced right-sided stroke. A, Diagnostic contrast-enhanced CT shows a significant stenosis in the right internal carotid artery because of a calcified plaque, whereas a noncalcified atherosclerotic plaque can be seen on the contralateral internal carotid artery. B, CT, inset on the symptomatic plaque. C, CT, inset on the asymptomatic plaque. D, The fused PET CT image denotes a focal area of high [¹⁸F] FCH uptake in the right symptomatic carotid plaque, whereas there is no visible [¹⁸F] FCH uptake in the left asymptomatic carotid plaque. E, Fused PET CT, inset on the symptomatic plaque. F, Fused PET-CT, inset on the asymptomatic plaque.