Comparison of symptomatic and asymptomatic atherosclerotic carotid plaques using parallel imaging and 3 T black-blood in vivo CMR

Abstract

Background: To determine if black-blood 3 T cardiovascular magnetic resonance (bb-CMR) can depict differences between symptomatic and asymptomatic carotid atherosclerotic plaques in acute ischemic stroke patients.

Methods: In this prospective monocentric observational study 34 patients (24 males; 70 ±9.3 years) with symptomatic carotid disease defined as ischemic brain lesions in one internal carotid artery territory on diffusion weighted images underwent a carotid bb-CMR at 3 T with fat-saturated pre- and post-contrast T1w-, PDw-, T2w- and TOF images using surface coils and Parallel Imaging techniques (PAT factor = 2) within 10 days after symptom onset. All patients underwent extensive clinical workup (lab, brain MR, duplex sonography, 24-hour ECG, transesophageal echocardiography) to exclude other causes of ischemic stroke. Prevalence of American Heart Association lesion type VI (AHA-LT6), status of the fibrous cap, presence of hemorrhage/thrombus and area measurements of calcification, necrotic core and hemorrhage were determined in both carotid arteries in consensus by two reviewers who were blinded to clinical information. McNemar and Wilcoxon's signed rank tests were use for statistical comparison. A p-value <0.05 was considered statistically significant.

Results: Symptomatic plaques showed a higher prevalence of AHA-LT6 (67.7% vs. 11.8%; p < 0.001; odds ratio = 12.5), ruptured fibrous caps (44.1% vs. 2.9%; p < 0.001; odds ratio = 15.0), juxtaluminal thrombus (26.5 vs. 0%; p < 0.01; odds ratio = 7.3) and intraplaque hemorrhage (58.6% vs. 11.8%; p = 0.01; odds ratio = 3.8). Necrotic core and hemorrhage areas were greater in symptomatic plaques (14.1 mm2 vs. 5.5 mm2 and 13.6 mm2 vs. 5.3 mm2; p < 0.01, respectively).

Conclusion: 3 T bb-CMR is able to differentiate between symptomatic and asymptomatic carotid plaques, demonstrating the potential of bb-CMR to differentiate between stable and vulnerable lesions and ultimately to identify patients with low versus high risk for cardiovascular complications. Best predictors of the symptomatic side were a ruptured fibrous cap, AHA-LT 6, juxtaluminal hemorrhage/thrombus, and intraplaque hemorrhage.

Figure 1

Imaging example. Figure 1 shows various CMR-images of a 66 years old patient who suffered an infarction 4 days before the CMR scan. a. T1w and DWI MR-images of the patient. Axial T1w images with fat suppression demonstrate atherosclerotic lesions in both internal carotid arteries (ICA). The lesion in the right ICA, ipsilateral to the symptoms, is hyperintense, consistent with intraplaque hemorrhage. The lesion in the left ICA is hypo- to isointense, consistent with a fibrous and calcified lesion. Axial DWI images show a diffusion restriction in the posterior part of the right middle cerebral artery, consistent with an acute brain infarction. b. Axial multi-sequence CMR images of the same patient demonstrating the complicated AHA lesion type VI plaque ipsilateral to the stroke in the right ICA. The arrow points to a region which is hyperintense on T1w and TOF images and hypointense on PDw and T2w images, consistent with type I hemorrhage into a large necrotic core. The dark band on TOF images is disrupted, the hyperintense area on TOF is located juxtaluminally and the fibrous cap cannot be visualized in the contrast enhanced T1w images, indicating rupture of the fibrous cap (ICA = Internal carotid artery, TOF = Time-of-Flight). c. Axial multi-sequence CMR images of the same patient demonstrating the uncomplicated AHA lesion type VII plaque contralateral to the stroke in the left ICA. The arrow points to a region which is hypointense on all images, consistent with a calcification, surrounding an area which is isointense to fatty tissue in T1w, T2w and PDw images and shows no contrast enhancement, consistent with a necrotic lipid core. The contrast enhancing fibrous cap separating the plaque from the lumen appears intact. (ICA = Internal carotid artery, TOF = Time-of-Flight).

Figure 2

Distribution of AHA lesion type. Figure 2 visualizes the distribution of AHA lesion types in the asymptomatic and the symptomatic groups. Note the higher prevalence of AHA lesion type 6 plaques in the symptomatic group and of types 3 and 7 in the asymptomatic group.

Figure 3

Quantitative analysis of plaque components. Figure 3 shows the absolute quantitative distribution of different plaque features in mm² on cross sectional images for symptomatic and asymptomatic plaques in comparison. Symptomatic plaques showed a greater maximum cross sectional area for lipid rich necrotic cores and hemorrhage while no differences were found for loose matrix and calcification areas.