Survey of the American Society of Neuroradiology Membership on the Use and Value of Extracranial Carotid Vessel Wall MRI.

BACKGROUND AND PURPOSE: Extracranial vessel wall MRI (EC-VWI) contributes to vasculopathy characterization. This survey study investigated EC-VWI adoption by American Society of Neuroradiology (ASNR) members and indications and barriers to implementation. MATERIALS AND METHODS: The ASNR Vessel Wall Imaging Study Group survey on EC-VWI use, frequency, applications, MR imaging systems and field strength used, protocol development approaches, vendor engagement, reasons for not using EC-VWI, ordering provider interest, and impact on clinical care was distributed to the ASNR membership between April 2, 2019, to August 30, 2019. RESULTS: There were 532 responses; 79 were excluded due to minimal, incomplete response and 42 due to redundant institutional responses, leaving 411 responses. Twenty-six percent indicated that their institution performed EC-VWI, with 66.3% performing it ≤1-2 times per month, most frequently on 3T MR imaging, with most using combined 3D and 2D protocols. Protocols most commonly included pre- and postcontrast T1-weighted imaging, TOF-MRA, and contrast-enhanced MRA. Inflammatory vasculopathy (63.3%), plaque vulnerability assessments (61.1%), intraplaque hemorrhage (61.1%), and dissection-detection/characterization (51.1%) were the most frequent applications. For those not performing EC-VWI, the reasons were a lack of ordering provider interest (63.9%), lack of radiologist time/interest (47.5%) or technical support (41.4%) for protocol development, and limited interpretation experience (44.9%) and knowledge of clinical applications (43.7%). Reasons given by 46.9% were that no providers approached radiology with interest in EC-VWI. If barriers were overcome, 51.1% of those not performing EC-VWI indicated they would perform it, and 40.6% were unsure; 48.6% did not think that EC-VWI had impacted patient management at their institution. CONCLUSIONS: Only 26% of neuroradiology groups performed EC-VWI, most commonly due to limited clinician interest. Improved provider and radiologist education, protocols, processing techniques, technical support, and validation trials could increase adoption.

[High-resolution magnetic resonance imaging of carotid atherosclerotic plaque]. / Hochauflösende Bildgebung atherosklerotischer Gefässwandläsionen der Karotiden durch die Magnetresonanztomografie.

Stroke is the third most common cause of mortality in the United States with an incidence rate of approximately 700 000 deaths per year. As a means to prevent cerebrovascular events, current concepts advocate endarterectomy or carotid stenting in patients with advanced carotid disease. Arterial stenosis alone has been shown to be a poor predictor of cardiovascular events and therefore both arterial stenosis and patient symptom status are taken as indications for interventional therapy. Several studies have shown that symptomatic subjects benefit more from a carotid endarterectomy than asymptomatic subjects: 3-6 carotid endarterectomies are needed to prevent one stroke per year in symptomatic subjects with > 70 % stenosis compared to 14 - 17 carotid endarterectomies in asymptomatic patients with > 50 % stenosis. It is commonly accepted today that factors other than the degree of luminal stenosis can determine a patient's symptom status, such as the composition or the superficial structure of atherosclerotic plaque. High-resolution magnetic resonance imaging has overcome the limitations of current angiographic techniques and has emerged as a leading non-invasive imaging modality for atherosclerotic disease, especially within carotid arteries and other large vessels. In this review, the state of the art in MRI of atherosclerosis is presented in terms of hardware and image acquisition protocols. Also, the results of validation studies for measuring lesion size, composition and inflammation will be summarized. Finally, the status of several clinical trials involving MRI of atherosclerosis will be reviewed.

High shear stress influences plaque vulnerability Part of the data presented in this paper were published in Stroke 2007;38:2379-81.

Shear stress of the blood at the vessel wall plays an important role in many processes in the cardiovascular system primarily focused on the regulation of vessel lumen and wall dimensions. There is ample evidence that atherosclerotic plaques are generated at low shear stress regions in the cardiovascular system, while high shear stress regions are protected. In the course of plaque progression, advanced plaques start to encroach into the lumen, and thereby start to experience high shear stress at the endothelium. Until now the consequences of high shear stress working at the endothelium of an advanced plaque are unknown. As high shear stress influences tissue regression, we hypothesised that high shear stress can destabilise the plaque by cap weakening leading to ulceration. We investigated this hypothesis in a magnetic resonance imaging (MRI) dataset of a 67-year-old woman with a plaque in the carotid artery at baseline and an ulcer at ten-month follow-up. The lumen, plaque components (lipid/necrotic core, intraplaque haemorrhage) and ulcer were reconstructed three dimensionally and the geometry at baseline was used for shear stress calculation using computational fluid dynamics. Correlation of the change in plaque composition with the shear stress at baseline showed that the ulcer was generated exclusively at the high shear stress location. In this serial MRI study we found plaque ulceration at the high shear stress location of a protruding plaque in the carotid artery. Our data suggest that high shear stress influences plaque vulnerability and therefore may become a potential parameter for predicting future events. (Neth Heart J 2008;16:280-3.).

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.

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.

Quantitative evaluation of carotid plaque composition by in vivo MRI.

OBJECTIVE: This study evaluates the ability of MRI to quantify all major carotid atherosclerotic plaque components in vivo. METHODS AND RESULTS: Thirty-one subjects scheduled for carotid endarterectomy were imaged with a 1.5T scanner using time-of-flight-, T1-, proton density-, and T2-weighted images. A total of 214 MR imaging locations were matched to corresponding histology sections. For MRI and histology, area measurements of the major plaque components such as lipid-rich/necrotic core (LR/NC), calcification, loose matrix, and dense (fibrous) tissue were recorded as percentages of the total wall area. Intraclass correlation coefficients (ICCs) were computed to determine intrareader and inter-reader reproducibility. MRI measurements of plaque composition were statistically equivalent to those of histology for the LR/NC (23.7 versus 20.3%; P=0.1), loose matrix (5.1 versus 6.3%; P=0.1), and dense (fibrous) tissue (66.3% versus 64%; P=0.4). Calcification differed significantly when measured as a percentage of wall area (9.4 versus 5%; P<0.001). Intrareader and inter-reader reproducibility was good to excellent for all tissue components, with ICCs ranging from 0.73 to 0.95. CONCLUSIONS: MRI-based tissue quantification is accurate and reproducible. This application can be used in therapeutic clinical trials and in prospective longitudinal studies to examine carotid atherosclerotic plaque progression and regression.

Carotid plaque composition differs between ethno-racial groups: an MRI pilot study comparing mainland Chinese and American Caucasian patients.

OBJECTIVE: Ethnicity-based research may identify new clues to the pathogenesis of atherosclerotic disease. Therefore, we sought to determine whether carotid lesions differ between 20 Chinese and 20 Caucasian Americans by MRI. METHODS AND RESULTS: Inclusion criteria were >50% stenosis as measured by duplex ultrasound and recent symptoms attributed to carotid artery disease. The patients were imaged in 2 centers (Beijing, China and Seattle, Wash) using a standardized protocol. Both carotid arteries were reviewed quantitatively (lumen, wall, outer wall, tissue components) and morphologically (lesion types, fibrous cap status). Significant differences between the Chinese and Americans were found for the mean size of the lipid/necrotic core (13.6 versus 7.8 mm2; P=0.002), percentage of slices with calcified type VII lesions (1.6 versus 12.4%; P=0.03), and percentage of slices with early type III lesions (19.3 versus 9.3%; P=0.02). Furthermore, the mean outer wall area in the common carotid artery was larger in the Chinese population (P=0.007). CONCLUSIONS: This pilot study suggests that composition and morphology of atherosclerotic lesions in symptomatic carotid disease differ between ethno-racial groups. Quantitative MRI-based review of carotid atherosclerosis comparing plaque morphology and composition between ethno-racial groups is feasible, and future MRI studies may improve our understanding of the pathophysiology of this disease.

Visualization of fibrous cap thickness and rupture in human atherosclerotic carotid plaque in vivo with high-resolution magnetic resonance imaging.

BACKGROUND: The results of studies of advanced lesions of atherosclerosis suggest that the thickness of the fibrous cap that overlies the necrotic core distinguishes the stable lesion from one that is at high risk for rupture and thromboembolic events. We have developed a high-resolution MRI technique that can identify the fine structure of the lesion, including the fibrous cap, in vivo. The aim of the present study was to determine the agreement between in vivo MRI and lesion architecture as seen on histology and gross tissue examination to identify fibrous cap thickness and rupture. METHODS AND RESULTS: Twenty-two subjects who were scheduled for carotid endarterectomy underwent MRI with a 3-dimensional multiple overlapping thin slab angiography protocol. The appearance of the fibrous cap was categorized as (1) an intact, thick, (2) an intact, thin, or (3) a ruptured fibrous cap on MRI, gross, and histological sections. Thirty-six sites were available for comparison between MRI and histology. There was a high level of agreement between MRI and histological findings: 89% agreement, kappa (95% CI)=0.83 (0.67 to 1. 0), weighted kappa=0.87. Spearman's correlation coefficient was 0.88 (significant to the 0.01 level). CONCLUSIONS: These findings indicate that high-resolution MRI with a 3-dimensional multiple overlapping thin slab angiography protocol is capable of distinguishing intact, thick fibrous caps from intact thin and disrupted caps in atherosclerotic human carotid arteries in vivo. This noninvasive technique has the potential to permit studies that examine the relationship between fibrous cap changes and clinical outcome and to permit trials that evaluate therapy intended to "stabilize" the fibrous cap.

In vivo accuracy of multispectral magnetic resonance imaging for identifying lipid-rich necrotic cores and intraplaque hemorrhage in advanced human carotid plaques.

BACKGROUND: High-resolution MRI has been shown to be capable of identifying plaque constituents, such as the necrotic core and intraplaque hemorrhage, in human carotid atherosclerosis. The purpose of this study was to evaluate differential contrast-weighted images, specifically a multispectral MR technique, to improve the accuracy of identifying the lipid-rich necrotic core and acute intraplaque hemorrhage in vivo. METHODS AND RESULTS: Eighteen patients scheduled for carotid endarterectomy underwent a preoperative carotid MRI examination in a 1.5-T GE Signa scanner using a protocol that generated 4 contrast weightings (T1, T2, proton density, and 3D time of flight). MR images of the vessel wall were examined for the presence of a lipid-rich necrotic core and/or intraplaque hemorrhage. Ninety cross sections were compared with matched histological sections of the excised specimen in a double-blinded fashion. Overall accuracy (95% CI) of multispectral MRI was 87% (80% to 94%), sensitivity was 85% (78% to 92%), and specificity was 92% (86% to 98%). There was good agreement between MRI and histological findings, with a value of kappa=0.69 (0.53 to 0.85). CONCLUSIONS: Multispectral MRI can identify the lipid-rich necrotic core in human carotid atherosclerosis in vivo with high sensitivity and specificity. This MRI technique provides a noninvasive tool to study the pathogenesis and natural history of carotid atherosclerosis. Furthermore, it will permit a direct assessment of the effect of pharmacological therapy, such as aggressive lipid lowering, on plaque lipid composition.

Differentiation of intraplaque versus juxtaluminal hemorrhage/thrombus in advanced human carotid atherosclerotic lesions by in vivo magnetic resonance imaging.

BACKGROUND: Intraplaque hemorrhage and juxtaluminal hemorrhage/thrombus may differ in cause and clinical implications. This study tested the hypothesis that MRI can distinguish between intraplaque hemorrhage and juxtaluminal hemorrhage/thrombus and investigated the association between hemorrhage and underlying lesion types. METHODS AND RESULTS: Twenty-six patients scheduled for carotid endarterectomy were imaged with a 1.5-T GE scanner by a multicontrast-weighted MRI technique. Hemorrhages were identified with previously established MRI criteria, and differentiations were made between intraplaque and juxtaluminal hemorrhage/thrombus. Corresponding histology was used to confirm the magnetic resonance findings. Tissues underlying areas of hemorrhage/thrombus were histologically categorized according to modified American Heart Association criteria. Of 190 matched sections, 140 contained areas of hemorrhage by histology, of which MRI correctly detected 134. The sensitivity and specificity for MRI to correctly identify cross sections that contained hemorrhage were 96% and 82%, respectively. Furthermore, MRI was able to distinguish juxtaluminal hemorrhage/thrombus from intraplaque hemorrhage with an accuracy of 96%. The distribution of lesion types underlying hemorrhages differed significantly (P=0.004). Intraplaque hemorrhage had an underlying lipid-rich type IV/V lesion in 55% of histological sections, whereas juxtaluminal hemorrhage/thrombus had an underlying calcified lesion type VII in 70% of sections. CONCLUSIONS: In vivo high-resolution MRI can detect and differentiate intraplaque hemorrhage from juxtaluminal hemorrhage/thrombus with good accuracy. The association of hemorrhage and lesion types suggests potential differences in origin. Noninvasive MRI therefore provides a possible tool for prospectively studying differences in origin of plaque hemorrhage and the association of plaque progression and instability.

Paraoxonase (PON1) phenotype is a better predictor of vascular disease than is PON1(192) or PON1(55) genotype.

The paraoxonase (PON1) PON1-Q192R and PON1-L55M polymorphisms have been inconsistently associated with vascular disease. Plasma PON1 activity phenotypes vary markedly within genotypes and were, therefore, expected to add to the informativeness of genotype for predicting vascular disease. The case-control sample included 212 age- and race-matched men (mean age 66.4 years). The 106 carotid artery disease (CAAD) cases had >80% carotid stenosis, and the 106 controls had <15%. Two PON1 substrate hydrolysis rates (paraoxon [POase] and diazoxon [DZOase]) were significantly lower in cases than in controls and were significant predictors of CAAD by use of logistic regression (POase, P=0.005; DZOase, P=0.019). DZOase predicted vascular disease independently of lipoprotein profile, high density lipoprotein subfractions, apolipoprotein A-I, and smoking. PON1-192 and PON1-55 genotypes or haplotypes did not predict case-control status unless the activity phenotype was also included as a predictor by use of logistic regression. When phenotype was included as a predictor, PON1-192 and PON1-55 genotypes or combined haplotypes were significant predictors (P<0.05). In conclusion, examining PON1-192 and/or PON1-55 genotypes alone may mistakenly lead to the conclusion that there is no role of PON1 in CAAD. These results support the benefit of a "level crossing" approach that includes intervening phenotypes in the study of complexly inherited disease.

Effects of prolonged intensive lipid-lowering therapy on the characteristics of carotid atherosclerotic plaques in vivo by MRI: a case-control study.

High-resolution magnetic resonance imaging (MRI) with flow suppression not only provides useful information on luminal and wall areas of the carotid artery but also can identify the principal tissue components of the carotid atherosclerotic plaque. The effects of intensive lipid-lowering therapy on these MRI tissue characteristics were examined in patients with coronary disease (CAD). Eight CAD patients who have been receiving intensive lipid-lowering treatment (niacin 2.5 g/d, lovastatin 40 mg/d, and colestipol 20 g/d) for 10 years in the Familial Atherosclerosis Treatment Study (FATS) follow-up were randomly selected from among 60 such treated patients. Eight CAD patients who were matched to the treated patients for age (+/-3 years), baseline low density lipoprotein (+/-5 mg/dL), and triglycerides (+/-50 mg/dL) but who had never been treated with lipid-lowering drugs were selected as controls. For each of these 32 carotid arteries, luminal and plaque areas were measured by planimetry, in a blinded protocol, from the magnetic resonance image that showed most plaque. Fibrous tissue, calcium, and lipid deposits were identified on the basis of established criteria. Plaque composition was estimated as a fraction of total planimetered area. Patients treated with 10-year intensive lipid-lowering therapy, compared with control subjects, had significantly lower low density lipoprotein cholesterol levels (84 versus 158 mg/dL, respectively; P<0.001) and higher high density lipoprotein cholesterol levels (51 versus 37 mg/dL, respectively; P<0.001). As a group, treated patients, compared with untreated control subjects, had a smaller core lipid area (0.7 versus 10.2 mm(2), respectively; P=0.01) and lipid composition (1% versus 17%, respectively). Group differences in luminal area (55 [treated] versus 44 [control] mm(2), P=NS) and plaque area (58 [treated] versus 64 [control] mm(2), P=NS) tended to favor treatment. MRI appears useful for estimating carotid plaque size and composition. Hyperlipidemic CAD patients frequently (97%) have at least moderate (>/=40% area stenosis) carotid plaque. In this case-control study, prolonged intensive lipid-lowering therapy is associated with a markedly decreased lipid content, a characteristic of clinically stable plaques.

Human carotid artery smooth muscle cells rarely express alpha(v)beta3 integrin at sites of recent plaque rupture.

Fibrin(ogen) is the major matrix ligand for beta3 integrins. If alpha(v)beta3 is the major receptor for fibrin(ogen) on intimal smooth muscle cells, we might expect to see this integrin associated with fibrin(ogen). Eighty-four specimens obtained from endarterectomies of 14 patients were studied. Fibrin was frequently observed in carotid intima even at the non-atherosclerotic areas. As for beta1 and beta3 integrins, beta1 was predominant in intima. The alpha(v)beta3 integrin expression was less frequent than alpha5beta1, another receptor for fibrin(ogen), in diffuse intimal thickening, fibrous cap and advanced plaques. Furthermore, alpha(v)beta3 was generally negative on smooth muscle cells in recent plaque ruptures. In conclusion, we suggest more attention should be paid on abundant fibrin matrix in intima. Histologically, the alpha5beta1 integrin rather than the alpha(v)beta3 is the major receptor for fibrin in intimal smooth muscle cells.

High-Resolution magnetic resonance imaging of normal and atherosclerotic human coronary arteries ex vivo: discrimination of plaque tissue components.

BACKGROUND: Noninvasive detection of plaque lipid and calcium in human atherosclerosis may have clinical utility, because the presence of each may be associated with increased risk of plaque disruption. Magnetic resonance imaging (MRI) has the potential to detect both plaque lipid and calcium. However, no previous studies have: 1) used an MR coil with sufficient resolution to image the components of human coronary arteries, 2) evaluated the utility of a combination of different MR contrast weightings in discriminating plaque components in human coronary arteries, or 3) used sensitive and specific histological stains for lipid and calcium to determine their MR image characteristics in human atherosclerosis. METHODS: Using a custom-made surface coil on a whole-body, 1.5T MRI scanner, high resolution MR images were obtained from 22 nonatherosclerotic and atherosclerotic human coronary artery segments and then compared with histological sections stained for neutral lipid, calcium, and ribrous and cellular components. RESULTS: With a multicontrast protocol using T1-, proton density-, and T2-weighted images, statistically significant differences were found among MR image contrast values for regions identified by histological stains as containing lipid only, calcium only, mixed lipid and calcium, or fibrous tissue. All four of these histologically defined region types could be differentiated from one another by a multicontrast MRI protocol. Of the 22 segments, 10 (45%) contained areas with combined plaque lipid and calcium; calcium would not have been recognized histologically in these regions without the use of a specific calcium stain. CONCLUSIONS: These results demonstrate that multicontrast MRI can produce remarkably high-resolution images and can discriminate between clinically relevant components of the atherosclerotic vessel wall.

Comparison of carotid vessel wall area measurements using three different contrast-weighted black blood MR imaging techniques.

Measuring carotid artery plaque burden from MRI is a reliable method for monitoring regression and progression of atherosclerosis. However, to measure all available images would be very time consuming, and in practice the image quality (IQ) of these images may be inconsistent, which can directly impact the quality of measurement. It is hypothesized that if IQ is comparable among different contrast weighted images, then carotid artery area measurements obtained from different contrast images of the same location will produce identical results. To test this, T1, proton density and T2 weighted images were acquired from ten patients (51 +/- 7 years old). Carotid lumen and vessel wall area was measured using a custom designed software program. The results showed strong agreement evidenced with only small differences on both lumen (mean: 40.5 mm(2)) and wall (mean: 52.6 mm(2)) area measurement among different weighted images. The maximum absolute mean differences are less than 2.7 mm(2) and 4.4 mm(2), and 90(th) percentile of the absolute differences are 5.6 mm(2) and 8.2 mm(2) respectively. In conclusion, different contrast weighted images with high and comparable IQ will yield similar results in lumen and vessel wall area measurement. At each matched location, it is recommended that the image with the highest IQ be used for area measurement.

Color Doppler characteristics in normal lower extremity arteries.

The purpose of this study was to determine the normal characteristics of the lower extremity arterial system as seen with color Doppler. A total of 420 arterial segments from the level of the proximal abdominal aorta to the distal tibial and peroneal vessels were examined with a color ultrasound scanner in 10 normal volunteers. Each arterial segment was examined for the presence of triphasic flow, wall irregularities, calcification, bruits, collaterals, and post-stenotic flow patterns. Standard duplex spectral waveform data were also obtained at each site. As expected, triphasic flow was present and detected by color Doppler in the majority of arterial segments. Color patterns suggesting the presence of bruits, collaterals, or post-stenotic flow were absent in all cases.

Echolucent regions in carotid plaque: preliminary analysis comparing three-dimensional histologic reconstructions to sonographic findings.

This study compares sonographic and histologic findings within defined spatial regions in carotid artery plaque, using computer generated three-dimensional reconstructions. Twenty-four patients (14 asymptomatic, 10 symptomatic) with angiographically documented 70% to 99% carotid artery stenosis were examined with ultrasonic B-mode imaging prior to endarterectomy. Using a standardized protocol for instrument set-up and scanning technique, echolucent regions in the plaque were identified. After endarterectomy, each plaque was sectioned at 0.5 to 1.0 millimeter increments throughout its length. Sites containing intraplaque hemorrhage, cholesterol clefts, foam cells, necrotic cores, dense calcification and speckled calcification were identified. These areas were outlined on a template, digitized and imported into a computer program that created three-dimensional reconstructions of the histologic findings. Each carotid plaque was divided into quadrants for analysis: (1) lateral wall proximal to the common carotid bifurcation (flow divider); (2) medial wall proximal to the flow divider; (3) lateral wall distal to the flow divider; and (4) medial wall distal to the flow divider. The odds of finding intraplaque hemorrhage, foam cells, necrotic cores and speckled calcification were significantly higher in quadrants with an echolucent region identified by ultrasonography (odds ratio (95% confidence interval) for intraplaque hemorrhage = 3.5 (1.4-8.6); foam cells = 4.0 (1.6-9.9); necrotic cores = 3.2 (1.2-8.4); speckled calcification = 4.0 (1.6-9.8). This preliminary analysis demonstrates the potential of these newly developed techniques for comparing ultrasonic imaging to histology.

A noninvasive imaging approach to assess plaque severity: the carotid atherosclerosis score.

BACKGROUND AND PURPOSE: The presence of IPH and/or FCR in the carotid atherosclerotic plaque indicates a high-risk lesion. The aim of this multicenter cross-sectional study was to establish the characteristics of lesions that may precede IPH and/or FCR. We further sought to construct a CAS that stratifies carotid disease severity. MATERIALS AND METHODS: Three hundred forty-four individuals from 4 imaging centers with 16%-99% carotid stenosis by duplex sonography underwent carotid MR imaging. In approximately 60% of the study sample (training group), multivariate analysis was used to determine factors associated with IPH and FCR. Statistically significant parameters identified during multivariate analysis were used to construct CAS. CAS was then applied to the remaining arteries (40%, test group), and the accuracy of classification for determining the presence versus absence of IPH or, separately, FCR was determined by ROC analysis and calculation of the AUC. RESULTS: The maximum proportion of the arterial wall occupied by the LRNC was the strongest predictor of IPH (P < .001) and FCR (P < .001) during multivariate analysis of the training group. The subsequently derived CAS applied to the test group was an accurate classifier of IPH (AUC = 0.91) and FCR (AUC = 0.93). Compared with MRA stenosis, CAS was a stronger classifier of both IPH and FCR. CONCLUSIONS: LRNC quantification may be an effective complementary strategy to stenosis for classifying carotid atherosclerotic disease severity. CAS forms the foundation for a simple imaging-based risk-stratification system in the carotid artery to classify severity of atherosclerotic disease.

Predictors of surface disruption with MR imaging in asymptomatic carotid artery stenosis.

BACKGROUND AND PURPOSE: Surface disruption, either ulceration or fibrous cap rupture, has been identified as a key feature of the unstable atherosclerotic plaque. In this prospective observational study, we sought to determine the characteristics of the carotid lesion that predict the development of new surface disruption. MATERIALS AND METHODS: One hundred eight asymptomatic individuals with 50%-79% carotid stenosis underwent carotid MR imaging at baseline and at 3 years. Multicontrast imaging criteria were used to determine the presence or absence of calcification, LRNC, intraplaque hemorrhage, and surface disruption. Volume measurements of plaque morphology and the LRNC and calcification, when present, were collected. RESULTS: At baseline, 21.3% (23/108) of participants were identified with a surface disruption. After 3 years, 9 (10.6%) of the remaining 85 individuals without disruption at baseline developed a new surface disruption during follow-up. Among all baseline variables associated with new surface disruption during regression analysis, the proportion of wall volume occupied by the LRNC (percentage LRNC volume; OR per 5% increase, 2.6; 95% CI, 1.5-4.6) was the strongest classifier (AUC = 0.95) during ROC analysis. New surface disruption was associated with a significant increase in percentage LRNC volume (1.7 +/- 2.0% per year, P = .035). CONCLUSIONS: This prospective investigation of asymptomatic individuals with 50%-79% stenosis provides compelling evidence that LRNC size may govern the risk of future surface disruption. Identification of carotid plaques in danger of developing new surface disruption may prove clinically valuable for preventing the transition from stable to unstable atherosclerotic disease.