3039Vulnerability of carotid atherosclerosis: relationship with plaque location, plaque eccentricity and vessel remodeling patterns. Insight from the the MAGNETIC observational study

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
O Catalano ◽  
C Cerabolini ◽  
E Eshja ◽  
G Bendotti ◽  
M De Salvo ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Wall Thickness ◽  
Carotid Atherosclerosis ◽  
Internal Carotid ◽  
Intraplaque Hemorrhage ◽  
Plaque Vulnerability ◽  
Cross Sectional ◽  
Fibrous Cap ◽  
Vessel Remodeling ◽  
Maximum Wall Thickness

Abstract Carotid atherosclerosis is a cause of brain ischemic events. Cardiovascular magnetic resonance (CMR) can assess plaque vulnerability. We investigated atherosclerosis vulnerability in relation to plaque location, eccentricity and vessel remodeling. Methods-Baseline CMR evaluations of the MAGNETIC observational study, were analyzed. We quantitated with MRI-Plaque View™, vessel lumen/wall and vulnerable plaque components of a 32-mm segment of common carotid artery (12 mm), bulb (8 mm) and internal carotid artery (12 mm). Lipid-rich necrotic core [LRNC], fibrous cap [CAP] and intraplaque hemorrhage [IPH] were expressed as percent of wall area. Results-A data-set of 8080 sections of adequate quality in 260 patients (198 male [76%], median age 71 years [65–76]), were analyzed. Patients were on therapy with antiplatelet, ACE-inhibitors/ARB and statins (196–229 out of 260 [75–88%]). We found significant differences in plaque composition according to longitudinal and circumferential location, eccentricity and vessel remodeling (table). At multivariate regression analysis, including classical RF and atherosclerotic burden, we found an independent association of: LRNC and IPH with longitudinal location, eccentricity and positive remodeling, and of CAP with eccentricity (p<0.001 for all). Lipid-rich necrotic core Fibrous cap Intraplaque hemorrhage Longitudinal distribution Common carotid artery 4% [1–10] p<0.001 6% [4–11] p<0.001 0% [0–3] p<0.001 Carotid bulb 7% [3–13] 9% [5–13] 1% [0–4] Internal carotid artery 3% [0–10] 7% [4–11] 0% [0–1] Circunferenzial location Antero-medial 4% [0–11] p<0.001 7% [4–12] p=0.07 0% [0–2] p<0.001 Antero-lateral 6% [1–12] 8% [5–12] 1% [0–4] Postero-lateral 5% [0–11] 7% [4–12] 0% [0–3] Postero-medial 5% [0–11] 7% [4–12] 0% [0–1] Plaque eccentricity Concentric 3% [0–9] p<0.001 7% [4–11] p<0.001 0% [0–2] p<0.001 Eccentric 9% [4–15] 9% [5–13] 1% [0–4] Remodelling pattern Negative 4% [0–10] p<0.001 7% [4–11] p<0.001 0% [0–2] p<0.001 Positive 7% [3–13] 8% [5–13] 1% [0–4] Plaque eccentricity was defined as eccentricity index (EI = [maximum wall thickness − minimum wall thickness]/maximum wall thickness) in the highest quartile. Positive remodeling was defined as remodeling index (= [vessel cross-sectional area − reference area]/cross-sectional area) in the highest quartile. Conclusions Carotid atherosclerotic plaque vulnerability seems to be independently associated with longitudinal location, plaque eccentricity and vessel positive remodeling. Acknowledgement/Funding Bayer AG, Leverkusen, Germany

Abstract P021: Association of Blood Lactate with Carotid Atherosclerosis: The Atherosclerosis Risk in Communities (ARIC) Carotid MRI Study

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Ghanshyam Palamaner Subash Shantha ◽  
Richey Sharrett ◽  
Brad C Astor ◽  
Josef Coresh ◽  
Frederick Brancati ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Carotid Artery ◽  
Blood Lactate ◽  
Wall Thickness ◽  
Carotid Atherosclerosis ◽  
Internal Carotid ◽  
Elevated Blood ◽  
Atherosclerosis Risk In Communities ◽  
Maximum Wall Thickness ◽  
Atherosclerosis Risk

Aim: Elevated blood lactate, a marker of decreased oxidative capacity, may be associated with high levels of oxidized LDL and consequent atherosclerosis. We assessed the association between elevated blood lactate and carotid atherosclerosis in a sample of 1496 adults, aged 60 - 82 years, in the general population. Methods: Maximum wall thickness of the internal carotid artery (MICA) was measured using gadolinium-enhanced magnetic resonance imaging (MRI) in 1496 participants from the Atherosclerosis Risk in Communities (ARIC) Study. Blood lactate was categorized into quartiles (Q1: < 5.9 mg/dl, Q2: 5.9 to 7.2mg/dl, Q3: 7.3 to 9.2 mg/dl, and Q4: >9.2 mg/dl). Results: Mean age was 70.3 years; 56% were women and 19% were African American. Higher lactate quartile was associated with greater odds of having MICA above the median (Odds ratio for Q1: 1.00, Q2: 1.06, Q3: 1.24 and Q4: 1.36; p for trend <0.001) after adjustment for age, gender, ethnicity, stature, body mass index (BMI), LDL, hypertension diagnosis, and diabetes diagnosis. The association between MICA and lactate was attenuated but remained significant (Q1: 1, Q2: 1.02, Q3: 1.12, Q4: 1.21, p for trend 0.011) after further adjustment for triglycerides/HDL ratio. Conclusion: Blood lactate is associated with internal carotid artery maximum wall thickness, a marker of carotid atherosclerosis. Attenuation of the association with adjustment for triglyceride/HDL ratio, a marker of insulin resistance, suggests that lactate’s association with wall thickness may be mediated through insulin resistance, at least in part.

scholarly journals Evolving determinants of carotid atherosclerosis vulnerability in asymptomatic patients from the MAGNETIC observational study

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Oronzo Catalano ◽  
Giulia Bendotti ◽  
Alessia Mori ◽  
Maria De Salvo ◽  
Marialuisa Falconi ◽  
...  
Keyword(s):  
Carotid Atherosclerosis ◽  
Angiotensin Receptor Blockers ◽  
Glycosylated Hemoglobin ◽  
Intraplaque Hemorrhage ◽  
Plaque Vulnerability ◽  
Plaque Composition ◽  
Asymptomatic Carotid ◽  
Cross Sectional ◽  
Data Set ◽  
Asymptomatic Patients

AbstractMRI can assess plaque composition and has demonstrated an association between some atherosclerotic risk factors (RF) and markers of plaque vulnerability in naive patients. We aimed at investigating this association in medically treated asymptomatic patients. This is a cross-sectional interim analysis (August 2013–September 2016) of a single center prospective study on carotid plaque vulnerability (MAGNETIC study). We recruited patients with asymptomatic carotid atherosclerosis (US stenosis > 30%, ECST criteria), receiving medical treatments at a tertiary cardiac rehabilitation. Atherosclerotic burden and plaque composition were quantified with 3.0 T MRI. The association between baseline characteristics and extent of lipid-rich necrotic core (LRNC), fibrous cap (CAP) and intraplaque hemorrhage (IPH) was studied with multiple regression analysis. We enrolled 260 patients (198 male, 76%) with median age of 71-y (interquartile range: 65–76). Patients were on antiplatelet therapy, ACE-inhibitors/angiotensin receptor blockers and statins (196–229, 75–88%). Median LDL-cholesterol was 78 mg/dl (59–106), blood pressure 130/70 mmHg (111–140/65–80), glycosylated hemoglobin 46 mmol/mol (39–51) and BMI 25 kg/m2 (23–28); moreover, 125 out of 187 (67%) patients were ex-smokers. Multivariate analysis of a data-set of 487 (94%) carotid arteries showed that a history of hypercholesterolemia, diabetes, hypertension or smoking did not correlate with LRNC, CAP or IPH. Conversely, maximum stenosis was the strongest independent predictor of LRNC, CAP and IPH (p < 0.001). MRI assessment of plaque composition in patients on treatment for asymptomatic carotid atherosclerosis shows no correlation between plaque vulnerability and the most well-controlled modifiable RF. Conversely, maximum stenosis exhibits a strong correlation with vulnerable features despite treatment.

scholarly journals Communication of inwardly projecting neovessels with the lumen contributes to symptomatic intraplaque hemorrhage in carotid artery stenosis

2015 ◽  
Vol 123 (5) ◽  
pp. 1125-1132 ◽  
Author(s):  
Nobutaka Horie ◽  
Yoichi Morofuji ◽  
Minoru Morikawa ◽  
Yohei Tateishi ◽  
Tsuyoshi Izumo ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Carotid Atherosclerosis ◽  
Vasa Vasorum ◽  
Intraplaque Hemorrhage ◽  
Plaque Morphology ◽  
Plaque Vulnerability ◽  
Carotid Artery Atherosclerosis ◽  
Key Factor ◽  
Baseline Characteristics ◽  
Ischemic Attack

OBJECT Recent studies have demonstrated that plaque morphology can contribute to identification of patients at high risk of carotid artery atherosclerosis as well as the degree of stenosis in those with carotid atherosclerosis. Neovascularization of carotid plaques is associated with plaque vulnerability. However, the mechanism of neovascularization in intraplaque hemorrhage (IPH) and its clinical contribution remain undetermined. In this study, the authors aimed to clarify the characteristics of neovessel appearance with a focus on inwardly projecting neovessels, which are reportedly important in plaque advancement. METHODS Consecutive patients with moderate to severe carotid atherosclerosis who underwent carotid endarterectomy were prospectively analyzed from 2010 to 2014. The neovessel appearance was categorized into 3 groups based on intraoperative indocyanine green (ICG) videoangiography: early appearance of neovessels from the endothelium (NVe), late appearance of neovessels from the vasa vasorum (NVv), and no appearance of vessels. Each neovessel pattern was evaluated with respect to clinical, radiological, and pathological findings including IPH, neovascularization, hemosiderin spots, and inflammation. RESULTS Of 57 patients, 13 exhibited NVe, 33 exhibited NVv, and 11 exhibited no neovessels. Overall, the interobserver and intraobserver reproducibilities of neovessel appearance were substantial for ICG videoangiography (κ = 0.76) and at 7 days postoperatively (κ = 0.76). There were no significant differences in baseline characteristics among the 3 groups, with the exception of a higher percentage of symptomatic presentations in patients with NVe (artery-to-artery embolic infarction in 61.5% and transient ischemic attack in 23.1%). Moreover, patients with NVe exhibited larger infarctions than did those with NVv (9675.0 ± 5601.9 mm3 vs 2306.6 ± 856.9 mm3, respectively; p = 0.04). Pathologically, patients with NVe had more severe IPH (47.2 ± 8.3 mm2 vs 19.8 ± 5.2 mm2, respectively; p < 0.01), hemosiderin spots (0.5 ± 0.2 mm2 vs 0.2 ± 0.1 mm2, respectively; p = 0.04), neovessels (0.4 ± 0.7 mm2 vs 0.1 ± 0.4 mm2, respectively; p = 0.11), and inflammation (1.0 ± 1.1 mm2 vs 0.6 ± 0.9 mm2, respectively; p = 0.26) around the endothelium than did patients with NVv, and all of these parameters were correlated with hyperintensity on time-of-flight MRI. However, the neovessel and inflammation differences were nonsignificant. Interestingly, inflammation was significantly correlated with neovessel formation (r = 0.43, p = 0.0008), hemosiderin spots (r = 0.62, p < 0.0001), and IPH (r = 0.349, p = 0.0097), suggesting that inflammation may be a key factor in plaque vulnerability. CONCLUSIONS Communication of inwardly projecting neovessels with the lumen and inflammation synergistically contribute to IPH and symptomatic presentations in patients with carotid stenosis and are more specific than the vasa vasorum. This condition could be a new therapeutic target, and regression of luminal neovessel sprouting and inflammation may help to prevent IPH development and a symptomatic presentation.

scholarly journals Chitinase 3 like 1 is a regulator of smooth muscle cell physiology and atherosclerotic lesion stability

2021 ◽  
Author(s):  
Pavlos Tsantilas ◽  
Shen Lao ◽  
Zhiyuan Wu ◽  
Anne Eberhard ◽  
Greg Winski ◽  
...  
Keyword(s):  
At Risk ◽  
Smooth Muscle ◽  
Carotid Artery ◽  
Atherosclerotic Lesion ◽  
Adverse Outcomes ◽  
Plaque Burden ◽  
Cell Physiology ◽  
Mechanistic Studies ◽  
Plaque Vulnerability ◽  
Fibrous Cap

Abstract Aims  Atherosclerotic cerebrovascular disease underlies the majority of ischaemic strokes and is a major cause of death and disability. While plaque burden is a predictor of adverse outcomes, plaque vulnerability is increasingly recognized as a driver of lesion rupture and risk for clinical events. Defining the molecular regulators of carotid instability could inform the development of new biomarkers and/or translational targets for at-risk individuals. Methods and results  Using two independent human endarterectomy biobanks, we found that the understudied glycoprotein, chitinase 3 like 1 (CHI3L1), is up-regulated in patients with carotid disease compared to healthy controls. Further, CHI3L1 levels were found to stratify individuals based on symptomatology and histopathological evidence of an unstable fibrous cap. Gain- and loss-of-function studies in cultured human carotid artery smooth muscle cells (SMCs) showed that CHI3L1 prevents a number of maladaptive changes in that cell type, including phenotype switching towards a synthetic and hyperproliferative state. Using two murine models of carotid remodelling and lesion vulnerability, we found that knockdown of Chil1 resulted in larger neointimal lesions comprised by de-differentiated SMCs that failed to invest within and stabilize the fibrous cap. Exploratory mechanistic studies identified alterations in potential downstream regulatory genes, including large tumour suppressor kinase 2 (LATS2), which mediates macrophage marker and inflammatory cytokine expression on SMCs, and may explain how CHI3L1 modulates cellular plasticity. Conclusion  CHI3L1 is up-regulated in humans with carotid artery disease and appears to be a strong mediator of plaque vulnerability. Mechanistic studies suggest this change may be a context-dependent adaptive response meant to maintain vascular SMCs in a differentiated state and to prevent rupture of the fibrous cap. Part of this effect may be mediated through downstream suppression of LATS2. Future studies should determine how these changes occur at the molecular level, and whether this gene can be targeted as a novel translational therapy for subjects at risk of stroke.

Abstract 3482: Increased Matrix Metalloproteinase-9 Expression is Correlated with Carotid Intraplaque hemorrhage in a Swine Model

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Zhong-Song Shi ◽  
Xiao-Bing Jiang ◽  
Jin-Shan Wang ◽  
Wei-Si Yuan ◽  
Dong-Hong Liu
Keyword(s):  
Carotid Artery ◽  
Matrix Metalloproteinase ◽  
Vulnerable Plaque ◽  
Carotid Plaque ◽  
Carotid Atherosclerosis ◽  
Intraplaque Hemorrhage ◽  
Swine Model ◽  
Carotid Plaques ◽  
Rete Mirabile ◽  
Atherosclerotic Changes

Purpose: The limited number of large animal carotid atherosclerotic models restricts the preclinical evaluation of endovascular therapies. Carotid intraplaque hemorrhage may be associated with a higher risk of ischemic stroke in patients with carotid disease. In this study, we assess the association of the lesional expression of matrix metalloproteinase (MMP)-9 with vulnerable atherosclerotic carotid plaque and intraplaque hemorrhage in a Swine model. Materials and Methods: Carotid atherosclerosis was induced in miniswines using the combination of partial ligation and high cholesterol diet, and a minimum 70% stenosis was confirmed by Doppler ultrasonography immediately post-ligation. Carotid artery sections were obtained for histopathological examination and immunohistochemical study for MMP-9 at three months. Distal embolism was determined by the presence of atheroemboli in the ipsilateral rete mirabile. Atherosclerotic changes were classified by AHA/Stary stage (type I to VI). The association of distal embolism in the rete mirabile with vulnerable carotid plaque was analyzed. The association of MMP-9 expression in the plaque with the vulnerable plaque and intraplaque hemorrhage was further analyzed. Results: One hundred ninety-one carotid segments from ten carotid artery models were assessed. Among 139 segments with atherosclerotic changes, 102 segments had vulnerable plaque (Stary IV to VI). Vulnerable atherosclerotic plaques were found more frequently in the vessel wall proximal to the partial ligation than distal ( P <0.0001). Distal embolism was found in all 10 rete mirabilis, and deemed to be from the ipsilateral vulnerable carotid plaques. Areas positive for MMP-9 tended to be greater in the vulnerable plaque than in the stable plaque (8.69 ± 0.73% vs. 7.04 ± 0.94%, p=0.35). Areas positive for MMP-9 were significantly greater in the plaque with intraplaque hemorrhage than in the plaque without intraplaque hemorrhage (11.84 ± 1.22% vs. 6.63 ± 0.59%, p<0.001). On multivariate analysis, positive expression of MMP-9 was an independent predictor of intraplaque hemorrhage (p=0.007). Conclusion: Vulnerable carotid plaques with distal embolism were created in a Swine model of carotid atherosclerosis. Increased expression of MMP-9 may be associated with vulnerable carotid plaques, especially having the feature of intraplaque hemorrhage.

scholarly journals Association of Carotid Atherosclerosis With White Matter Hyperintensity in an Asymptomatic Japanese Population: A Cross-Sectional Study

2021 ◽  
Vol 8 ◽  
Author(s):  
Li Zhang ◽  
Quan Zhou ◽  
Li Hua Shao ◽  
Jun Wen ◽  
Jun Xia
Keyword(s):  
White Matter ◽  
Carotid Artery ◽  
Japanese Population ◽  
Carotid Atherosclerosis ◽  
Smoking Status ◽  
White Matter Hyperintensity ◽  
Large Artery ◽  
Cross Sectional ◽  
Carotid Artery Plaque ◽  
Plaque Score

Objective: A limited number of scholars concentrated on the relationship between carotid atherosclerosis (CAS) and white matter hyperintensity (WMH) (i.e., CAS-WMH relationship). The current research aimed to clarify the CAS-WMH relationship in Japanese population.Methods: All participants underwent MRI of head and ultrasonography of the carotid artery. WMH was diagnosed from MRI results. The carotid ultrasound findings, carotid artery plaque score (PS), and plaque number (PN) could be achieved to indicate the severity of CAS. We also employed multivariate logistic regression models to estimate the CAS-WMH relationship. Interaction and stratified analyses were undertaken on the basis of a number of factors (e.g., gender, age, smoking status, drinking habit, and history of chronic diseases).Results: A total of 1,904 Japanese subjects were included, and the prevalence of WMH was 54.8% (1,044/1,904). It was unveiled that frequency of CAS was greater in cases with WMH. In a fully adjusted model, high PS was associated with the frequency of WMH, followed by high PN. Further analyses revealed a dose-response relationship between PS and incidence of WMH.Conclusion: PS and PN exhibited the greatest influences on determining the frequency of WMH, highlighting the potentially important pathophysiological role of large artery atherosclerosis in intensifying WMH.

Abstract WP162: Impact of Carotid Artery Remodeling by T1 weighted MR Imaging for the Assessment of Plaque Vulnerability in High-grade Carotid Stenosis

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Kenji Fukuda ◽  
Koji Iihara ◽  
Naoaki Yamada ◽  
Hatsue Ueda
Keyword(s):  
Carotid Artery ◽  
Carotid Stenosis ◽  
Average Rate ◽  
Intraplaque Hemorrhage ◽  
High Grade ◽  
Plaque Vulnerability ◽  
Rapid Acquisition ◽  
Asymptomatic Patients ◽  
Artery Remodeling ◽  
The Relationship

Background- The relationship between coronary artery remodeling and plaque vulnerability has been described on the basis of symptomatology and histology. However, the association with carotid artery remodeling has not been explored in detail. The aim of this study was to validate the relationship between carotid artery remodeling and plaque vulnerability by comparing the degree of outward remodeling calculated using 3D inversion-recovery-based T1-weighted imaging (magnetization-prepared rapid acquisition gradient-echo [MPRAGE]) with the symptomatology and histology of plaques extracted during carotid endarterectomy (CEA). Methods and Results- Sixty-one patients with high-grade carotid stenosis who underwent CEA and whose plaque could be examined were included. The average rate of stenosis as per the NASCET criteria was 79.8%. The carotid remodeling index (CRI) was determined by measuring the external cross-sectional vessel area (CSVA) of the maximum stenosis of the internal carotid artery (ICA) and dividing it by the external CSVA of the distal ICA unaffected by atherosclerosis using MPRAGE imaging. The relationship between the CRI and plaque vulnerability was evaluated on the basis of symptomatology and histology. The CRI was significantly higher in symptomatic patients than in asymptomatic patients (1.98 ± 0.26 vs. 1.68 ± 0.24, p < 0.0001). A higher CRI was positively correlated with the necrotic core area (r = 0.568, p < 0.0001) as well as significantly associated with severe intraplaque hemorrhage (p < 0.0001) and the prevalence of cap inflammation with macrophage (p = 0.03) and lymphocyte (p = 0.01) infiltration. Conclusion- These results validate the relationship between carotid artery remodeling and plaque vulnerability in high-grade carotid stenosis. MPRAGE imaging is effective to assess plaque vulnerability in terms of the CRI in addition to the signal intensity of carotid plaques.

3041Wall shear stress measurement by ultrafast vector flow imaging for atherosclerotic carotid stenosis

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
G Goudot ◽  
L Khider ◽  
O Pedreira ◽  
J M Poree ◽  
P Julia ◽  
...  
Keyword(s):  
Shear Stress ◽  
Carotid Artery ◽  
Wall Shear Stress ◽  
Internal Carotid Artery ◽  
Carotid Stenosis ◽  
Common Carotid Artery ◽  
Carotid Plaque ◽  
Internal Carotid ◽  
Plaque Vulnerability ◽  
Wall Shear

Abstract Background Carotid plaque vulnerability assessment is an important factor in guiding the decision to treat significant carotid stenosis. Ultrafast Ultrasound Imaging (UF) offers the possibility of evaluating local flow velocities over an entire 2D image, allowing access to velocity measurements in contact with the arterial wall and to measure the wall shear stress (WSS). Purpose To evaluate the feasibility of WSS measurement in a prospective series of patients with carotid stenosis. Methods A 7.5 MHz linear probe of an Aixplorer scanner was used. UF acquisitions had 3 tilted plane waves transmits (−10; 0; 10°) and an effective frame rate of 5000Hz. We evaluated the flow velocity in 5 areas of the carotid wall: common carotid artery (1), plaque ascent (2), plaque peak (3), plaque descent (4), internal carotid artery (5) (Figure). WSS was computed with the vector field speed using the following formula, WSS=μ·δn·v with v the blood velocity, n the normal vector to the vessel wall and μ, the blood viscosity, calculated from the hematocrit value for each patient. WSS measurement method was first validated using a laminar flow phantom and known viscosity. And then, 33 patients were then prospectively evaluated, with a median carotid stenosis degree of 80% [75–85]. Results Significant correlation was found between in vitro measurement and the theoretical WSS values (R2=0.95; p<0.001).In patients,the maximum WSS value over the cardiac cycle follows the shape of the plaque with an increase during the ascend, reaching its maximum value of 3.57 Pa [2.47–4.45] at the peak of the plaque, and a fall after passing the peak (0.99 Pa [0.8–1.32]) lower than the WSS values in the non-stenotic areas (1.55 Pa [1.13–1.90] for the common carotid artery) (Table). Table 1 Wall's area Wall shear stress (Pa) Min Max Delta 1. Common carotid artery 0.14 [0.05–0.27] 1.55 [1.13–1.90] 0.73 [0.55–0.96] 2. Plaque's ascent 0.39 [0.24–0.59] 2.63 [1.89–3.28] 1.20 [0.89–1.79] 3. Plaque's peak 0.60 [0.32–0.89] 3.57 [2.47–4.45] 1.78 [1.44–2.46] 4. Plaque's descent 0.16 [0.13–0.22] 0.99 [0.80–1.32] 0.52 [0.34–0.73] 5. Internal carotid artery 0.17 [0.13–0.35] 1.37 [1.04–1.75] 0.72 [0.50–0.87] Results are median [25th–75th percentile]. Figure 1 Conclusion UF provide reliable WSS values. High WSS was present at the peak of the plaque, whereas lowest WSS values were found at the post-stenotic zone. WSS evaluation may help to better characterize the carotid plaque vulnerability.

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