scholarly journals Carotid Plaque Morphology is Similar in Patients with Reduced and Normal Renal Function

2020 ◽  
Vol 14 ◽  
pp. 117954682095179
Author(s):  
Caroline Heijl ◽  
Fredrik Kahn ◽  
Andreas Edsfeldt ◽  
Christoffer Tengryd ◽  
Jan Nilsson ◽  
...  
Keyword(s):  
Renal Function ◽  
Carotid Plaque ◽  
Continuous Variable ◽  
Intraplaque Hemorrhage ◽  
Plaque Morphology ◽  
Plaque Vulnerability ◽  
Vulnerable Atherosclerotic Plaque ◽  
Increased Risk ◽  
Plaque Phenotype ◽  
Tissue Calcium

Background: Chronic Kidney Disease (CKD) is associated with an increased risk for cardiovascular events such as stroke. However, it is still unclear if decreased kidney function is associated with a vulnerable atherosclerotic plaque phenotype. To explore if renal function was associated with carotid plaque vulnerability we analyzed carotid plaques obtained at surgery from the Carotid Plaque Imaging Project (CPIP). Methods: Patients were enrolled through the CPIP cohort. The indication for surgery was plaques with stenosis >70%, associated with ipsilateral symptoms or plaques with stenosis >80% not associated with symptoms. Transversal sections from the most stenotic plaque region were analyzed for connective tissue, calcium, lipids, macrophages, intraplaque hemorrhage, and smooth muscle cells. Homogenates were analyzed for collagen and elastin. Results: Carotid endarterectomy specimens from 379 patients were obtained. The median GFR was 73 ml/min/1.73 m2. Plaque characteristics showed no significant association with eGFR, neither when eGFR was divided in CKD groups nor when eGFR was handled as a continuous variable and adjusting for other known risk factors (ie, age, diabetes, hypertension, and smoking). Conclusions: The higher risk of cardiovascular disease such as stroke in CKD is not associated with increased plaque vulnerability and other factors have to be sought.

scholarly journals Ultrasound Elastography: another piece in the puzzle of carotid plaque vulnerability?

2021 ◽  
Author(s):  
Andjoli Davidhi ◽  
Vasileios Rafailidis ◽  
Evangelos Destanis ◽  
Panos Prassopoulos ◽  
Stefanos Foinitsis
Keyword(s):  
Shear Wave ◽  
Carotid Plaque ◽  
Diagnostic Yield ◽  
Imaging Modality ◽  
Shear Wave Elastography ◽  
Ultrasound Elastography ◽  
Intraplaque Hemorrhage ◽  
Plaque Vulnerability ◽  
Carotid Plaques ◽  
Increased Risk

Recent literature has shown that various carotid plaque features, other than stenosis, contribute to plaque vulnerability. Features such as surface morphology and plaque composition with distinct components (e.g. intraplaque hemorrhage, lipid core) have been associated with the increased risk of future cerebrovascular events. Ultrasonography constitutes the first line modality for the assessment of carotid disease and has traditionally been used to grade stenosis with high accuracy. Recenttechnological advances such as contrast-enhanced ultrasound and elastography increased the diagnostic yield of ultrasound in assessing the morphology of carotid plaques. The purpose of this review is to present the available literature on ultrasound elastography of the atherosclerotic carotid. Strain and shear wave elastography allow for the characterization of plaque components, thus indicating its nature and importantly, the plaque’s vulnerability. Shear wave elastography indices appear morerobust than Strain indices. Overall, elastography is a feasible method to distinguish vulnerable carotid plaques. There is, however, a need for larger and longer prospective controlled clinical studies in order to validate elastography as an imaging modality used for the detection of unstable carotid plaques.

scholarly journals SUR1-E1506K mutation impairs glucose tolerance and promotes vulnerable atherosclerotic plaque phenotype in hypercholesterolemic mice

PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0258408
Author(s):  
Erika Gurzeler ◽  
Anna-Kaisa Ruotsalainen ◽  
Anssi Laine ◽  
Teemu Valkama ◽  
Sanna Kettunen ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Atherosclerotic Plaque ◽  
Plaque Morphology ◽  
Atherosclerotic Plaques ◽  
Positive Staining ◽  
Sulfonylurea Receptor ◽  
Vulnerable Atherosclerotic Plaque ◽  
Increased Risk ◽  
Plaque Phenotype

Background and aims Diabetes is a major risk factor of atherosclerosis and its complications. The loss-of-function mutation E1506K in the sulfonylurea receptor 1 (SUR1-E1506K) induces hyperinsulinemia in infancy, leading to impaired glucose tolerance and increased risk of type 2 diabetes. In this study, we investigate the effect of SUR1-E1506K mutation on atherogenesis in hypercholesterolemic LDLR-/- mice. Methods SUR1-E1506K mutated mice were cross-bred with LDLR-/- mice (SUR1Δ/LDLR-/-), 6 months old mice were fed a western-diet (WD) for 6 months to induce advanced atherosclerotic plaques. At the age of 12 months, atherosclerosis and plaque morphology were analyzed and mRNA gene expression were measured from aortic sections and macrophages. Glucose metabolism was characterized before and after WD. Results were compared to age-matched LDLR-/- mice. Results Advanced atherosclerotic plaques did not differ in size between the two strains. However, in SUR1Δ/LDLR-/- mice, plaque necrotic area was increased and smooth muscle cell number was reduced, resulting in higher plaque vulnerability index in SUR1Δ/LDLR-/- mice compared to LDLR-/- mice. SUR1Δ/LDLR-/- mice exhibited impaired glucose tolerance and elevated fasting glucose after WD. The positive staining area of IL-1β and NLRP3 inflammasome were increased in aortic sections in SUR1Δ/LDLR-/- mice compared to LDLR-/- mice, and IL-18 plasma level was elevated in SUR1Δ/LDLR-/- mice. Finally, the mRNA expression of IL-1β and IL-18 were increased in SUR1Δ/LDLR-/- bone marrow derived macrophages in comparison to LDLR-/- macrophages in response to LPS. Conclusions SUR1-E1506K mutation impairs glucose tolerance and increases arterial inflammation, which promotes a vulnerable atherosclerotic plaque phenotype in LDLR-/- mice.

Effect of renal function (RF) on outcomes in the adjuvant treatment of older women with breast cancer (>65 years): CALGB/CTSU 49907 (CC) ancillary data study.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 9515-9515
Author(s):  
Stuart M. Lichtman ◽  
Constance Cirrincione ◽  
Arti Hurria ◽  
Aminah Jatoi ◽  
Maria Theodoulou ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Renal Function ◽  
Renal Insufficiency ◽  
Continuous Variable ◽  
Hematologic Toxicity ◽  
Logrank Test ◽  
Dose Modification ◽  
Increased Risk ◽  
Therapy Completion ◽  
The Relationship

9515 Background: CC 49907 showed superiority of standard therapy (cyclophosphamide/doxorubicin [AC] or cyclophosphamide/methotrexate/5-fluorouracil [CMF]) over capecitabine[C]. Dose adjustments made for renal insufficiency (RI) for methotrexate and C; ideal body weight used. Purpose was to analyze the relationship between RF at baseline and 5 endpoints: toxicity, dose modification, therapy completion, relapse-free survival [RFS] and overall survival [OS]. Methods: Pre-treatment RF was calculated (Cockcroft-Gault). Endpoints assessed by regimen. RF was tested as a dichotomous and continuous variable of stages 1,2 vs. 3,4 kidney disease (National Kidney Foundation). Logistic regression modeled the relationship between renal stage and the first three endpoints of toxicity, dose modification and therapy completion. Toxicity divided by hematologic or not. The relationship of RFS and OS with RF was assessed with the logrank test and as a continuous variable with Wald chi square. Results: 619 patients; incidence of stage 3/4 RI(<60 ml/min) was: CMF=72%; AC=64%; C=75%. With AC the incidence of toxicity differed by renal function. 31% of patients with poorer function >grade 3 non-hematologic toxicity vs. 14% with better function(p=0.011). There was a suggestion of effect of RF on OS and RFS for C-treated patients. RF was not associated with dose modification, premature therapy termination, RFS or OS for the CMF-treated patients. Conclusions: 1) AC: declining RF was associated with increased non-hematologic toxicity. 2)Patients with RI who received dose modifications were not at increased risk for complications in comparison to those who did not have renal insufficiency and received full dose. 3)Declining RF did not affect therapy completion. 4)C: suggestion that worse RF was related to poorer RFS or OS. 5)Exclusion of patients from clinical trials with RI based on concern of excessive hematologic toxicity may not be justified with appropriate modification. 6)Results should be considered in the design of clinical trials for older patients.

scholarly journals The proteoglycan mimecan is associated with carotid plaque vulnerability and increased risk of future cardiovascular death

2020 ◽  
Vol 313 ◽  
pp. 88-95
Author(s):  
Christoffer Tengryd ◽  
Signe Holm Nielsen ◽  
Michele Cavalera ◽  
Eva Bengtsson ◽  
Federica Genovese ◽  
...  
Keyword(s):  
Carotid Plaque ◽  
Cardiovascular Death ◽  
Plaque Vulnerability ◽  
Increased Risk

Abstract 464: Knockout of Insulin-like Growth Factor-1 Receptor in Monocyte/Macrophage Promotes Atherosclerosis and Induces an Unstable Plaque Phenotype

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Yusuke Higashi ◽  
Shaw-yung Shai ◽  
Sergiy Sukhanov ◽  
Catherine Kim ◽  
Patrice Delafontaine
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Actin ◽  
Intraplaque Hemorrhage ◽  
Insulin Like Growth Factor ◽  
Plaque Vulnerability ◽  
Cell Content ◽  
Atherosclerotic Burden ◽  
Tgfβ Receptor ◽  
Plaque Phenotype

We have previously shown that infusion of insulin-like growth factor-1 (IGF-1) exerts anti-inflammatory and anti-oxidant effects and reduces atherosclerotic burden in apolipoprotein E deficient (Apoe-/-) mice. Monocytes/macrophages play a pivotal role in atherogenesis and express high levels of IGF-1 receptor (IGF-1R); however the potential effects of IGF-1 on their function are unknown. Thus, we created monocyte/macrophage specific IGF-1R knockout mice (MΦIgf1rKO) by crossing Igf1r floxed mice with Lysozyme-Cre mice, both on Apoe-/- background, and evaluated atherosclerosis by feeding a high fat diet for 8 wks. MΦIgf1rKO mice had a marked increase in atherosclerotic burden; 41± 12 % and 57 ± 15 % increase in plaque size by en face and cross-section analysis respectively, compared to Igf1r floxed mice (control; n=8, p<0.05). Plaque composition in the aortic root was also substantially altered; MΦIgf1rKO had increased monocyte/macrophage content (anti-Mac3 staining, MΦIgf1rKO, 31 ± 3 % vs. Igf1r floxed, 23 ± 4 %) and a decrease in smooth muscle cell content (anti-α-smooth muscle actin staining, MΦIgf1rKO, 15 ± 4 % vs. Igf1r floxed, 23 ± 3 %), whilst there was no significant change in levels of circulating Ly-6Chi monocyte subpopulation. These changes in composition are consistent with a more inflammatory and less stable plaque phenotype. In fact, the frequency of intraplaque hemorrhage and elastin layer breaks (signs of plaque vulnerability) was higher in MΦIgf1rKO mice (5 in 8 mice positive) than in Igf1r floxed mice (2 in 8 positive). Gene expression analysis in aorta showed that MΦIgf1rKO downregulated TGFβ receptor 1 and 2 (by 37±12 % and 36±10 %, P<0.05, n=10), thrombospondin-1 (by 50±14 %, P<0.01, n=10), LXRβ (by 33±9 %, P<0.01, n=10), RXRα (by 38±11 %, P<0.01, n=10), and ABCA1 and ABCG1 (by 32±14 % and 45±19 %, P<0.05, n=10), and upregulated ACAT-1 (by 58±16 %, P<0.05, n=10) and DGAT-2 (by 115±55 %, P<0.05, n=10). These changes are consistent with decreased SMC content and increased lipid accumulation in macrophages. Taken together, our data indicate that monocyte/macrophage IGF-1R signaling suppresses macrophage accumulation in lesions and reduces plaque vulnerability, providing a novel mechanism whereby IGF-1 exerts its anti-atherogenic effects.

Abstract WP125: Comparison Of Carotid Intraplaque Hemorrhage With Other Markers Of Plaque Vulnerability.

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Joseph S McNally ◽  
Seong-Eun Kim ◽  
Hyo-Chun Yoon ◽  
John Roberts ◽  
Krishna Narra ◽  
...  
Keyword(s):  
Relative Risk ◽  
Acute Stroke ◽  
Carotid Plaque ◽  
Systemic Disease ◽  
The Body ◽  
Intraplaque Hemorrhage ◽  
Plaque Vulnerability ◽  
Intraluminal Thrombus ◽  
Brain Images ◽  
Ischemic Events

Background: MR detected carotid intraplaque hemorrhage (IPH) has been associated with acute ischemic events. Other markers of plaque vulnerability can also be imaged by MRI/MRA and include >70% carotid stenosis, plaque ulceration, and intraluminal thrombus. Atherosclerosis is a systemic disease, and many of these markers are found bilaterally in patients. Objective: To determine the relative risk acute ischemic events with carotid IPH compared to other markers of plaque vulnerability, and to determine whether IPH is associated with these markers and contralateral IPH. Methods: Over 2 years, 159 patients with suspected acute stroke were evaluated with brain DTI and MRA neck workup. Carotid MRA included lumen evaluation as well as carotid plaque imaging with the MPRAGE sequence. This provided 318 carotid artery and ipsilateral brain images for analysis. 48 arteries were excluded due to extracarotid sources of brain ischemia and 4 were excluded due to carotid occlusion. 266 arteries were eligible for data analysis. Results: Acute territorial ischemic events were associated with carotid IPH, >70% stenosis, ulceration and intraluminal thrombus (relative risk=6.4 (4.3-8.7), 4.4 (2.8-5.9), 3.8 (2.4-5.6), and 5.7 (3.6-5.7) respectively, p<0.001). Within the same carotid plaque, IPH was associated with ulceration and >70% stenosis (relative risk=7.8 (4.4-13.1) and 6.0 (2.6-13.8) respectively, p<0.001). There was a trend toward association with intraluminal thrombus, but this did not reach significance (relative risk=3.4 (0.9-12.4), p=0.056). Carotid IPH also increased the relative risk of contralateral carotid IPH (relative risk=6.3, (3.4-10.9), p<0.001). Conclusions: Carotid IPH is associated with acute stroke, with a relative risk on par with other markers of plaque vulnerability. Carotid IPH is highly associated with ulceration or >70% stenosis. Carotid IPH is also associated with contralateral IPH, suggesting that systemic factors result in plaque hemorrhage elsewhere in the body.

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.

Carotid Plaques From Symptomatic Patients With Mild Stenosis Is Associated With Intraplaque Hemorrhage

Hypertension ◽  
2021 ◽  
Author(s):  
Valentina Nardi ◽  
John Benson ◽  
Melanie C. Bois ◽  
Luca Saba ◽  
Anthony S. Larson ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Carotid Artery Stenosis ◽  
Continuous Variable ◽  
Interquartile Range ◽  
Artery Stenosis ◽  
Intraplaque Hemorrhage ◽  
Plaque Vulnerability ◽  
Carotid Plaques ◽  
Mild Stenosis ◽  
Cerebrovascular Events

Carotid plaque vulnerability features beyond the degree of stenosis may play a key role in the pathogenesis and recurrence of ischemic cerebrovascular events. This study sought to compare intraplaque hemorrhage (IPH) as a marker of plaque vulnerability in symptomatic patients with mild (<50%), moderate (50%–69%), and severe (≥70%) carotid artery stenosis. We included patients who experienced ischemic cerebrovascular events with no other identifiable sources and underwent carotid endarterectomy for mild (n=32), moderate (n=47), and severe (n=58) carotid artery stenosis. The degree of stenosis and imaging hallmarks were assessed by computed tomography angiography or magnetic resonance angiography. Plaque specimens were stained with hematoxylin and eosin and Movat pentachrome staining. Carotid plaques of patients with mild stenosis had a higher extent of IPH (%) on tissue analysis compared with patients with moderate (mild, 15.7% [interquartile range, 7.8%–26.7%]; moderate, 3.9% [0.0%–9.2%]; P <0.001) and severe carotid artery stenosis (mild, 15.7% [interquartile range, 7.8%–26.7%]; severe, 2.5% [interquartile range, 0.0%–11.2%]; P <0.001). When considering the degree of carotid artery stenosis as a continuous variable, a lower lumen narrowing was associated with higher extent of IPH ( P <0.001; R, −0.329). Our major finding is the association of IPH with mild carotid artery stenosis based on histological analysis. The current study may suggest that IPH potentially plays a role in the mechanism of stroke in patients with nonobstructive carotid stenosis.

scholarly journals Cigarette Smoking and Carotid Plaque Echodensity in the Northern Manhattan Study

2015 ◽  
Vol 40 (3-4) ◽  
pp. 136-143 ◽  
Author(s):  
Dixon Yang ◽  
Sunil Iyer ◽  
Hannah Gardener ◽  
David Della-Morte ◽  
Milita Crisby ◽  
...  
Keyword(s):  
Cigarette Smoking ◽  
Carotid Plaque ◽  
Multinomial Logistic Regression ◽  
Plaque Morphology ◽  
Current Cigarette Smoking ◽  
Vascular Events ◽  
Logistic Regression Models ◽  
Increased Risk ◽  
Former Smokers ◽  
The Mean

Background: We sought to determine the association between cigarette smoking and carotid plaque ultrasound morphology in a multiethnic cohort. Methods: We analyzed 1,743 stroke-free participants (mean age 65.5 ± 8.9 years; 60% women; 18% white, 63% Hispanic, 19% black; 14% current and 38% former smokers, 48% never smoked) from the Northern Manhattan Study using an ultrasound index of plaque echodensity, the Gray-Scale Median (GSM). Echolucent plaque (low GSM) represents soft plaque and echodense (high GSM) more calcified plaque. The mean GSM weighted by plaque area for each plaque was calculated for those with multiple plaques. Quintiles of GSM were compared to no plaque. Multinomial logistic regression models were used to assess associations of cigarette smoking with GSM, adjusting for demographics and vascular risk factors. Results: Among subjects with carotid plaque (58%), the mean GSM scores for quintiles 1-5 were 48, 72, 90, 105, and 128, respectively. Current smokers had over a two fold increased risk of having GSM in quintile 1 (odds ratio (OR) = 2.17; 95% confidence interval (CI), 1.34-3.52), quintile 2 (OR = 2.33; 95% CI, 1.42-3.83), quintile 4 (OR = 2.05; 95% CI, 1.19-3.51), and quintile 5 (OR = 2.13; 95% CI, 1.27-3.56) but not in quintile 3 (OR = 1.18; 95% CI, 0.67-2.10) as compared to never smokers in fully adjusted models. Former smokers had increased risk in quintile 2 (OR = 1.46; 95% CI, 1.00-2.12), quintile 3 (OR = 1.56; 95% CI, 1.09-2.24), quintile 4 (OR = 1.66; 95% CI, 1.13-2.42), and quintile 5 (OR = 1.73; 95% CI, 1.19-2.51), but not in quintile 1 (OR = 1.05; 95% CI, 0.72-1.55). Conclusions: A nonlinear, V-shaped-like relationship between current cigarette smoking and plaque echodensity was observed. Former smokers were at the highest risk for plaques in high GSM quintiles. Thus, current smokers were more likely to have either soft or calcified plaques and former smokers were at greater risk of having only echodense plaques when compared to those who have never smoked. Further research is needed to determine if plaque morphology mediates an association between smoking and clinical vascular events.

scholarly journals Search for Reliable Circulating Biomarkers to Predict Carotid Plaque Vulnerability

2020 ◽  
Vol 21 (21) ◽  
pp. 8236
Author(s):  
Núria Puig ◽  
Elena Jiménez-Xarrié ◽  
Pol Camps-Renom ◽  
Sonia Benitez
Keyword(s):  
Carotid Plaque ◽  
Imaging Techniques ◽  
Intraplaque Hemorrhage ◽  
Circulating Biomarkers ◽  
Plaque Vulnerability ◽  
Vascular Events ◽  
Carotid Revascularization ◽  
Fibrous Cap ◽  
Current Review ◽  
Inflammatory Molecules

Atherosclerosis is responsible for 20% of ischemic strokes, and the plaques from the internal carotid artery the most frequently involved. Lipoproteins play a key role in carotid atherosclerosis since lipid accumulation contributes to plaque progression and chronic inflammation, both factors leading to plaque vulnerability. Carotid revascularization to prevent future vascular events is reasonable in some patients with high-grade carotid stenosis. However, the degree of stenosis alone is not sufficient to decide upon the best clinical management in some situations. In this context, it is essential to further characterize plaque vulnerability, according to specific characteristics (lipid-rich core, fibrous cap thinning, intraplaque hemorrhage). Although these features can be partly detected by imaging techniques, identifying carotid plaque vulnerability is still challenging. Therefore, the study of circulating biomarkers could provide adjunctive criteria to predict the risk of atherothrombotic stroke. In this regard, several molecules have been found altered, but reliable biomarkers have not been clearly established yet. The current review discusses the concept of vulnerable carotid plaque, and collects existing information about putative circulating biomarkers, being particularly focused on lipid-related and inflammatory molecules.

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