# Blood Tests for Carotid Artery Disease: A Patient's Guide to Biomarkers That May Predict Stroke Risk Carotid atherosclerosis (narrowing of the neck arteries due to cholesterol plaque buildup) is a major cause of stroke, but doctors struggle to identify which patients with no symptoms are at highest risk and would benefit most from surgery. This review examined blood-based biomarkers (measurable substances in the blood) that might signal the presence, progression, or instability of carotid plaque. After analyzing studies from the Cochrane Library and MEDLINE databases through September 2018, the authors found that while several inflammatory, lipid, and metabolic biomarkers show promise—including hs-CRP, interleukin-6, MMP-9, and oxidized LDL—no single blood test has yet proven robust enough to become standard of care. The researchers conclude that prospective studies combining multiple biomarkers are essential to prove their clinical usefulness in stroke prevention. # Blood Tests for Carotid Artery Disease: A Patient's Guide to Biomarkers That May Predict Stroke Risk ## Table of Contents - Key Points - Why Carotid Artery Disease Matters - How This Research Review Was Conducted - Inflammatory Biomarkers: The Body's Warning Signals - Endothelial and Cell Adhesion Markers - Matrix-Degrading Enzymes: The Plaque Destabilizers - Lipid Biomarkers: Beyond Basic Cholesterol - Metabolic and Other Biomarkers - What This Means for Patients - Study Limitations - Recommendations for Moving Forward - Frequently Asked Questions - Source Information ## Key Points - No single blood biomarker has yet proven robust enough to become standard of care for carotid artery disease. - Inflammatory markers like hs-CRP, IL-6, MMP-9, and oxidized LDL show promise but have mixed results across studies. - Combining multiple blood biomarkers with imaging features may help identify high-risk patients who need intervention. - LDL particle size, oxidation state, and apolipoprotein content influence risk, not just total cholesterol levels. - Managing inflammation through lifestyle changes—quitting smoking, diet, exercise, cholesterol control—is important for vascular health. ## Why Carotid Artery Disease Matters Carotid atherosclerosis is a buildup of fatty plaque inside the two large arteries in your neck that supply blood to the brain. This condition is a major and potentially preventable cause of ischemic stroke (a stroke caused by a blocked blood vessel). Carotid endarterectomy (surgical removal of the plaque) and carotid stenting (inserting a mesh tube to hold the artery open) are proven techniques for preventing strokes. However, the number of procedures needed to prevent a single stroke in patients without symptoms remains high. This has prompted a trend toward a nonsurgical approach—even in patients with significant narrowing of the artery, known as stenosis. **This is the central challenge:** doctors need better tools to identify which asymptomatic patients with 60% to 99% carotid stenosis are most likely to benefit from intervention. This would reduce the "number needed to treat" and spare low-risk patients from unnecessary procedures. Several markers have been proposed to identify high-risk plaque, including clinical factors, ultrasound features, magnetic resonance (MR) plaque characteristics, and transcranial Doppler signals. The European Society for Vascular Surgery guidelines recommend that imaging features—such as silent brain infarction, intraplaque hemorrhage on MR imaging, stenosis progression, large plaque area, or large juxtaluminal black area on ultrasound analysis—may be used to select patients with asymptomatic carotid stenosis who might benefit from intervention. During plaque progression, specific molecules may diffuse from the plaque into the bloodstream. This means blood tests could act as "surrogate markers" of plaque presence, status, and risk of complications. A biomarker is defined as a characteristic that is objectively measured and evaluated as an indicator of normal biological processes, disease processes, or the body's response to treatment. For a biomarker to be clinically useful, it must satisfy several criteria: 1. **Proof of concept:** Different levels are found in patients with a certain outcome 1. **Prospective validation:** The biomarker predicts the development of the outcome 1. **Incremental value:** It adds information beyond existing markers 1. **Clinical usefulness:** It can change current therapy decisions 1. **Improved outcomes:** Its use should improve patient outcomes 1. **Cost effectiveness:** Its benefits justify its costs ## How This Research Review Was Conducted The authors searched the Cochrane Library and MEDLINE databases through September 2018 for studies evaluating the association between carotid plaque and serum biomarkers of atherosclerotic disease in humans. The search crossed the terms *biomarker, inflammation, lipids, lipoproteins, diabetes, adipokines, calcification, coagulation, and thrombosis* with keywords including *asymptomatic carotid, symptomatic carotid, plaque progression, transient ischemic attack, amaurosis fugax, and stroke*. From 2,601 abstracts on biomarkers and carotid disease, the researchers selected 487 for screening. They prioritized randomized controlled trials, cohort studies, and case-control studies over non-controlled studies, favoring larger sample sizes, stronger statistical associations, and greater methodologic validity. Studies focused on plaque presence, progression, instability, or symptom development. Nonhuman, basic science, and histology-only studies were excluded, as were studies that did not focus on human clinical data. The remaining articles were read in full and included in the review. ## Inflammatory Biomarkers: The Body's Warning Signals Atherosclerosis is now understood as a chronic, low-grade inflammatory disorder of the arterial wall. A key concept is **trained immunity**—a process in which innate immune cells adopt a long-term proinflammatory state after brief exposure to a trigger, such as oxidized low-density lipoprotein (ox-LDL). This contributes to persistent inflammation, increased production of proatherogenic cytokines (cell signaling proteins) and chemokines (proteins that attract immune cells), and increased foam cell formation (cells that engulf cholesterol and contribute to plaque). ### High-Sensitivity C-Reactive Protein (hs-CRP) C-reactive protein (CRP) was the first described atherosclerosis biomarker. It belongs to the pentraxin superfamily of proteins and is one of the most representative acute-phase proteins—proteins whose levels rise during inflammation. High-sensitivity (hs)-CRP testing measures low but persistent levels of inflammation. The European Society of Cardiology guidelines state that hs-CRP may be measured as part of refined risk assessment only in patients with an unusual or moderate risk profile (class IIb/B recommendation), but not in asymptomatic low-risk or high-risk individuals (class III/B). The American College of Cardiology/American Heart Association guidelines say hs-CRP measurement may be considered when, after a quantitative risk assessment, a treatment decision is still uncertain (class IIb/B). **A major study found:** - More than 1,600 patients with asymptomatic carotid atherosclerosis were followed for a median of 11.81 years - The risk of all-cause and cardiovascular mortality significantly increased with elevated hs-CRP levels - Patients with carotid narrowing greater than 50% and hs-CRP levels above 0.29 mg/dL had **nearly twice the risk of cardiovascular mortality** compared with patients who had less than 50% stenosis and hs-CRP below 0.29 mg/dL However, the association between hs-CRP and carotid disease is controversial. Some studies found that high hs-CRP levels can predict the presence of carotid plaque, while others could not establish this association or any correlation with the degree of stenosis. Results are also mixed regarding plaque type: some studies report associations with echolucent plaques (plaques that appear dark on ultrasound and are considered more dangerous), while others correlated hs-CRP with increased plaque volume but not echolucency. hs-CRP may also predict plaque instability on MR imaging (shown as hypointensity on T1-weighted images). Levels of 5 mg/L or greater were significantly associated with a greater number of new cerebral lesions detected on diffusion-weighted MR imaging during carotid artery stenting—but hs-CRP did not correlate with plaque inflammation as measured by FDG uptake on PET scans. The authors noted a large recent series finding no significant association between progression of carotid intima-media thickness (cIMT, a measure of arterial wall thickness) over 2 years and average hs-CRP levels. This suggests hs-CRP might be considered a **risk marker rather than a causal factor** in carotid disease progression. That said, a meta-analysis of 12 studies including more than 2,000 patients found that elevated baseline hs-CRP levels were independently associated with increased ischemic stroke risk. Elevated hs-CRP also predicted early restenosis (re-narrowing) after carotid endarterectomy. ### Pentraxin-3 (PTX3) PTX3 is another acute-phase protein that has been associated with the presence of atherosclerotic plaques. Elevated PTX3 levels were found in patients with plaque instability undergoing carotid stenting. However, the association with the presence and severity of carotid stenosis is questioned in other studies. A population-based study of more than 2,400 subjects showed that PTX3 does not predict incident cardiovascular events—meaning its clinical usefulness remains uncertain. ### Serum Amyloid-A Protein (SAA) SAA is an acute-phase apolipoprotein related to high-density lipoprotein (HDL, the "good" cholesterol). **Levels greater than 10 mg/L** were significantly associated with a greater number of new cerebral lesions detected on diffusion-weighted MR imaging during carotid artery stenting. Higher SAA levels were also significantly associated with progressive atherosclerosis measured by ultrasound, and can help identify patients with ischemic stroke caused by atherothrombosis (plaque-related clots) versus cardioembolic stroke (clots originating from the heart). ### Interleukin-6 (IL-6) IL-6 is a "master" proinflammatory and procoagulant cytokine (a protein that promotes both inflammation and blood clotting). It has been linked to coronary artery events and is also elevated in patients with carotid atherosclerotic lesions. IL-6 is associated with increased cIMT but not with the degree of stenosis. IL-6 appears to reflect local inflammatory activity within the plaque: it is upregulated in patients with plaque instability features on MR imaging, increased in patients who underwent carotid endarterectomy, and found in the debris retrieved from cerebral embolic protection devices used during carotid artery stenting. ### Interleukin-1 beta (IL-1b) IL-1b is an important mediator of the inflammatory response involved in cell proliferation, differentiation, and apoptosis (programmed cell death). In a key clinical trial, subcutaneous injection of **canakinumab**—a human monoclonal antibody that neutralizes IL-1b—in patients with well-controlled diabetes and high cardiovascular risk significantly decreased systemic inflammation (measured by hs-CRP and IL-6 levels) without major effects on LDL or HDL cholesterol. This supports IL-1b's significance as a mediator of atherosclerosis activity. IL-1b was also found independently and significantly associated with the presence of carotid artery stenosis in patients who underwent carotid endarterectomy. ### Tumor Necrosis Factor-alpha (TNF-a) TNF-a (also known as cachectin) is a major proinflammatory cytokine involved in early inflammatory events. It is associated with larger plaque size and has an inverse correlation with plaque GSM (grey-scale median, a measure of plaque echogenicity on ultrasound—lower values suggest more dangerous, lipid-rich plaque). TNF-a is also increased in patients with plaque instability and significantly increased in symptomatic patients. ### Monocyte Chemotactic Protein 1 (MCP-1) MCP-1 (also known as chemokine C-C motif ligand-2) is one of the key chemokines that regulate the migration of monocytes and macrophages across the vascular endothelium. It was found associated with carotid artery stenosis in patients who underwent carotid endarterectomy, and levels were higher in patients with symptomatic carotid stenosis compared with asymptomatic carotid stenosis. ### Plasma-Soluble Urokinase Plasminogen Activator Receptor (suPAR) suPAR is released by endothelial and immune cells in an inflammatory environment. It is predictive of both prevalent (existing) carotid and peripheral atherosclerosis and of incident (future) events. **Levels were higher in patients with symptomatic carotid stenosis**, and among symptomatic patients, higher in those with stroke or transient ischemic attack (a "mini-stroke") than in those with amaurosis fugax (temporary vision loss in one eye). These results suggest suPAR may be a biomarker of plaque instability and the severity of thrombotic (clotting) consequences. ## Endothelial and Cell Adhesion Markers Selectins (P, E, and L) are cell-surface glycoproteins involved in the rolling and anchoring of white blood cells on the vascular wall. Intercellular adhesion molecules (ICAMs) and vascular cell adhesion molecules (VCAMs) induce firm adhesion of inflammatory cells to the vessel surface. Their soluble forms circulate in the blood and can be measured. ### VCAM-1 VCAM-1 levels are positively associated with cardiovascular mortality, the presence of carotid atherosclerotic lesions, and MR markers of plaque instability. However, VCAM-1 plasma concentration was not correlated with the degree of stenosis or with FDG uptake on PET imaging of the carotid artery. ### ICAM-1 There is evidence for a predictive role of circulating ICAM-1 levels in initially healthy people, with a significant association with cardiovascular mortality. ICAM-1 was found elevated in more than 300 patients who underwent carotid endarterectomy compared with healthy controls. ### Selectins L-selectin is expressed on granulocytes, monocytes, and most lymphocytes. It has been related to larger plaque size estimated by ultrasound in patients with carotid atherosclerotic plaque. E-selectin levels were significantly associated with carotid artery stenosis in endarterectomy patients. ### Endothelial Microparticles (EMPs) EMPs are tiny submicron particles (0.1 to 1.0 micrometers) released when endothelial cells are activated or undergo apoptosis (cell death). They promote oxidative stress and vascular inflammation. **EMP concentrations were significantly higher in patients with carotid stenosis of 70% or greater** and in asymptomatic patients with unstable plaques compared with controls. Certain specific EMP subsets were also higher in unstable plaques confirmed by histologic analysis after surgery in a cohort of endarterectomy patients. ## Matrix-Degrading Enzymes: The Plaque Destabilizers Matrix metalloproteinases (MMPs) are a class of enzymes involved in degrading the extracellular matrix—the structural scaffolding of the artery wall. This degradation can lead to plaque destabilization and cap erosion (thinning of the fibrous cap that covers the plaque). An imbalance between these enzymes and their inhibitors (tissue inhibitors of metalloproteinases, or TIMPs) may lead to plaque rupture. Key findings include: - Carotid plaques from surgical samples showed features of instability in patients with **higher serum levels of TIMP-1, MMP-1, and MMP-7** - MMP-7 was elevated in the blood of patients who had a stroke 2 to 6 months before - MMP-9 levels were higher in patients with active carotid plaques on PET imaging - Symptomatic patients who underwent carotid endarterectomy showed **higher serum levels of MMP-2 and MMP-9** - Elevated MMP-9 levels were found in debris retrieved from cerebral embolic protection devices during carotid stenting ## Lipid Biomarkers: Beyond Basic Cholesterol Lipid factors, along with inflammatory factors, are the main actors in the onset, evolution, and destabilization of atheroma plaque. But their specific roles are complex. ### LDL Cholesterol (LDL-c) There is compelling evidence of cardiovascular benefit from lowering LDL-c—by decreasing the availability of cholesterol particles that enter the artery wall. However, the concept of **residual cardiovascular risk** has emerged: patients treated with statins still face risk even after achieving significant LDL-c reduction. This is caused by the atherogenic effects of triglyceride-rich lipoproteins (TRLs), especially very low-density lipoproteins (VLDL). This led to the concept of **non-HDL cholesterol**, which reflects cholesterol in all atherogenic particles containing Apo B (LDL-c + VLDL-c + lipoprotein(a) + cholesterol remnants). Non-HDL cholesterol may outperform LDL-c as a risk marker, particularly in patients with atherogenic dyslipidemia. Recently, LDL-c—even at normal levels—was found to be independently associated with the presence and extent of early systemic atherosclerosis in patients without major cardiovascular risk factors. LDL-c contains multiple subfractions. **Small and dense LDL particles** have greater atherogenic potential due to decreased clearance, greater binding, increased penetrability into the artery wall, and greater susceptibility to oxidation. They have been associated with both coronary heart disease and carotid atherosclerosis. Higher levels independently predicted increased cIMT and proinflammatory activation of peripheral mononuclear cells and endothelial cells. ### Oxidized LDL (Ox-LDL) Oxysterols are oxidized end-products of cholesterol metabolism, enhanced by risk factors like tobacco exposure. They are toxic to cells, stimulate foam cell formation, and contribute to plaque vulnerability by increasing MMP-9 production in macrophages. **Ox-LDL plasma levels are inversely correlated with carotid plaque GSM**, meaning higher oxidation levels are linked to more vulnerable plaques. ### HDL Cholesterol (HDL-c) HDL-c protects the vessel wall by transforming plaque to higher echogenicity (more stable appearance on ultrasound) through reduction of lipid content and inflammation. Epidemiologic studies confirm the association between HDL-c levels and cIMT. Low HDL-c and higher total cholesterol/HDL-c ratios were associated with lower GSM and other characteristics of carotid plaque instability. HDL particle size matters: - An HDL size greater than 8.22 nm was independently associated with low cIMT - There was an **inverse association between HDL3-c (smaller particles) and plaque area** - There was a **positive association between HDL2-c (larger, more effective particles) and plaque thickness** ### Triglyceride-Rich Lipoproteins (TRLs) TRLs include chylomicrons, VLDL, intermediate-density lipoproteins (IDL), and other remnant particles. They can predict increased cIMT and are associated with proinflammatory activation of peripheral blood cells. **Elevated TRL levels are an independent risk factor for future ischemic strokes and for echolucent carotid plaques.** ### Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) Lp-PLA2 travels with circulating LDL-c and induces a proinflammatory reaction in the vessel wall. Its levels are higher at the shoulder and necrotic lipid core areas of plaque histology samples. Interestingly, secretory PLA2 levels—but not Lp-PLA2 levels—have been associated with atherosclerotic plaques and outcomes in some studies. However, circulating Lp-PLA2 was found to be increased in patients with high-grade carotid stenosis and unstable plaques in a small series of endarterectomy patients. ### Lipoprotein(a) [Lp(a)] Lp(a) is an LDL-like particle, rich in cholesterol and strongly influenced by genetics. Elevated levels are associated with increased risk for cardiovascular diseases—but not with carotid atherosclerosis in a group of patients with statin-treated familial hyperlipidemia. Other studies report increased Lp(a) in patients with high-grade unstable carotid stenosis, and a strong correlation with hypoechoic (dangerous-looking) plaques. **Lp(a) apheresis (a filtration treatment that removes Lp(a) from the blood) resulted in cIMT and plaque reduction.** While Lp(a) independently predicted carotid stenosis and occlusion in one study, it was not related to plaque area in another. ### Apolipoproteins (Apos) Apolipoproteins are the protein components of plasma lipoproteins. The most relevant subtypes are: - **Apo A-I:** the main protein on HDL, considered atheroprotective - **Apo B-100:** the main protein on LDL, considered atheroprone - **Apo C-II:** important in chylomicrons and VLDL, activates lipoprotein lipase - **Apo E:** present in chylomicrons, VLDL, and IDL, allows binding to liver cells Anti-ApoA-I immunoglobulin G levels were independently associated with cardiovascular disease in the general population. A meta-analysis of eight cohort and four case-control studies concluded that reduced ApoA-I, increased ApoB, and a higher ApoB/A-I ratio were risk factors for a **first ischemic stroke—but not hemorrhagic stroke**. A clinical study confirmed lower ApoA-I levels in ischemic stroke cases versus controls. ApoB showed no significant correlation with major cardiovascular events in one large cohort study, though the existence of two allele proteins (ApoB100 and ApoB48) may bias these findings. A large meta-analysis of 22 studies including **30,879 participants** demonstrated a significant association between the APOE genotype and cIMT. ## Metabolic and Other Biomarkers The original article also references metabolic biomarkers including adipokines (resistin, adiponectin, FABP4), homocysteine, and osteoprotegerin (OPG), as well as hematologic markers such as red blood cell distribution width (RDW), white blood cell count, neutrophil count, T lymphocytes, and monocytes. Additional categories include angiogenic factors like vascular endothelial growth factor (VEGF), thrombosis-related markers like PAI-1, and micro-RNAs (miRNA). One notable finding in the metabolic category: **lower levels of bilirubin correlated with silent cerebral infarction on brain MR imaging**, which may precede symptomatic ischemic events. Calcification markers include osteoprotegerin (OPG), which plays a role in vascular calcification and has been studied in relation to plaque burden and stability. ## What This Means for Patients This review carries several important messages for patients with carotid artery disease: **No single blood test can yet determine your stroke risk.** While many biomarkers show statistical associations with plaque presence, instability, or symptom development, none has yet met all the criteria needed to become a standard clinical tool. **Combinations may be the future.** The authors suggest that combining serum biomarkers with imaging features (such as MR-detected intraplaque hemorrhage or ultrasound plaque analysis) may help vascular specialists select high-risk patients who need intervention. This personalized approach could reduce unnecessary surgeries in low-risk patients while ensuring high-risk patients receive timely treatment. **Inflammation matters.** The consistent finding across multiple inflammatory markers—hs-CRP, IL-6, IL-1b, suPAR, and others—confirms that inflammation plays a central role in plaque instability. This is why lifestyle changes that reduce inflammation (smoking cessation, diet, exercise, cholesterol management) are so important for vascular health. **Cholesterol is more complex than "good" and "bad."** Particle size, oxidation state, and apolipoprotein content all influence risk. For example, small dense LDL particles are more dangerous than large fluffy ones, and the ApoB/ApoA-I ratio may matter more than simple LDL levels for predicting stroke. ## Study Limitations This was a review of existing literature, not a new clinical trial. As such, it inherits the limitations of the underlying studies: - The included studies varied widely in design, sample size, and methodology—making direct comparisons difficult - Many findings are conflicting: for example, some studies show hs-CRP predicts plaque presence while others do not, and PTX3 results are similarly divided - Several biomarkers (such as E-selectin, Lp-PLA2, and Lp(a) in carotid disease) have been studied primarily in small patient series, limiting the strength of conclusions - Most studies are observational, meaning they can show associations but cannot prove causation - None of the reviewed biomarkers has yet undergone rigorous prospective validation to demonstrate that using it improves clinical outcomes—the critical test for any new medical tool - Cost-effectiveness data were not systematically assessed ## Recommendations for Moving Forward The authors make a clear call to action: 1. **Prospective studies applying a combination of biomarkers are essential** to prove clinical usefulness. Single markers studied in isolation have repeatedly produced conflicting results. 1. Future research should focus on **multimodal risk assessment**—combining blood biomarkers with imaging features to create a composite risk score. 1. Biomarker panels should be tested in well-designed randomized controlled trials to demonstrate that their use actually changes treatment decisions and improves patient outcomes. 1. Researchers should prioritize biomarkers that have shown the most consistent results across studies, particularly those related to plaque instability (such as MMPs, suPAR, and certain inflammatory cytokines). For patients today, the practical takeaway is to continue working with your vascular specialist to manage established risk factors: high cholesterol, high blood pressure, diabetes, smoking, and inactivity. While blood biomarker testing is not yet standard of care for carotid disease, the field is rapidly evolving—and combination biomarker panels may soon help refine treatment decisions for asymptomatic carotid stenosis. ## Frequently Asked Questions ### What is carotid atherosclerosis? Carotid atherosclerosis is a buildup of fatty plaque inside the two large neck arteries that supply blood to the brain. It is a major and potentially preventable cause of ischemic stroke, which happens when a blood vessel to the brain becomes blocked. Doctors can treat it with surgery to remove plaque or with a stent to hold the artery open. ### Can a blood test determine my stroke risk? No single blood test has yet proven robust enough to become standard of care for predicting stroke risk in people with asymptomatic carotid artery narrowing. While several inflammatory, lipid, and metabolic markers show promise, none has met all criteria needed for routine clinical use. Researchers say future studies combining multiple biomarkers are essential to prove their usefulness. ### What blood markers are most promising for carotid disease? Inflammatory markers such as hs-CRP, interleukin-6, and suPAR are linked to plaque instability. Matrix-degrading enzymes like MMP-9 and oxidized LDL also show promise. However, results have been mixed in different studies, and no single marker is reliable enough yet. Combining several biomarkers together may be the way forward, researchers say. ### What does a high hs-CRP level mean? hs-CRP is a blood test that measures low-level inflammation. In a major study, patients with greater than 50% carotid narrowing and hs-CRP above 0.29 mg/dL had nearly twice the risk of cardiovascular death than those with less narrowing and lower hs-CRP. However, other studies found no association, so its exact role remains controversial. ### What can I do to reduce my risk of stroke from carotid disease? Managing established risk factors is key: high cholesterol, high blood pressure, diabetes, smoking, and inactivity. Because inflammation plays a central role in plaque instability, lifestyle changes that reduce inflammation—like quitting smoking, eating a healthy diet, exercising, and managing cholesterol—are particularly important for vascular health and stroke prevention. ### Why are doctors looking for new blood tests for carotid disease? Even in patients with significant narrowing, many surgeries are needed to prevent one stroke. Doctors want better tools to identify which asymptomatic patients with 60% to 99% carotid stenosis are most likely to benefit from intervention. Blood biomarkers could serve as surrogate markers of plaque presence, status, and risk, helping spare low-risk patients from unnecessary procedures. ### Should I get a second opinion before carotid endarterectomy for asymptomatic carotid stenosis when blood tests to predict stroke risk are uncertain? No single blood biomarker has been proven robust enough to become standard of care for predicting stroke risk in carotid artery disease. Because doctors still struggle to identify which asymptomatic patients with 60–99% stenosis benefit most from surgery, a second opinion can help you weigh whether endarterectomy or stenting is necessary or whether a nonsurgical approach is reasonable. The review highlights conflicting biomarker results and notes that combining blood markers with imaging features may ultimately guide this decision. Diagnostic Detectives Network provides independent expert second opinions on your diagnosis and treatment options. ## Source Information **Original Article Title:** Barcelona serum biomarkers in carotid atherosclerosis **Authors:** Esaú Martinez, MD; Jordi Martorell, PhD; and Vincent Riambau, MD, PhD — Barcelona, Spain **Journal:** Journal of Vascular Surgery, 2020; Volume 71, pages 329-341 **Published By:** Society for Vascular Surgery, Elsevier Inc. (https://doi.org/10.1016/j.jvs.2019.04.488) **Note:** This patient-friendly article is based on peer-reviewed research. It is intended for educational purposes and does not constitute medical advice. Patients should discuss their individual risk factors and treatment options with their healthcare providers. --- Publisher: Diagnostic Detectives Network (https://diagnosticdetectives.com) — independent multi-expert medical second opinions, worldwide, private-pay. Author byline: Anton Titov, MD, PhD. Contact: https://diagnosticdetectives.com/pages/contact Canonical page: https://diagnosticdetectives.com/products/blood-tests-for-carotid-artery-disease-a-patients-guide-to-biomarkers-that-may-predict-stroke-risk