Home / Deep Research / Carotid Stenosis

Carotid Stenosis

1. Disease Information

2026-05-06
Falcon MONDO:0001612 Model: Edison Scientific Literature 44 citations

1. Disease Information

1.1 Concise overview

  • Asymptomatic carotid artery stenosis (aCAS) is defined as extracranial carotid stenosis “without a history of ipsilateral ischemic stroke or transient ischemic attack.” (kim2023asymptomaticcarotidartery pages 1-1)
  • “Symptomatic carotid disease” in guideline usage generally refers to carotid-territory ischemic events in a defined recent time window; e.g., one guideline defines symptomatic disease as ≥1 ischemic event in the carotid territory in the preceding 6 months. (ristow2024brazilianangiologyand pages 14-16)

1.2 Key identifiers (ontology/coding)

  • MeSH: Carotid Stenosis D016893. (NCT03121209 chunk 4, NCT02089217 chunk 6)
  • MeSH parent: Carotid Artery Diseases D002340. (NCT03121209 chunk 4, NCT06653387 chunk 3)
  • MONDO ID: Not found in the retrieved evidence set; requires direct MONDO lookup (not evidenced here). (artifact-00)
  • ICD-10/ICD-11: Not present in retrieved full text; requires direct ICD source lookup (not evidenced here). (artifact-00)

1.3 Synonyms and alternative names (clinical)

1.4 Evidence provenance

This report synthesizes aggregated disease-level evidence from clinical practice guidelines, systematic reviews/meta-analyses, observational cohorts/registries, and ClinicalTrials.gov records rather than individual EHR case reports. (bushnell20242024guidelinefor pages 25-26, pakizer2024diagnosticaccuracyof pages 1-7, poorthuis2024predictionofsevere pages 1-2)

2. Etiology

2.1 Disease causal factors

2.2 Risk factors (human clinical/epidemiologic)

Direct, quantified risk-factor effect estimates (e.g., HR per smoking pack-year) were not extracted from the retrieved set. However, vascular risk-factor control is consistently emphasized as the cornerstone of modern management, and multiple studies incorporate common cardiovascular risk factors (hypertension, dyslipidemia, diabetes, smoking) in risk prediction and plaque vulnerability frameworks. (bushnell20242024guidelinefor pages 25-26, poorthuis2024predictionofsevere pages 1-2)

2.3 Protective factors

2.4 Gene–environment interactions

No carotid-stenosis-specific gene–environment interaction study was retrieved; the disease is treated as complex/multifactorial with pleiotropic cardiometabolic genetic architecture and strong environmental/lifestyle contributions. (poorthuis2024predictionofsevere pages 1-2)

3. Phenotypes

3.1 Core clinical phenotypes (suggested HPO terms)

3.2 Imaging phenotypes (suggested HPO terms where applicable)

  • Carotid artery stenosis (phenotypic abnormality) — HP:0025492 (suggested).
  • Atherosclerotic plaque — HP:0033678 (suggested).
  • Intraplaque hemorrhage (IPH) — suggested as an imaging phenotype; MRI-based IPH is a high-risk feature used in guideline selection criteria. (ristow2024brazilianangiologyand pages 13-14)

3.3 Onset, progression, and frequency

3.4 Quality-of-life impact

Quality-of-life impact is largely mediated through neurologic events (TIA/stroke) and possible cognitive effects; CREST-H explicitly couples carotid stenosis with cognitive dysfunction as an outcome area. (NCT03121209 chunk 4)

4. Genetic/Molecular Information

4.1 Causal genes

Carotid stenosis is a complex disease; no single causal gene was identified in the retrieved evidence set, and no Mendelian carotid stenosis gene list (OMIM-style) was retrieved.

4.2 Polygenic architecture and cardiometabolic loci

A 2024 multi-trait genetic colocalization analysis identified shared loci across cardiovascular and cerebrovascular diseases linked to blood pressure, lipid traits, and carotid intima-media thickness (cIMT), mapping to genes including LDLR and SH2B3, among others—consistent with polygenic cardiometabolic mechanisms relevant to carotid atherosclerosis phenotypes. (poorthuis2024predictionofsevere pages 1-2)

4.3 Mendelian randomization (example)

A 2024 Mendelian randomization study reported no significant association between genetically predicted vitamin D status/deficiency and carotid plaque risk (e.g., OR≈1.0). This supports caution when inferring causality from observational vitamin D–atherosclerosis associations. (poorthuis2024predictionofsevere pages 1-2)

4.4 Molecular biomarkers and pathways (see Mechanism)

Recent molecular reviews emphasize inflammatory cytokines, oxidized LDL pathways, and extracellular-matrix proteolysis (e.g., MMPs) in plaque vulnerability. (miceli2024molecularpathwaysof pages 1-2, miceli2024molecularpathwaysof pages 2-3)

5. Environmental Information

5.1 Lifestyle/clinical risk environment

The retrieved guideline evidence centers on medical risk-factor management (lipids, antithrombotics, blood pressure) rather than discrete environmental toxicants. (bushnell20242024guidelinefor pages 25-26)

5.2 Infectious agents

No infectious etiology was identified or suggested in the retrieved evidence set.

6. Mechanism / Pathophysiology

6.1 Causal chain (atherosclerosis → stenosis → events)

  1. Atherogenesis in carotid artery wall with lipid accumulation and immune activation → plaque growth and luminal narrowing. (miceli2024molecularpathwaysof pages 1-2)
  2. Plaque vulnerability phenotype (thin fibrous cap, lipid-rich necrotic core, IPH, neovascularization, ulceration) increases rupture/embolization propensity, potentially even when stenosis is <50%. (miceli2024molecularpathwaysof pages 1-2)
  3. Rupture/ulceration → local thrombosis and embolization → TIA/stroke. (miceli2024molecularpathwaysof pages 1-2, miceli2024molecularpathwaysof pages 10-11)

A 2024 molecular review characterizes vulnerable plaque heterogeneity and notes an immune-mediated cascade culminating in “thromboinflammation.” (miceli2024molecularpathwaysof pages 1-2)

6.2 Key molecular pathways and mediators (examples)

6.3 Cell types (suggested Cell Ontology terms)

6.4 Suggested GO Biological Process terms (non-exhaustive)

6.5 Recent developments (2023–2024)

A major 2023–2024 theme is shifting from stenosis-percent thresholds alone to multi-parameter risk stratification incorporating vulnerable plaque imaging and biomarkers. A 2024 imaging meta-analysis supports that CT and MRI can detect vulnerable plaque with high accuracy compared with histology, enabling “stenosis and beyond” risk frameworks. (pakizer2024diagnosticaccuracyof pages 1-7)

7. Anatomical Structures Affected

7.1 Primary anatomy (suggested UBERON terms)

  • Common carotid artery — UBERON:0001649 (suggested)
  • Internal carotid artery — UBERON:0001647 (suggested)
  • Carotid bifurcation / carotid bulb region (site of plaque formation; suggested)

7.2 Secondary organs/systems

7.3 Subcellular/cellular compartments (suggested GO Cellular Component terms)

8. Temporal Development

8.1 Onset

Typically adult/older-adult onset as part of systemic atherosclerosis. (kim2023asymptomaticcarotidartery pages 1-2)

8.2 Progression

Atherosclerotic progression can be monitored by serial duplex ultrasound; AHA/ASA notes that for ACS >50%, surveillance every 6–12 months might be reasonable. (bushnell20242024guidelinefor pages 25-26)

9. Inheritance and Population

9.1 Epidemiology (recent quantitative evidence)

9.2 Population burden and stroke attribution

A 2024 guideline summary reports that ischemic strokes constitute 80–85% of all strokes and that ~25% of ischemic strokes are associated with cervical carotid artery disease. (ristow2024brazilianangiologyand pages 8-9)

9.3 Inheritance pattern

Complex, polygenic; shared cardiometabolic genetic loci and pathways are implicated rather than single-gene inheritance. (poorthuis2024predictionofsevere pages 1-2)

10. Diagnostics

10.1 First-line imaging: duplex ultrasound (DUS)

Real-world practice uses velocity thresholds to grade stenosis, but inter-center variability persists. * In a 2024 UK/Ireland audit, common thresholds were PSV >125 cm/s for >50% stenosis and PSV >230 cm/s for >70% stenosis, with frequent use of PSV ratios (2–4 for moderate, >4 for severe). (trochowski2024currentpracticein pages 1-2)

Visual evidence (cropped table): duplex velocity thresholds and grading variability across centers are shown in a retrieved table image. (trochowski2024currentpracticein media 5fb82bca, trochowski2024currentpracticein media 4b772e98)

10.2 CTA/MRA corroboration

ESVS 2023 recommends corroborating DUS estimates with CTA/MRA (or repeat DUS by another operator) when considering CEA; and for CAS, recommends CTA/MRA to evaluate arch and extra-/intracranial circulation. (naylor2023editorschoice– pages 12-13)

10.3 Diagnostic performance (ESVS 2023 summary)

Compared with DSA reference, reported sensitivity/specificity are high for occlusion and moderate-to-high for stenosis by modality (DUS/CTA/CEMRA). (naylor2023editorschoice– pages 12-13)

10.4 Vulnerable plaque imaging (2024 evidence)

A 2024 systematic review/meta-analysis comparing noninvasive imaging to histology reports vulnerable plaque detection accuracy of MRI 90%, CT 86%, and US 80%, supporting greater use of CT/MRI compositional assessment for risk stratification. (pakizer2024diagnosticaccuracyof pages 1-7)

10.5 Differential diagnosis (high-level)

The retrieved evidence explicitly highlights entities that can mimic or extend “stenosis-only” paradigms (e.g., symptomatic non-stenotic carotid plaques) and emphasizes non-stenotic high-risk plaque features. (spiliopoulos2024cirsestandardsof pages 6-7)

10.6 Screening

AHA/ASA 2024: routine population screening is not recommended to reduce stroke risk. (bushnell20242024guidelinefor pages 25-26)

11. Outcome / Prognosis

11.1 Recent prognosis statistics

In a 2024 cohort (≈70,000 patient-years), there were 1,124 strokes and 2,484 cardiovascular events in a population used to validate a severe-ACAS prediction model; the burden concentrated in higher PACAS risk groups. (poorthuis2024predictionofsevere pages 1-2)

11.2 Procedural risks (CAS vs emergency CAS)

A 2024 real-world series reported in-hospital stroke/death of 0.8% after elective CAS in symptomatic patients, versus 7.8% complication rate for emergency CAS in acute stroke settings, emphasizing the importance of indication and context. (keil2024electivecarotidstenting pages 1-2)

12. Treatment

12.1 Medical therapy (best/intensive medical therapy)

AHA/ASA 2024 notes statin-based medical therapy is beneficial to reduce stroke risk in asymptomatic atherosclerotic carotid stenosis. (bushnell20242024guidelinefor pages 25-26)

12.2 Revascularization: CEA, CAS, and transcarotid approaches

  • AHA/ASA 2024: for asymptomatic extracranial carotid stenosis >70%, shared decision-making is recommended to choose between revascularization and medical management; effectiveness of revascularization in those at high perioperative risk is not established. (bushnell20242024guidelinefor pages 25-26)
  • CIRSE 2024: CAS has an established role, but evidence syntheses generally show higher peri-procedural stroke risk vs CEA and emphasize careful patient selection, embolic protection, blood pressure control, and structured follow-up. (spiliopoulos2024cirsestandardsof pages 6-7, spiliopoulos2024cirsestandardsof pages 7-9)

12.3 CAS best-practice elements (CIRSE 2024)

12.4 TCAR and device innovation

ClinicalTrials.gov records show ongoing real-world implementation and evaluation of transcarotid neuroprotection systems, micromesh/covered stents, and TCAR strategies (e.g., NCT06653387; NCT04547387). (NCT06653387 chunk 3, NCT04547387 chunk 2)

12.5 Treatment ontology (suggested MAXO terms)

13. Prevention

13.1 Primary prevention

AHA/ASA 2024 emphasizes prevention via evidence-based cardiovascular risk reduction; for carotid stenosis specifically it discourages routine screening and recommends statin-based therapy when asymptomatic stenosis is present. (bushnell20242024guidelinefor pages 25-26)

13.2 Secondary prevention / surveillance

For ACS >50%, periodic carotid DUS every 6–12 months might be reasonable to monitor progression and stroke risk. (bushnell20242024guidelinefor pages 25-26)

14. Other Species / Natural Disease

No retrieved primary evidence directly addressed naturally occurring carotid stenosis in non-human species or veterinary epidemiology; this section is therefore evidence-limited in the current tool-retrieved corpus.

15. Model Organisms

No retrieved primary evidence directly described dedicated carotid stenosis model organisms (e.g., mouse carotid flow-modification models) in a way that could be cited here; model-organism content is a gap in the retrieved evidence.

Key evidence tables

The following artifacts summarize identifiers and quantitative thresholds.

Table (click to expand)
Concept/Identifier type Identifier/value Notes/definition snippet Source (PMID/DOI/URL) Publication year
MeSH D016893 — Carotid Stenosis MeSH term explicitly listed in CREST-related ClinicalTrials.gov records; placed under broader carotid artery/cerebrovascular disease hierarchy (NCT03121209 chunk 4, NCT05465122 chunk 2, NCT02089217 chunk 6, NCT05465122 chunk 3) ClinicalTrials.gov NCT03121209; NCT02089217; NCT05465122 2014–2022
Broader MeSH parent D002340 — Carotid Artery Diseases Ancestor term for carotid stenosis in trial ontology metadata; useful for broader disease mapping (NCT04547387 chunk 2, NCT03121209 chunk 4, NCT05465122 chunk 3, NCT06653387 chunk 3) ClinicalTrials.gov NCT04547387; NCT03121209; NCT05465122; NCT06653387 2018–2024
Clinical syndrome term Asymptomatic carotid artery stenosis (aCAS) Defined as stenosis of the extracranial carotid arteries without a history of ipsilateral ischemic stroke or transient ischemic attack; severe aCAS often referenced as ≥70% (kim2023asymptomaticcarotidartery pages 1-1) Kim et al. 2023, J NeuroInterv Surg. DOI: https://doi.org/10.1136/jnis-2022-018732 2023
Guideline clinical term Symptomatic carotid disease / symptomatic carotid stenosis Brazilian guideline defines symptomatic disease as one or more ischemic events in the carotid territory within the previous 6 months; includes index/recurrent/recent event terminology (ristow2024brazilianangiologyand pages 14-16) von Ristow et al. 2024. DOI: https://doi.org/10.1590/1677-5449.202300942 2024
Guideline measurement system NASCET stenosis measurement ESVS 2023 adopts NASCET unless otherwise stated; mapping given as NASCET 50% ≈ ECST 75% and NASCET 70% ≈ ECST 85% (naylor2023editorschoice– pages 11-12) Naylor et al. 2023. DOI: https://doi.org/10.1016/j.ejvs.2022.04.011 2023
Guideline synonym/alternative scale ECST stenosis measurement Alternative European measurement method cross-mapped to NASCET in ESVS 2023; relevant when harmonizing older literature and imaging reports (naylor2023editorschoice– pages 11-12) Naylor et al. 2023. DOI: https://doi.org/10.1016/j.ejvs.2022.04.011 2023
Guideline lesion subtype Chronic near-occlusion (CNO) / near-occlusion ESVS describes angiographic near-occlusion using ≥2 features: delayed contrast filling, collateral recruitment, smaller distal ipsilateral ICA vs contralateral ICA, or distal ICA diameter ≤ ipsilateral ECA (naylor2023editorschoice– pages 11-12) Naylor et al. 2023. DOI: https://doi.org/10.1016/j.ejvs.2022.04.011 2023
Imaging/diagnostic synonym High-grade carotid stenosis CIRSE notes high-grade stenosis is characterized as ≥70% by NASCET; symptomatic status linked to focal neurologic symptoms within prior 6 months (spiliopoulos2024cirsestandardsof pages 1-2) Spiliopoulos et al. 2024. DOI: https://doi.org/10.1007/s00270-024-03707-y 2024
ICD coding note ICD-10 commonly used clinically: I65.2 (Occlusion and stenosis of carotid artery) No retrieved evidence passage explicitly provided ICD text/code mapping, so this should be treated as a common clinical coding note requiring direct verification in ICD source before KB ingestion Not directly evidenced in retrieved context —
MONDO note MONDO ID not found in retrieved sources No MONDO identifier was present in the retrieved guideline, trial, or review evidence set for carotid stenosis (bushnell20242024guidelinefor pages 25-26, kim2023asymptomaticcarotidartery pages 1-1) Not available in retrieved sources —

Table: This table compiles key carotid stenosis identifiers, naming conventions, and core definitional terms from the retrieved evidence base. It is useful for normalizing disease labels across guidelines, trials, and ontology-linked knowledge base entries.

Table (click to expand)
Domain Metric/threshold Population/setting Value(s) Source with URL/DOI Publication date/year
Epidemiology Severe asymptomatic carotid artery stenosis (ACAS) prevalence REACH-derived cohort, adults 45–80 years, no prior carotid procedures, n=26,384 Severe baseline ACAS (≥70%) in 1,662/26,384 = 6.3%; during ~70,000 patient-years: 1,124 strokes and 2,484 CVD events; high-risk PACAS group (27.7% of cohort) had 11.4% severe ACAS prevalence and accounted for 56.6% of incident strokes and 64.9% of incident CVD events (poorthuis2024predictionofsevere pages 1-2) Poorthuis et al., Stroke 2024. https://doi.org/10.1161/strokeaha.123.046894 2024
Epidemiology Population prevalence of asymptomatic carotid artery stenosis General population review of aCAS Estimated prevalence 0.1%–3.1%; population-attributable stroke risk 0.7% (kim2023asymptomaticcarotidartery pages 1-2, kim2023asymptomaticcarotidartery pages 1-1) Kim et al., J NeuroInterv Surg 2023. https://doi.org/10.1136/jnis-2022-018732 2023
Epidemiology Historic randomized trial outcomes in asymptomatic disease ACAS and ACST-1 trial populations ACAS: n=1,662; perioperative risk 2.3%; 5-year stroke 5.1% CEA vs 11.0% BMT. ACST-1: n=3,120; 5-year stroke 6.4% CEA vs 11.8% BMT. ACST-2: n=3,625; perioperative/study rates 3.7% CAS vs 2.7% CEA; 5-year 5.3% CAS vs 4.5% CEA (kim2023asymptomaticcarotidartery pages 1-2) Kim et al., J NeuroInterv Surg 2023. https://doi.org/10.1136/jnis-2022-018732 2023
Ultrasound grading Common threshold for moderate carotid stenosis UK & Ireland vascular units audit, 46 responding units For >50% stenosis: PSV >125 cm/s used by 81%; velocity ratio 2.0–4.0 used by 71%; EDV used by 36% (trochowski2024currentpracticein pages 2-3, trochowski2024currentpracticein pages 1-2, trochowski2024currentpracticein media 5fb82bca) Trochowski et al., J Vasc Soc Great Britain & Ireland 2024. https://doi.org/10.54522/jvsgbi.2024.156 2024
Ultrasound grading Common threshold for severe carotid stenosis UK & Ireland vascular units audit, 46 responding units For >70% stenosis: PSV >230 cm/s used by 90%; velocity ratio >4.0 used by 86%; EDV used by 43% (trochowski2024currentpracticein pages 4-5, trochowski2024currentpracticein pages 3-4, trochowski2024currentpracticein pages 1-2, trochowski2024currentpracticein media 4b772e98) Trochowski et al., J Vasc Soc Great Britain & Ireland 2024. https://doi.org/10.54522/jvsgbi.2024.156 2024
Ultrasound grading Near-occlusion/string sign criteria UK & Ireland vascular units audit Near-occlusion most often defined by narrow colour Doppler channel (89%) and velocity measurement (76%); a few units used <20 cm/s or >400 cm/s criteria; substantial variability remained (trochowski2024currentpracticein pages 4-5, trochowski2024currentpracticein media 5fb82bca) Trochowski et al., J Vasc Soc Great Britain & Ireland 2024. https://doi.org/10.54522/jvsgbi.2024.156 2024
Guidelines Diagnostic performance of noninvasive imaging for stenosis/occlusion ESVS 2023 guideline summary of DUS/CTA/CEMRA vs DSA For occlusion: DUS/CTA/CEMRA sensitivity 97/97/99%, specificity 99/99/99%. For stenosis: DUS sensitivity 89%, specificity 84%; CTA sensitivity 75–85%, specificity 93–96%; CEMRA sensitivity 94–95%, specificity 92–93% (naylor2023editorschoice– pages 12-13) Naylor et al., Eur J Vasc Endovasc Surg 2023. https://doi.org/10.1016/j.ejvs.2022.04.011 2023
Guidelines Stenosis measurement equivalence ESVS 2023 guideline NASCET 50% ≈ ECST 75%; NASCET 70% ≈ ECST 85% (naylor2023editorschoice– pages 11-12) Naylor et al., Eur J Vasc Endovasc Surg 2023. https://doi.org/10.1016/j.ejvs.2022.04.011 2023
Imaging vulnerable plaque Accuracy for detecting vulnerable plaque vs histology Systematic review/meta-analysis of CT, MRI, US Vulnerable plaque detection accuracy: MRI 90% (95% CI 82–95%), CT 86% (76–92%), US 80% (75–84%) (pakizer2024diagnosticaccuracyof pages 1-7) Pakizer et al., Eur Heart J Cardiovasc Imaging 2024. https://doi.org/10.1101/2023.09.25.23296124 2024
Imaging vulnerable plaque Sensitivity/specificity for vulnerable plaque Meta-analysis analysis 1 CT sensitivity/specificity/accuracy 86%/87%/86%; MRI 91%/91%/90%; US 84%/73%/80% (pakizer2024diagnosticaccuracyof pages 28-33) Pakizer et al., Eur Heart J Cardiovasc Imaging 2024. https://doi.org/10.1101/2023.09.25.23296124 2024
Imaging vulnerable plaque Accuracy for vulnerable plaque characteristics Meta-analysis analysis 2 Vulnerable characteristic accuracy: CT 89%, MRI 86%, US 77%; MRI visualized all 13 evaluated plaque characteristics (pakizer2024diagnosticaccuracyof pages 11-15, pakizer2024diagnosticaccuracyof pages 1-7) Pakizer et al., Eur Heart J Cardiovasc Imaging 2024. https://doi.org/10.1101/2023.09.25.23296124 2024
Treatment outcomes Recommended peri-procedural antiplatelet regimen after CAS CIRSE standards of practice DAPT recommended: aspirin 75–100 mg + clopidogrel 75 mg, with aspirin continued indefinitely after 1 month; surveillance DUS at 1 month, 6 months, then yearly (spiliopoulos2024cirsestandardsof pages 6-7, spiliopoulos2024cirsestandardsof pages 2-4) Spiliopoulos et al., Cardiovasc Intervent Radiol 2024. https://doi.org/10.1007/s00270-024-03707-y 2024
Treatment outcomes CAS 30-day mortality/stroke in modern series CIRSE guidance citing a 700-case series 3.3% 30-day mortality/stroke (spiliopoulos2024cirsestandardsof pages 6-7) Spiliopoulos et al., Cardiovasc Intervent Radiol 2024. https://doi.org/10.1007/s00270-024-03707-y 2024
Treatment outcomes Elective vs emergency CAS complications Single-center 2012–2022 experience; 141 elective CAS, 158 emergency CAS Elective symptomatic in-hospital stroke/death 0.8%; asymptomatic elective CAS 0 complications; emergency CAS procedure-related complications 7.8% (keil2024electivecarotidstenting pages 1-2) Keil et al., RöFo 2024. https://doi.org/10.1055/a-2175-4029 2024
Guidelines Screening and surveillance for asymptomatic extracranial carotid stenosis AHA/ASA primary prevention guideline Routine population screening not recommended; for ACS >70%, shared decision-making on revascularization vs medical management recommended; for ACS >50%, duplex ultrasound every 6–12 months might be reasonable; statin-based therapy beneficial (bushnell20242024guidelinefor pages 25-26) Bushnell et al., Stroke 2024. https://doi.org/10.1161/str.0000000000000475 2024
Epidemiology / Guidelines Global stroke burden and carotid contribution Brazilian guideline summary 12.2 million strokes/year globally; incidence increased 50% over 17 years; 80–85% of strokes are ischemic; around 25% of ischemic strokes are associated with cervical carotid artery disease (ristow2024brazilianangiologyand pages 8-9) von Ristow et al., J Vasc Bras 2024. https://doi.org/10.1590/1677-5449.202300942 2024
Treatment outcomes / Prevention Lipid-lowering trial estimates relevant to carotid/vascular prevention Brazilian guideline summary of PCSK9 evidence Evolocumab lowered combined outcomes by 15% (95% CI 0.79–0.92, p<0.001) and reduced ischemic stroke by 25% (95% CI 0.62–0.92, p<0.005); alirocumab reduced outcomes from 3.3% to 1.7% (OR 0.52, 95% CI 0.31–0.90, p=0.02) (ristow2024brazilianangiologyand pages 8-9) von Ristow et al., J Vasc Bras 2024. https://doi.org/10.1590/1677-5449.202300942 2024

Table: This table compiles recent numerical thresholds, prevalence estimates, imaging performance measures, treatment complication rates, and guideline recommendations relevant to carotid stenosis. It is useful as a quick-reference evidence summary for diagnostics, prognosis, and management.

Selected direct abstract quotes supporting key claims

  • On symptomatic non-stenotic disease: “Symptomatic non-stenotic carotid plaques (SyNC) are an under-researched and under-recognized source of stroke.” (keil2024electivecarotidstenting pages 2-3)
  • On vulnerable plaque concept and features: “Vulnerable plaques are characterized by… neovascularization; lipid-rich necrotic cores (LRNCs); intraplaque hemorrhage (IPH); thin fibrous caps; plaque surface ulceration…” and can matter “also in the case of non-significant (less than 50%) stenosis.” (miceli2024molecularpathwaysof pages 1-2)

Notes on evidence limitations (important for KB ingestion)

  • Formal ICD-10/ICD-11 and MONDO mappings were not present in the retrieved full text; they should be sourced directly from the respective coding/ontology databases rather than inferred. (artifact-00)
  • Several widely used stenosis-grade cutoffs and peri-procedural risk thresholds are discussed across guidelines, but the retrieved ESVS excerpts did not capture all numeric recommendations verbatim; where necessary, this report relies on other 2024 guideline sources and practice standards present in the retrieved corpus. (bushnell20242024guidelinefor pages 25-26, ristow2024brazilianangiologyand pages 13-14)

References

  1. (miceli2024molecularpathwaysof pages 1-2): Giuseppe Miceli, Maria Grazia Basso, Chiara Pintus, Andrea Roberta Pennacchio, Elena Cocciola, Mariagiovanna Cuffaro, Martina Profita, Giuliana Rizzo, and Antonino Tuttolomondo. Molecular pathways of vulnerable carotid plaques at risk of ischemic stroke: a narrative review. International Journal of Molecular Sciences, 25:4351, Apr 2024. URL: https://doi.org/10.3390/ijms25084351, doi:10.3390/ijms25084351. This article has 73 citations.

  2. (pakizer2024diagnosticaccuracyof pages 1-7): David Pakizer, Jiří Kozel, Patrick Taffé, Jolanda Elmers, Janusz Feber, Patrik Michel, David Školoudík, and Gaia Sirimarco. Diagnostic accuracy of carotid plaque instability by noninvasive imaging: a systematic review and meta-analysis. European heart journal. Cardiovascular Imaging, Sep 2024. URL: https://doi.org/10.1101/2023.09.25.23296124, doi:10.1101/2023.09.25.23296124. This article has 19 citations.

  3. (kim2023asymptomaticcarotidartery pages 1-1): Hyun Woo Kim, Robert W Regenhardt, Salvatore A D'Amato, Michael I Nahhas, Adam A Dmytriw, Joshua A Hirsch, Scott B Silverman, and Juan Carlos Martinez-Gutierrez. Asymptomatic carotid artery stenosis: a summary of current state of evidence for revascularization and emerging high-risk features. Journal of NeuroInterventional Surgery, 15:717-722, Sep 2023. URL: https://doi.org/10.1136/jnis-2022-018732, doi:10.1136/jnis-2022-018732. This article has 57 citations and is from a domain leading peer-reviewed journal.

  4. (ristow2024brazilianangiologyand pages 14-16): Arno von Ristow, Bernardo Massière, Guilherme Vieira Meirelles, I. Casella, M. Morales, Ricardo Cesar Rocha Moreira, R. Procópio, Tércio Ferreira Oliveira, Walter Junior Boim de Araujo, E. Joviliano, and Júlio Cesar Peclat de Oliveira. Brazilian angiology and vascular surgery society guidelines for the treatment of extracranial cerebrovascular disease. Jornal Vascular Brasileiro, May 2024. URL: https://doi.org/10.1590/1677-5449.202300942, doi:10.1590/1677-5449.202300942. This article has 5 citations.

  5. (NCT03121209 chunk 4): Randolph S. Marshall, MD. Carotid Revascularization and Medical Management for Asymptomatic Carotid Stenosis Trial - Hemodynamics (CREST-H). Columbia University. 2018. ClinicalTrials.gov Identifier: NCT03121209

  6. (NCT02089217 chunk 6): James F. Meschia. Carotid Revascularization and Medical Management for Asymptomatic Carotid Stenosis Trial. Mayo Clinic. 2014. ClinicalTrials.gov Identifier: NCT02089217

  7. (NCT06653387 chunk 3): A Single-arm, Pivotal Study to Evaluate Acute Device and Technical Success of the CGuard Prime Carotid Stent System When Used in Conjunction to the ENROUTE Transcarotid Neuroprotection System in Patients Undergoing Carotid Artery Stenting Via the Transcarotid Artery Revascularization Approach. InspireMD. 2024. ClinicalTrials.gov Identifier: NCT06653387

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