Carotid stenting
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Muhammad Saad, M.B.B.S.[2]
Overview
Carotid artery stenting (CAS) is a percutaneous, endovascular procedure used to treat carotid stenosis (narrowing of the carotid artery lumen by atheroma). Carotid stenosis may be asymptomatic (diagnosed incidentally on imaging) or symptomatic, presenting with transient ischemic attacks (TIAs) or cerebrovascular accidents (CVAs, strokes). The goal of CAS is to prevent stroke by restoring adequate blood flow through the stenotic internal carotid artery. CAS is performed as an alternative to carotid endarterectomy (CEA), particularly in patients at elevated surgical risk due to anatomic or medical comorbid conditions. Over 14,000 patients have been enrolled in randomized controlled trials evaluating CAS, and the procedure has been shown to be noninferior to CEA in appropriately selected patients.[1][2]
Approaches to CAS include:
Transfemoral CAS (tfCAS): The traditional approach via femoral artery access, with navigation through the aortic arch to the carotid arteries. An embolic protection device (EPD) is used to capture debris during the procedure.
Transcarotid artery revascularization (TCAR): A newer approach involving direct surgical exposure of the common carotid artery in the neck with temporary carotid flow reversal for cerebral protection, avoiding aortic arch manipulation.
Landmark Studies
CAS vs CEA in Symptomatic Patients
Multiple landmark randomized controlled trials have compared CAS to CEA in patients with symptomatic carotid stenosis:
| Trial | Year | N | Population | Key Findings |
|---|---|---|---|---|
| SAPPHIRE | 2004 | 334 | High-surgical-risk; ~70% asymptomatic, ~30% symptomatic; >50% symptomatic or >80% asymptomatic stenosis | CAS noninferior to CEA for primary composite (death, stroke, or MI at 30 days plus death or ipsilateral stroke to 1 year): 12.2% CAS vs 20.1% CEA (P=0.004 for noninferiority). Benefits maintained at 3 years.[1][3] |
| EVA-3S | 2006 | 527 | Symptomatic; ≥60% stenosis | Stopped early. 30-day stroke or death: 9.6% CAS vs 3.9% CEA (P=0.01).[4] |
| SPACE | 2006 | 1,214 | Symptomatic; ≥50% stenosis | 30-day stroke or death: 7.4% CAS vs 6.6% CEA; failed to prove noninferiority of CAS.[4] |
| ICSS | 2010 | 1,713 | Symptomatic; ≥50% stenosis | 30-day stroke, death, or procedural MI: 8.5% CAS vs 5.2% CEA (P=0.006). At 5 years, fatal or disabling stroke did not differ significantly.[5][4] |
| CREST | 2010 | 2,502 | Symptomatic (1,321) and asymptomatic (1,181); ≥50% symptomatic or ≥60% asymptomatic stenosis by angiography | No significant difference in primary composite (periprocedural stroke, MI, or death plus ipsilateral stroke at 4 years): 7.2% CAS vs 6.8% CEA (P=0.51). Periprocedural stroke higher with CAS (4.1% vs 2.3%; P=0.01); periprocedural MI higher with CEA (2.3% vs 1.1%; P=0.03). At 10 years: 11.8% CAS vs 9.9% CEA (HR 1.10; 95% CI 0.83–1.44).[2][6] |
CAS vs CEA in Asymptomatic Patients
| Trial | Year | N | Key Findings |
|---|---|---|---|
| ACST-2 | 2021 | 3,625 | Procedural disabling stroke or death: ~1% in both groups. 5-year nonprocedural stroke: 5.3% CAS vs 4.5% CEA (RR 1.16; P=0.33). No significant difference between CAS and CEA.[7] |
| ACT-1 | 2016 | 1,453 | Procedural stroke or death: 2.9% CAS vs 1.7% CEA (not significant). 5-year outcomes comparable.[4][8] |
Revascularization vs Medical Therapy Alone (Asymptomatic Stenosis)
| Trial | Year | N | Key Findings |
|---|---|---|---|
| CREST-2 (Stenting Arm) | 2026 | 1,245 | CAS + intensive medical therapy vs intensive medical therapy alone. 4-year primary outcome (stroke or death): 2.8% CAS + medical therapy vs 6.0% medical therapy alone (P=0.02; NNT=31).[9] |
| CREST-2 (CEA Arm) | 2026 | 1,240 | CEA + intensive medical therapy vs intensive medical therapy alone. 4-year primary outcome: 3.7% CEA + medical therapy vs 5.3% medical therapy alone (P=0.24; not significant).[9] |
| ECST-2 | 2025 | 429 | Low-to-intermediate stroke risk patients (asymptomatic or symptomatic). 2-year interim results: no benefit of revascularization over optimized medical therapy alone (win ratio 1.01; P=0.97).[10] |
| Meta-analysis (Gao et al.) | 2026 | 3,426 | Pooled analysis of SPACE-2, ECST-2, and CREST-2. No significant difference between revascularization and medical management for the primary composite outcome (RR 0.91; 95% CI 0.47–1.74; P=0.77).[11] |
Cochrane Systematic Review
A 2020 Cochrane review of 8 trials found that CEA conferred benefit over CAS for early stroke or death (40 vs 66 per 1,000 patients). This benefit was maintained at ≥4 years (235 vs 273 per 1,000). Cranial nerve palsy was less frequent with CAS (5 vs 51 per 1,000). No clear benefit of CEA over CAS was observed in patients aged <70 years.[12]
A meta-analysis of 13 randomized controlled trials (7,484 patients) confirmed that CAS was associated with a higher risk of any stroke (RR 1.45; 95% CI 1.06–1.99) but a lower risk of periprocedural myocardial infarction (RR 0.43; 95% CI 0.26–0.71) compared to CEA.[13]
Transcarotid Artery Revascularization (TCAR)
TCAR has emerged as an alternative to transfemoral CAS (tfCAS), with growing registry data suggesting improved periprocedural outcomes:
A Vascular Quality Initiative (VQI) analysis of 198,166 procedures (2016–2023) reported stroke/death rates of 1.6% for TCAR vs 2.9% for tfCAS (aOR 1.84 for tfCAS vs TCAR; P<0.001). CEA had the lowest rate at 1.3% (aOR 0.83 for CEA vs TCAR; P<0.001).[14]
TCAR was safer than tfCAS regardless of aortic arch type or degree of atherosclerosis.[15]
The ROADSTER-1 and ROADSTER-2 trials demonstrated a combined periprocedural stroke rate of 0.6% and combined stroke/death rate of 1.2% in symptomatic patients undergoing TCAR.[16]
Indications
The aim of CAS is to prevent the adverse sequelae of carotid artery stenosis secondary to atherosclerotic disease, primarily stroke.
Symptomatic Patients
CAS is indicated for symptomatic patients (TIA or nondisabling stroke within the preceding 6 months) with ≥50% carotid stenosis by angiography (or ≥70% by noninvasive imaging), provided the anticipated rate of periprocedural stroke or death is <6%.[8][17]
CAS may be preferred over CEA in symptomatic patients who are:
Aged <70 years (where CAS and CEA outcomes are comparable)[12]
At high surgical risk for CEA (see below)
With unfavorable neck anatomy for surgery
Revascularization should typically occur within 2 weeks after symptom onset.[13]
Asymptomatic Patients
CAS is indicated for asymptomatic patients with ≥70% stenosis (by validated duplex ultrasound) or ≥80% stenosis (by CTA or MRA), provided the anticipated rate of periprocedural stroke or death is <3%, and the patient has a life expectancy of at least 3–5 years.[8][17]
The CREST-2 trial demonstrated that CAS plus intensive medical therapy was superior to intensive medical therapy alone for asymptomatic carotid stenosis (4-year stroke or death: 2.8% vs 6.0%; P=0.02).[9] However, the ECST-2 interim results and a pooled meta-analysis did not show a significant benefit of revascularization over optimized medical therapy alone.[10][11]
High-Risk Features Favoring CAS Over CEA
CAS is particularly considered in patients with at least one anatomic or comorbid risk factor placing them at high risk for adverse events from CEA:
Anatomic Risk Factors:
Contralateral carotid artery occlusion
Contralateral laryngeal nerve palsy
Scarring of the neck post radiation therapy or following neck surgery
Recurrent stenosis after prior carotid endarterectomy
High cervical carotid artery lesions (distal to the second cervical vertebra)
Carotid artery stenosis below the clavicle or proximal (intrathoracic) arterial stenosis
Previous carotid endarterectomy
Contralateral vocal cord paralysis
Comorbid Conditions:
Congestive heart failure (NYHA Class III/IV) and/or known severe left ventricular dysfunction (LVEF ≤30%)
Open-heart surgery needed within 6 weeks
Recent myocardial infarction (>24 hours and <4 weeks)
Unstable angina (CCS class III/IV)
Synchronous severe cardiac and carotid disease requiring open heart surgery and carotid revascularization
Severe pulmonary disease (chronic oxygen therapy, resting PO2 <60 mmHg, baseline hematocrit >50%, FEV1 or DLCO <50% of normal)
Abnormal stress test
Age greater than 80 years (note: age >80 is also associated with higher CAS periprocedural risk)[17][1]
Carotid Revascularization in Patients Undergoing CABG
Symptomatic Stenosis
CAS (with embolic protection) before or concurrent with CABG is reasonable in patients with >80% stenosis who have experienced ipsilateral retinal or hemispheric cerebral ischemic symptoms within 6 months (Class I, Level C).[17]
Asymptomatic Stenosis
The safety and efficacy of carotid revascularization before or concurrent with myocardial revascularization are not well established (Class IIb, Level C).[17]
Risk Stratification
High-Risk Lesion Characteristics
Evidence of intraluminal thrombus thought to increase the risk of plaque fragmentation and distal embolization
Lesion(s) that may require more than two stents
Very tortuous lesions
Total occlusion of the target vessel
Lesions of the ostium of the common carotid artery
Highly calcified lesions resistant to balloon inflation
Concurrent treatment of bilateral lesions
High-Risk Access Characteristics
Patients with known peripheral vascular, supra-aortic, or internal carotid artery tortuosity that would preclude the use of catheter-based techniques
Type III aortic arch anatomy (strongly associated with increased periprocedural risk with transfemoral CAS)[15]
Patients in whom femoral or brachial access is not possible
High-Risk Patient Characteristics
Patients at low-to-moderate risk for adverse events from carotid endarterectomy (where CEA is generally preferred)
Patients experiencing acute ischemic neurologic stroke or who experienced a stroke within 48 hours
Patients with an intracranial mass lesion (i.e., abscess, tumor, or infection) or aneurysm (>9 mm)
Patients with arteriovenous malformations of the territory of the target carotid artery
Patients with coagulopathies
Patients with poor renal function, who may be at high risk for a reaction to contrast medium
Patients with perforated vessels evidenced by extravasation of contrast media
Patients with aneurysmal dilation immediately proximal or distal to the lesion
Pregnant patients or patients under the age of 18
Age as a Risk Modifier
Age is an important modifier of CAS outcomes. The Cochrane review demonstrated no clear benefit of CEA over CAS in patients aged <70 years, whereas patients aged ≥70 years had significantly better outcomes with CEA.[12] CAS may be preferred in younger symptomatic patients, while CEA may be preferred in older patients.[4]
Stenting (CAS) vs Carotid Endarterectomy (CEA)
Outcomes
A meta-analysis by Sardar et al. (2017) demonstrated that CAS was associated with lower periprocedural myocardial infarction (OR ~0.5) but higher periprocedural stroke (~double) compared to CEA.[18]
Key comparative findings across trials:
Periprocedural stroke: Higher with CAS than CEA (CREST: 4.1% vs 2.3%, P=0.01)[2]
Periprocedural MI: Higher with CEA than CAS (CREST: 2.3% vs 1.1%, P=0.03)[2]
Cranial nerve palsy: Significantly less frequent with CAS (5 vs 51 per 1,000)[12]
Long-term ipsilateral stroke: No significant difference at 10 years (CREST: 6.9% CAS vs 5.6% CEA; HR 0.99)[6]
Restenosis: Moderate (≥50%) restenosis more frequent after CAS; severe (≥70%) restenosis rates similar (5–12% CAS vs 8–10% CEA at 5–10 years). Restenosis after CEA (but not CAS) was associated with increased stroke risk.[5][4]
- Summary table comparing CAS vs CEA recommendations by symptom status and stenosis severity
- [17]
| Symptomatic Patients | Asymptomatic Patients | ||
|---|---|---|---|
| 50–69% Stenosis | 70–99% Stenosis | 70–99% Stenosis | |
| Endarterectomy | Class I | Class I | Class IIa |
| Level of Evidence | B | A | A |
| Stenting | Class I | Class I | Class IIb |
| Level of Evidence | B | B | B |
Scenarios Where Carotid Endarterectomy is Preferred
CEA is generally preferred in the setting of:
Age ≥70 years (particularly in symptomatic patients)[12]
Impaired renal function with increased risk of contrast-induced nephropathy
A tortuous, calcified aorta
Complex, eccentric, calcified lesions
Severe aortic arch atherosclerosis[4]
Scenarios Where Carotid Artery Stenting is Preferred
CAS is generally preferred in the setting of:
Neck anatomy unfavorable for arterial surgery (Class IIa, Level B)
High carotid bifurcation where it is technically difficult for surgeons to perform the surgery
Arterial stenosis distal to the second cervical vertebra or proximal (intrathoracic) arterial stenosis
Previous ipsilateral carotid endarterectomy
Contralateral vocal cord paralysis
History of previous radical neck surgery
History of radiation therapy[17]
Age <70 years in symptomatic patients[12]
Procedure
Patient Preparation
Informed consent obtained
Dual antiplatelet therapy (DAPT): Aspirin 325 mg plus clopidogrel 75 mg initiated at least 48 hours prior to the procedure. Alternatives for clopidogrel-intolerant patients include ticagrelor 60–90 mg twice daily or prasugrel 5–10 mg daily.[9][4]
Pre-procedural statin therapy is reinforced[19]
Local anesthetic administered (general anesthesia is discouraged for transfemoral CAS)[19]
Transfemoral CAS Technique
Preparation of both groins with antiseptic and draping
Puncture into femoral artery and access through short sheath
Guidewire passed through aorta and into the aortic arch
Arch aortogram obtained if not previously performed to confirm suitability to continue
Selective carotid and cerebral angiogram performed
Long access sheath or guide catheter placed after cannulation of common carotid artery (CCA)
Guidewire passed through area of carotid narrowing
Placement of embolic protection device (EPD) above the area of narrowing (distal filter) or proximal flow-reversal device
Pre-dilation angioplasty of carotid narrowing (optional; many operators proceed directly to stent deployment)
Deployment of stent into area of narrowing
Post-stent angioplasty (with caution; balloons >5.0 mm are discouraged)[19]
Removal of protection device, guidewires, and sheath
Aftercare of groin puncture site
Intraprocedural anticoagulation with heparin (target activated clotting time 250–300 seconds)
Transcarotid Artery Revascularization (TCAR) Technique
Direct surgical exposure of the common carotid artery in the neck via a small incision
Arterial sheath inserted directly into the CCA
Establishment of temporary carotid flow reversal via an arteriovenous circuit (CCA to internal jugular vein) for cerebral embolic protection
Stent deployment under flow reversal
Restoration of antegrade flow and closure of the arteriotomy
Embolic Protection Devices
Embolic protection is considered essential during CAS to reduce the risk of distal cerebral embolism:[17][16]
Distal filter devices:
Capture embolic debris on a filter placed distal to the lesion in the internal carotid artery
Examples: Rx Accunet, Emboshield Nav6, FilterWire EZ, Angioguard, Spider Fx, Gore embolic filter[19]
Proximal flow-reversal/occlusion devices:
Achieve cerebral protection by reversing or arresting flow in the ICA during the procedure
Examples: MoMa device, Gore flow-reversal device[19]
Associated with fewer microembolic signals on transcranial Doppler compared to distal filters
Stent Types
First-generation stents:
Open-cell design (e.g., Acculink, Wallstent, Precise): Greater flexibility and conformability to vessel anatomy but larger free cell area, which may allow plaque prolapse.[20]
Closed-cell design (e.g., Xact): Smaller free cell area providing better plaque coverage but less conformability.[20]
Second-generation (dual-layer/mesh-covered) stents:
Feature an inner mesh layer designed to trap and exclude plaque debris from the vessel lumen, reducing distal embolization.
Examples: CGuard (InspireMD), Roadsaver/Casper (Terumo/MicroVention).
A systematic review and meta-analysis of 68,422 patients demonstrated significantly lower 30-day death/stroke/MI rates with second-generation stents compared to first-generation stents (1.30% vs 4.11%; P<0.01).[20]
A patient-based meta-analysis of 556 patients treated with dual-layer stents reported a 30-day stroke rate of 1.25% and 30-day mortality of 0.17%.[21]
Complications
Periprocedural Stroke
Periprocedural stroke is the most significant complication of CAS. In the CREST trial, the periprocedural stroke rate was 4.1% for CAS vs 2.3% for CEA (P=0.01).[2] The risk is higher in patients aged ≥70 years, those with severe aortic arch atherosclerosis, and those with tortuous vascular anatomy.[12][4]
Cerebral Hyperperfusion Syndrome
Cerebral hyperperfusion syndrome (CHS) is a potentially life-threatening complication characterized by ipsilateral headache, seizures, focal neurologic deficits, and/or intracerebral hemorrhage occurring after restoration of normal carotid blood flow.
Pooled CHS risk after CAS: 4.6% (meta-analysis).[22]
VQI data: CHS incidence 0.15% CEA, 0.18% TCAR, 0.53% tfCAS.[23]
Risk factors include: impaired cerebrovascular reserve, contralateral carotid stenosis ≥70%, and post-procedure hypertension.[22][23]
Strict blood pressure control (systolic <140 mmHg) in the periprocedural period is essential for prevention.[22]
Hemodynamic Complications
Bradycardia and hypotension due to baroreflex stimulation during stent deployment at the carotid sinus occur in 5–10% of CAS cases. These are usually transient but may require atropine or temporary pacing.[17]
Sustained hemodynamic depression (>1 hour) is more common in patients with contralateral carotid stenosis and calcified lesions.
Other Complications
Myocardial infarction: ~1% (lower than with CEA)[2]
Arterial dissection or thrombosis: <1%
Cranial nerve palsy: Rare with CAS (5 per 1,000 vs 51 per 1,000 with CEA)[12]
Access site complications (hematoma, pseudoaneurysm, arteriovenous fistula)
In-stent restenosis (see below)
Post-Procedural Care and Long-Term Management
Immediate Post-Procedural Care
Neurologic monitoring for at least 24 hours post-procedure
Strict blood pressure control: systolic blood pressure <140 mmHg to reduce the risk of cerebral hyperperfusion syndrome[22]
Monitoring for hemodynamic instability (bradycardia, hypotension)
Groin/access site assessment
Antithrombotic Therapy
Dual antiplatelet therapy (DAPT): Aspirin 325 mg plus clopidogrel 75 mg daily for a minimum of 30 days post-procedure[4][9]
After 30 days: Aspirin (81–325 mg) continued indefinitely
Alternatives for clopidogrel-intolerant patients: ticagrelor 60–90 mg twice daily or prasugrel 5–10 mg daily[4]
Medical Therapy Optimization
Intensive medical therapy is a critical component of long-term management regardless of revascularization status:
Statin therapy: High-intensity statin (e.g., atorvastatin 40–80 mg or rosuvastatin 20–40 mg) with target LDL cholesterol <70 mg/dL[9]
Antihypertensive therapy: Target blood pressure <130/80 mmHg
Diabetes mellitus management: Target HbA1c <7%
Lifestyle modifications: Exercise, Mediterranean diet, weight management
Surveillance for Restenosis
Duplex ultrasound surveillance is recommended post-CAS to monitor for in-stent restenosis.
Moderate (≥50%) restenosis is more frequent after CAS than CEA; however, severe (≥70%) restenosis rates are similar (5–12% CAS vs 8–10% CEA at 5–10 years).[5][4]
Restenosis after CEA (but not CAS) was associated with increased stroke risk in the ICSS secondary analysis.[5]
Annual stroke risk with severe in-stent restenosis is approximately 1%.[4]
Suggested surveillance schedule: duplex ultrasound at 1 month, 6 months, and 12 months post-procedure, then annually thereafter.[16]
Treatment Algorithm
The following algorithm summarizes the approach to management of carotid stenosis:
Step 1: Determine Symptom Status
Symptomatic: TIA or nondisabling stroke within the preceding 6 months
Asymptomatic: Incidental finding on imaging
Step 2: Confirm Degree of Stenosis
Noninvasive imaging: Duplex ultrasound, CTA, or MRA
Catheter angiography if noninvasive results are discordant
Step 3: Assess Candidacy for Revascularization
| Clinical Scenario | Recommended Approach |
|---|---|
| Symptomatic, ≥50% stenosis (angiography) or ≥70% (noninvasive), standard surgical risk | CEA preferred (Class I); CAS acceptable alternative especially if age <70 years[17][12] |
| Symptomatic, ≥50% stenosis, high surgical risk for CEA | CAS with EPD (Class I)[17][1] |
| Asymptomatic, ≥70% stenosis (duplex) or ≥80% (CTA/MRA), life expectancy ≥3–5 years | CEA or CAS with intensive medical therapy; benefit of revascularization over medical therapy alone remains debated[9][10][11] |
| Asymptomatic, <70% stenosis | Intensive medical therapy alone[8] |
| Symptomatic, <50% stenosis | Medical therapy alone[17] |
Step 4: Choose Revascularization Modality
CEA preferred: Age ≥70 years, severe aortic arch disease, tortuous anatomy, calcified lesions, impaired renal function
CAS (transfemoral) preferred: Hostile neck (prior surgery, radiation, high bifurcation), contralateral vocal cord paralysis, age <70 years
TCAR preferred: When CAS is indicated but unfavorable aortic arch anatomy (Type III arch, severe arch atherosclerosis) precludes safe transfemoral access[14][15]
Step 5: Optimize Medical Therapy
All patients should receive intensive medical therapy regardless of revascularization decision: high-intensity statin, antiplatelet therapy, blood pressure control, diabetes management, and smoking cessation.[9]
External links
References
- ↑ 1.0 1.1 1.2 1.3 Yadav JS, Wholey MH, Kuntz RE, et al. (2004). "Protected carotid-artery stenting versus endarterectomy in high-risk patients". N Engl J Med. 351 (15): 1493–1501. doi:10.1056/NEJMoa040127. PMID 15470212.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Brott TG, Hobson RW, Howard G, et al. (2010). "Stenting versus endarterectomy for treatment of carotid-artery stenosis". N Engl J Med. 363 (1): 11–23. doi:10.1056/NEJMoa0912321. PMID 20505173.
- ↑ Gurm HS, Yadav JS, Fayad P, et al. (2008). "Long-term results of carotid stenting versus endarterectomy in high-risk patients". N Engl J Med. 358 (15): 1572–1579. doi:10.1056/NEJMoa0708028. PMID 18354102.
- ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 Bonati LH, Jansen O, de Borst GJ, Brown MM (2022). "Management of atherosclerotic extracranial carotid artery stenosis". Lancet Neurol. 21 (3): 273–283. doi:10.1016/S1474-4422(21)00359-8. PMID 35065036 Check
|pmid=value (help). - ↑ 5.0 5.1 5.2 5.3 Bonati LH, Gregson J, Dobson J, et al. (2018). "Restenosis and risk of stroke after stenting or endarterectomy for symptomatic carotid stenosis in the International Carotid Stenting Study (ICSS): secondary analysis of a randomised trial". Lancet Neurol. 17 (7): 587–596. doi:10.1016/S1474-4422(18)30195-9. PMID 29861139.
- ↑ 6.0 6.1 Brott TG, Howard G, Roubin GS, et al. (2016). "Long-term results of stenting versus endarterectomy for carotid-artery stenosis". N Engl J Med. 374 (11): 1021–1031. doi:10.1056/NEJMoa1505215. PMID 26886419.
- ↑ Halliday A, Bulbulia R, Bonati LH, et al. (2021). "Second Asymptomatic Carotid Surgery Trial (ACST-2): a randomised comparison of carotid artery stenting versus carotid endarterectomy". Lancet. 398 (10305): 1065–1073. doi:10.1016/S0140-6736(21)01910-3. PMID 34469763 Check
|pmid=value (help). - ↑ 8.0 8.1 8.2 8.3 White CJ, Brott TG, Gray WA, et al. (2022). "Carotid artery stenting: JACC state-of-the-art review". J Am Coll Cardiol. 80 (2): 155–170. doi:10.1016/j.jacc.2022.05.005.
- ↑ 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.7 Brott TG, Howard G, Lal BK, et al. (2026). "Medical management and revascularization for asymptomatic carotid stenosis". N Engl J Med. doi:10.1056/NEJMoa2411488. PMID 41269206 Check
|pmid=value (help). - ↑ 10.0 10.1 10.2 Donners S, van Velzen TJ, Cheng SF, et al. (2025). "Optimised medical therapy alone versus optimised medical therapy plus revascularisation for asymptomatic or low-to-intermediate risk symptomatic carotid stenosis (ECST-2): 2-year interim results of a multicentre randomised trial". Lancet Neurol. 24 (5): 389–399. doi:10.1016/S1474-4422(25)00107-3. PMID 40252662 Check
|pmid=value (help). Vancouver style error: initials (help) - ↑ 11.0 11.1 11.2 Gao Y, Wang L, Zhang H, et al. (2026). "Medical management and revascularization for asymptomatic carotid stenosis: a meta-analysis of randomized controlled trials". J Neurol. 273 (4): 220. doi:10.1007/s00415-026-13766-5. PMID 41860631 Check
|pmid=value (help). - ↑ 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.7 12.8 Müller MD, Lyrer P, Brown MM, Bonati LH (2020). "Carotid artery stenting versus endarterectomy for treatment of carotid artery stenosis". Cochrane Database Syst Rev. 2: CD000515. doi:10.1002/14651858.CD000515.pub5. PMID 32096560 Check
|pmid=value (help). - ↑ 13.0 13.1 Furie KL, Kelly PJ (2026). "Secondary prevention after ischemic stroke". N Engl J Med. doi:10.1056/NEJMra2404772.
- ↑ 14.0 14.1 Straus S, Yadavalli SD, Allievi S, et al. (2024). "Seven years of the transcarotid artery revascularization surveillance project, comparison to transfemoral stenting and endarterectomy". J Vasc Surg. 80 (4): 1072–1082. doi:10.1016/j.jvs.2024.05.040. PMID 38821431 Check
|pmid=value (help). - ↑ 15.0 15.1 15.2 Hamouda M, Alqrain S, Zarrintan S, et al. (2024). "Transcarotid artery revascularization outperforms transfemoral carotid artery stenting regardless of aortic arch type or degree of atherosclerosis". J Vasc Surg. doi:10.1016/j.jvs.2024.08.030. PMID 39134214 Check
|pmid=value (help). - ↑ 16.0 16.1 16.2 AbuRahma AF, Avgerinos ED, Chang RW, et al. (2022). "The Society for Vascular Surgery implementation document for management of extracranial cerebrovascular disease". J Vasc Surg. 75 (1): 26S–98S. doi:10.1016/j.jvs.2021.04.074.
- ↑ 17.00 17.01 17.02 17.03 17.04 17.05 17.06 17.07 17.08 17.09 17.10 17.11 Brott TG, Halperin JL, Abbara S, et al. (2011). "2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management of patients with extracranial carotid and vertebral artery disease". J Am Coll Cardiol. 57 (8): e16–e94. doi:10.1016/j.jacc.2010.11.006.
- ↑ Sardar P, Chatterjee S, Aronow HD, et al. (2017). "Carotid artery stenting versus endarterectomy for stroke prevention: a meta-analysis of clinical trials". J Am Coll Cardiol. 69 (18): 2266–2275. doi:10.1016/j.jacc.2017.02.053.
- ↑ 19.0 19.1 19.2 19.3 19.4 Lal BK, Roubin GS, Rosenfield K, et al. (2019). "Quality assurance for carotid stenting in the CREST-2 registry". J Am Coll Cardiol. 74 (25): 3071–3079. doi:10.1016/j.jacc.2019.10.031.
- ↑ 20.0 20.1 20.2 Mazurek A, Malinowski K, Rosenfield K, et al. (2022). "Clinical outcomes of second- versus first-generation carotid stents: a systematic review and meta-analysis". J Clin Med. 11 (17): 5003. doi:10.3390/jcm11175003. PMID 36013058 Check
|pmid=value (help). - ↑ Stabile E, de Donato G, Musialek P, et al. (2018). "Use of dual-layered stents in endovascular treatment of extracranial stenosis of the internal carotid artery: results of a patient-based meta-analysis of 4 clinical studies". JACC Cardiovasc Interv. 11 (22): 2324–2331. doi:10.1016/j.jcin.2018.06.050.
- ↑ 22.0 22.1 22.2 22.3 Huibers AE, Westerink J, de Vries EE, et al. (2018). "Editor's choice - Cerebral hyperperfusion syndrome after carotid artery stenting: a systematic review and meta-analysis". Eur J Vasc Endovasc Surg. 56 (3): 322–333. doi:10.1016/j.ejvs.2018.05.012. PMID 30196814.
- ↑ 23.0 23.1 Hsu AC, Williams B, Ding L, et al. (2023). "Risk factors for cerebral hyperperfusion syndrome following carotid revascularization". Ann Vasc Surg. 95: 198–206. doi:10.1016/j.avsg.2023.05.040. PMID 37356658 Check
|pmid=value (help).