Successful Carotid Endarterectomy for Carotid Web Presenting with Recurrent Ischemic Stroke in an Elderly Patient: A Case Report

Article information

J Neurosonol Neuroimag. 2026;18(1):39-43
Publication date (electronic) : 2026 June 30
doi : https://doi.org/10.31728/jnn.2026.00181
Stroke Center, Department of Neurology, Biomedical Research Institute, Pusan National University Hospital, School of Medicine, Pusan National University, Busan, Korea
Correspondence: Yoon Jung Kang, MD Stroke Center, Department of Neurology, Biomedical Research Institute, Pusan National University Hospital, School of Medicine, Pusan National University, 179 Gudeok-ro, Seo-gu, Busan 49241, Korea Tel: +82-51-240-7317 Fax: +82-51-245-2783 E-mail: entire2387@naver.com
Received 2026 May 7; Revised 2026 June 15; Accepted 2026 June 24.

Abstract

Carotid web is an intimal variant of fibromuscular dysplasia that has been increasingly recognized as a cause of embolic stroke. Although typically reported in younger individuals, it may also present in elderly patients and can be underrecognized due to overlapping atherosclerotic features. We report a 73-year-old woman who presented with transient left arm weakness and was found to have acute infarction in the right frontal lobe with a shelf-like filling defect in the proximal internal carotid artery. Despite antiplatelet therapy, she developed recurrent ischemic stroke one week later, with imaging showing new infarctions and progression of the filling defect. Digital subtraction angiography confirmed carotid web with superimposed thrombus. Carotid endarterectomy was performed, enabling complete removal of the lesion and thrombus. The patient remained free of recurrent stroke at one-year follow-up. This case highlights that carotid web should be considered regardless of age and that surgical management may prevent recurrence.

Carotid web (CaW) is a rare vascular abnormality characterized by a shelf-like projection of fibrotic intimal tissue into the lumen of the carotid bulb.1 Although typically reported in younger individuals, carotid web may remain clinically silent and become manifest later in life, particularly in elderly patients, where it can be underrecognized due to overlapping atherosclerotic features.2-4 Importantly, CaW is associated with a high recurrence rate of embolic stroke despite medical therapy, whereas carotid revascularization has been shown to reduce the risk of recurrence.5 We report a case of recurrent ischemic stroke caused by CaW in a 73-year-old woman who was successfully treated with carotid endarterectomy (CEA).

CASE

A 73-year-old woman presented to the emergency department with sudden onset of left arm weakness that had occurred one hour prior to arrival. The neurological symptoms lasted several minutes and resolved spontaneously. On examination, her National Institutes of Health Stroke Scale (NIHSS) score was 0. One month earlier, she had been diagnosed with diabetes mellitus (DM) but had not taken the prescribed medication. She had no history of prior stroke or transient ischemic attack, was a non-smoker, and had no other conventional vascular risk factors. Laboratory evaluation revealed marked hyperglycemia with a serum glucose level of 424 mg/dL and a glycated hemoglobin level of 12.84%. Low-density lipoprotein cholesterol was 133 mg/dL, and D-dimer was 0.52 μg/mL. Complete blood count as well as renal and liver function tests were within normal limits. No potential cardioembolic source was identified on electrocardiography or transthoracic echocardiography.

Non-contrast brain computed tomography (CT) showed no acute abnormalities. Brain magnetic resonance imaging (MRI) demonstrated acute ischemic lesions in the right frontal region (Fig. 1A). Magnetic resonance angiography (MRA) revealed a shelf-like intraluminal projection arising from the posterior wall of the proximal right internal carotid artery (ICA) and extending into the lumen without causing significant stenosis, consistent with the characteristic imaging appearance of carotid web (Fig. 1B). At the time of treatment decision, the patient had complete resolution of symptoms with no residual neurological deficits (NIHSS score 0). Because the symptoms were no longer present and were considered non-disabling, intravenous thrombolytic therapy was not administered. During hospitalization, glycemic control was initiated with combination oral antidiabetic therapy. The patient was treated with dual antiplatelet therapy consisting of aspirin 100 mg and clopidogrel 75 mg, together with high-intensity statin therapy (atorvastatin 40 mg daily). She was discharged on hospital day 9 without neurological deterioration.

Fig. 1.

(A, B) At the initial event, diffusion-weighted imaging (DWI) demonstrated discrete acute ischemic lesions in the right frontal lobe (A), and magnetic resonance angiography (MRA) revealed a shelf-like filling defect (red arrow) in the right carotid bulb (B). (C, D) On follow-up imaging, DWI showed newly developed acute infarcts in the right frontal cortex and subcortical white matter within the external and internal watershed territories (C), while MRA demonstrated extension of the filling defect (red arrow) at the site of the carotid web (CaW) (D). (E, F) Computed tomography perfusion imaging obtained during the recurrent event. Cerebral blood flow map (E) and time-to-maximum map (F) demonstrated no significant perfusion deficit or substantial salvageable penumbra. (G) Digital subtraction angiography showed CaW (red arrow) of the right internal carotid artery with distal intraluminal thrombosis (white arrow). (H) CaW (black arrow) and red thrombus (white arrow) were observed during operation.

One week after discharge, the patient was readmitted with newly developed left hemiplegia and dysarthria noted upon awakening. On arrival, her NIHSS score was 9, with deficits involving the left upper and lower extremities and dysarthria. Brain MRI demonstrated newly developed acute ischemic lesions in the right frontoparietal region superimposed on the previous infarcts (Fig. 1C). MRA showed progressive enlargement of the shelf-like filling defect at the site of the carotid web in the proximal right ICA, resulting in a more prominent intraluminal projection than on the initial examination, suggestive of evolving thrombus associated with the carotid web (Fig. 1D). As the patient presented with a wake-up stroke, imaging-based eligibility for reperfusion therapy was assessed. CT perfusion imaging did not demonstrate a significant perfusion deficit or substantial salvageable penumbra (Fig. 1E, 1F). Therefore, acute reperfusion therapy was not pursued.

To further characterize the vascular abnormality, digital subtraction angiography (DSA) was performed the following day. Angiography demonstrated a filling defect consistent with CaW, with a superimposed intraluminal thrombus in the distal portion (Fig. 1G). Given the recurrent ischemic events despite dual antiplatelet therapy and high-intensity statin treatment, together with the presence of a superimposed thrombus, surgical intervention was considered. CEA was planned to remove both the thrombus and the underlying web structure in order to prevent further thrombus formation and recurrent embolic events. In preparation for surgery, clopidogrel was discontinued 5 days before the procedure, while aspirin was continued.

After stabilization of the acute neurological deficits and completion of diagnostic evaluation, CEA was performed on hospital day 8. Intraoperatively, a web-like intimal structure projecting into the lumen of the ICA was identified, along with an attached thrombus (Fig. 1H). An intraoperative shunt was used to maintain cerebral blood flow during carotid cross-clamping, and patch angioplasty was performed using bovine pericardium after endarterectomy. Complete removal of the thrombus and CaW was successfully achieved without perioperative complications. Postoperatively, no neurological deterioration was observed. Follow-up CT angiography demonstrated no residual abnormality in the proximal right ICA. After CEA, the patient was maintained on clopidogrel and high-intensity statin therapy, together with continued management of vascular risk factors including DM. The patient’s neurological deficits gradually improved during hospitalization, and she was transferred to a rehabilitation facility on postoperative day 8 with an NIHSS score of 6 and a modified Rankin Scale (mRS) score of 3. At one-year follow-up, she had mild residual neurological deficits with an mRS score of 2 and remained free of recurrent ischemic stroke.

DISCUSSION

CaW has been increasingly recognized as a potential cause of cryptogenic ischemic stroke. Although traditionally described in younger patients, recent studies suggest that CaW can occur across a broader age range and may remain clinically silent until a thromboembolic event occurs.3-6 In elderly patients, CaW may be overlooked or misattributed to atherosclerotic disease, potentially leading to underdiagnosis.

The diagnosis of CaW is primarily based on characteristic imaging findings. On brain CT angiography and MRA, CaW typically appears as a thin shelf-like intraluminal projection arising from the posterior wall of the carotid bulb or proximal ICA.1,7 On DSA, it is visualized as a linear or triangular filling defect projecting into the lumen, often accompanied by delayed contrast clearance distal to the lesion.8 These features help distinguish CaW from atherosclerotic plaque, which generally presents as a broader-based lesion associated with calcification, lipid-rich components, or irregular luminal narrowing.

The proposed mechanism of ischemic stroke in CaW involves flow stagnation and disturbed flow distal to the web, creating a prothrombotic environment that promotes thrombus formation and embolization. These pathological flow characteristics appear to be driven by the geometry of the web itself rather than by the degree of luminal stenosis.9,10 In the present case, serial MRA demonstrated interval enlargement of the intraluminal filling defect before DSA confirmation of thrombus, suggesting ongoing thrombus formation within the flow stagnation zone created by the web. Although the recurrent infarcts involved both external and internal watershed territories, significant cerebral hypoperfusion was not demonstrated on CT perfusion imaging. Together with the progressive enlargement of the filling defect and subsequent thrombus confirmation on DSA, these findings suggest that thromboembolism arising from the carotid web likely contributed to the recurrent ischemic events.

Previous studies have demonstrated a high risk of recurrent stroke in patients with symptomatic CaW treated with medical therapy alone, whereas carotid revascularization substantially reduces recurrence risk.2,5,7 In the present case, recurrent stroke occurred despite dual antiplatelet therapy, and serial MRA demonstrated progressive enlargement of the intraluminal filling defect with subsequent DSA confirmation of superimposed thrombus. Because ongoing thrombus formation and recurrent embolization were considered likely despite medical therapy, surgical intervention was pursued after neurological stabilization and completion of diagnostic evaluation. CEA was favored over CAS to allow direct removal of both the web and thrombus while avoiding the potential risk of distal embolization during endovascular manipulation. The patient remained free of recurrent stroke during one year of follow-up.

This report has several limitations. Carotid duplex ultrasonography, late venous-phase angiographic images, and histopathological examination of the resected specimen were not available. Nevertheless, the diagnosis was supported by characteristic serial MRA findings, angiographic confirmation of a corresponding filling defect with superimposed thrombus on DSA, and direct intraoperative visualization of a web-like intimal projection with attached thrombus.

Our study highlights that carotid web (CaW) should not be overlooked as a potential cause of recurrent ischemic stroke, even in elderly patients, and that superimposed thrombus formation may contribute to stroke recurrence. Recognition of CaW as a potential embolic source is therefore important regardless of patient age. In selected symptomatic patients who develop recurrent ischemic events despite medical therapy, particularly in the presence of superimposed thrombus, CEA may be considered to reduce the risk of further stroke recurrence.

Notes

Ethics Statement

This study was approved by the Institutional Review Board of Pusan National University Hospital. Written informed consent for publication of this case report and the accompanying images was obtained from the patient.

Availability of Data and Material

The data supporting the findings of this study are available from the corresponding author upon reasonable request.

Author Contributions

Sang Min Sung: Conceptualization, data collection, and manuscript drafting. Yoon Jung Kang: Manuscript drafting, critical revision of the manuscript, supervision, and final approval. All authors have read and approved the manuscript.

Acknowledgments

None.

Sources of Funding

This work was supported by a New Faculty Research Grant of Pusan National University, 2025.

Conflicts of Interest

The authors have no conflicts of interest to declare.

References

1. Choi PM, Singh D, Trivedi A, Qazi E, George D, Wong J, et al. Carotid webs and recurrent ischemic strokes in the era of CT angiography. AJNR Am J Neuroradiol 2015;36:2134–2139.
2. Guglielmi V, Compagne KCJ, Sarrami AH, Sluis WM, van den Berg LA, van der Sluijs PM, et al. Assessment of recurrent stroke risk in patients with a carotid web. JAMA Neurol 2021;78:826–833.
3. Olindo S, Chausson N, Signate A, Mecharles S, Hennequin JL, Saint-Vil M, et al. Stroke recurrence in first-ever symptomatic carotid web: A cohort study. J Stroke 2021;23:253–262.
4. Yang T, Yoshida K, Maki T, Fushimi Y, Yamada K, Okawa M, et al. Prevalence and site of predilection of carotid webs focusing on symptomatic and asymptomatic Japanese patients. J Neurosurg 2021;135:1370–1376.
5. Haynes J, Raz E, Tanweer O, Shapiro M, Esparza R, Zagzag D, et al. Endarterectomy for symptomatic internal carotid artery web. J Neurosurg 2020;135:1–8.
6. Wang Y, Li HL, Xu XH, Ye JH, Li J. New asymptomatic thrombosis caused by carotid web during the acute period of cerebral infarction. BMC Neurol 2023;23:264.
7. Ahmad M, Tan M, Abuarqoub M, Patel K, Siracusa F, Shalhoub J, et al. Carotid webs: a review of diagnosis and management strategies in current literature. J Vasc Soc G B Irel 2025;4:99–110.
8. Liang S, Qin P, Xie L, Niu S, Luo J, Chen F, et al. The carotid web: Current research status and imaging features. Front Neurosci 2023;17:1104212.
9. Compagne KCJ, Dilba K, Postema EJ, van Es ACGM, Emmer BJ, Majoie CBLM, et al. Flow patterns in carotid webs: A patient-based computational fluid dynamics study. AJNR Am J Neuroradiol 2019;40:703–708.
10. El Sayed R, Lucas CJ, Cebull HL, Nahab FB, Haussen DC, Allen JW, et al. Subjects with carotid webs demonstrate pro-thrombotic hemodynamics compared to subjects with carotid atherosclerosis. Sci Rep 2024;14:10092.

Article information Continued

Fig. 1.

(A, B) At the initial event, diffusion-weighted imaging (DWI) demonstrated discrete acute ischemic lesions in the right frontal lobe (A), and magnetic resonance angiography (MRA) revealed a shelf-like filling defect (red arrow) in the right carotid bulb (B). (C, D) On follow-up imaging, DWI showed newly developed acute infarcts in the right frontal cortex and subcortical white matter within the external and internal watershed territories (C), while MRA demonstrated extension of the filling defect (red arrow) at the site of the carotid web (CaW) (D). (E, F) Computed tomography perfusion imaging obtained during the recurrent event. Cerebral blood flow map (E) and time-to-maximum map (F) demonstrated no significant perfusion deficit or substantial salvageable penumbra. (G) Digital subtraction angiography showed CaW (red arrow) of the right internal carotid artery with distal intraluminal thrombosis (white arrow). (H) CaW (black arrow) and red thrombus (white arrow) were observed during operation.