INTRODUCTION
Carotid web (CW) is a well-documented but often under-recognized vascular anomaly increasingly identified as a significant mechanism of recurrent ischemic stroke, particularly in young patients with cryptogenic strokes. However, its management remains suboptimal, warranting greater awareness and standardized approaches in clinical practice.
CW is characterized as a shelf-like intimal projection into the lumen of the proximal internal carotid artery, likely representing a focal variant of fibromuscular dysplasia [1]. This structure disrupts laminar blood flow, creating regions of stasis that predispose to thrombus formation and subsequent embolism. The prevalence of CW in cryptogenic stroke populations has been reported to range from 9.4% to 34.0%, with notable ethnic and age-related variations [2-5].
Despite observational evidence linking CW with ischemic stroke recurrence, its optimal management remains uncertain. While antiplatelet therapy is commonly used, accumulating evidence suggests that carotid revascularization (endarterectomy or stenting) may be more effective in preventing recurrence, given the high relapse rates observed with medical therapy alone [6-9]. However, current prevention strategies lack robust evidence, leading to variability in practice.
Recurrent stroke is a major concern in CW, with rates up to 44% in some series [5,9-13]. These findings underscore the importance of early recognition and targeted interventions to mitigate the burden of recurrent ischemic events. A critical but underexplored issue is recurrent thrombus formation within CW, which may precede clinical stroke events. To our knowledge, no previous studies have emphasized acute monitoring of CW patients to detect early thrombus formation, which could provide a window for timely intervention.
This case series addresses both stroke recurrence and asymptomatic thrombus formation after endovascular treatment (EVT)—an underrecognized but clinically relevant risk. Because early thrombus often remains undetected without targeted imaging, we underscore the role of neuroimaging and neurosonology for early detection, risk stratification, and tailored treatment. Silent thrombi, identifiable only with close surveillance, may precede embolic events, reinforcing the importance of acute monitoring in CW management.
METHODS AND MATERIALS
Study Design and Patient Selection
We performed a retrospective analysis of patients diagnosed with CW at Dr. Balmis General University Hospital (a comprehensive stroke center in Spain). Among consecutive patients who presented with acute ischemic stroke between January 2021 and December 2024, cases with radiologically confirmed CW were identified.
Patients were included based on the presence of CW, defined as a shelf-like intimal projection into the proximal internal carotid artery lumen, identified by computed tomography angiography (CTA) or digital subtraction angiography (DSA). Clinical data—including demographic characteristics, vascular risk factors, imaging findings, stroke recurrence, and treatment modalities—were collected retrospectively from electronic medical records. An extensive etiological workup was performed in all cases according to current clinical guidelines to exclude alternative stroke mechanisms.
Imaging Definition of Carotid Web and Assessment of Patients
CW was defined on CTA as a thin, shelf-like intraluminal filling defect along the posterior wall of the carotid bulb just beyond the bifurcation [14]. The lesion was best appreciated on oblique sagittal reconstructions and appeared as a septum on axial sections. All CTA examinations were systematically reviewed by experienced neuroradiologists and neuroint-erventionists to ensure diagnostic consistency. On DSA, the CW lesion was suspected when a thin, shelf-like filling defect was observed at the posterior wall of the proximal internal carotid artery bulb, together with contrast stasis in the pocket rostral to the web [15]. All patients underwent a standardized etiological evaluation in accordance with Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria and American Heart Association/American Stroke Association (AHA/ASA) guidelines [16,17].
Early Ultrasound Monitoring
In patients who underwent EVT and were suspected of having CW, early duplex sonography was systematically performed within 48 hours post-procedure to detect in vivo thrombus formation. No standardized long-term imaging protocol was applied during the follow-up period, and additional imaging was performed at the discretion of the treating physician based on clinical evolution or suspicion of recurrence. All examinations were performed with the same Toshiba Aplio 500 ultrasound system (Canon Medical Systems), using a 7–12 MHz linear array transducer for cervical imaging and a 1–5 MHz phased array probe for transcranial insonation.
Statistical Analysis
We assessed recurrent ischemic events and thrombus reappearance during follow-up, along with secondary prevention strategies, including antiplatelet therapy and carotid intervention. Descriptive statistics summarized baseline and clinical data, with continuous variables reported as means±-standard deviation or medians [interquartile range], and categorical variables as counts and percentages. Patients were grouped by treatment—antiplatelet alone versus carotid intervention—and recurrence rates were compared descriptively. Given the small sample, no inferential analysis was conducted; results are hypothesis-generating. Clopper–Pearson 95% confidence intervals were used to illustrate uncertainty.
RESULTS
A total of 23 patients were identified with CW as the underlying cause of the acute ischemic stroke. Their demographic and clinical characteristics are summarized in Table 1. Most patients were female (n=14, 60.9%), with a mean age of 56.1±10.7 years at the time of their first stroke. The majority (n=19, 82.6%) received reperfusion therapy during the acute phase, including intravenous thrombolysis, EVT, or both.
Of the 23 patients, 11 were initially managed with antiplatelet therapy alone, and all 6 cases of recurrence (2 clinical strokes and 4 asymptomatic thrombi) occurred in this group, yielding a recurrence rate of 54.5% (6/11; 95% CI: 23.4–83.3%). In contrast, 12 patients underwent early carotid intervention (9 stenting and 3 endarterectomy) after the index event, and none of them experienced any clinical or radiologic recurrence during follow-up (0/12, 0.0%; 95% CI: 0.0–26.5%). While the study was not powered for inferential statistics, this observed difference suggests a potential protective effect of anatomical correction compared to antiplatelet therapy alone.
Recurrent ipsilateral ischemic stroke occurred in 2 patients (8.7%; 95% CI: 1.1–28.0%) despite secondary prevention. An additional 4 patients (17.4%; 95% CI: 5.0–38.8%) developed thrombus formation within the ipsilateral CW on follow-up imaging after initial stroke, in the absence of new neurological symptoms. An illustrative case of thrombus recurrence is shown in Fig. 1, demonstrated through sonography and CTA imaging. We present the post-endarterectomy results in Supplementary Fig. 1.
All 6 patients with evidence of recurrence (either clinical or radiographic) subsequently underwent definitive treatment of the CW—4 received carotid artery stenting and 2 underwent carotid endarterectomy (CEA), as detailed in Table 2. Among the 2 patients with recurrent stroke, all underwent EVT and acute stenting was performed during the endovascular procedure. In the remaining 4 cases, the choice of treatment was based on patient-specific factors and the availability of each procedure. All cases were reviewed collaboratively by a multidisciplinary team comprising specialists in neurology, neurointerventional radiology, and vascular surgery to determine the optimal management strategy.
No complications were observed during the procedures. Notably, after CW correction via stenting or CEA, no further strokes were observed during follow-up, suggesting a protective effect against recurrent embolic events.
DISCUSSION
Our study suggests a notable risk of stroke recurrence in patients with CW, underscoring its probable clinical importance as a contributor of recurrent ischemic events. Among the 23 patients identified with CW, 2 experienced recurrent ischemic stroke, yielding a recurrence rate of 8.7%, which is slightly lower than rates reported in previous studies (11.1–44.0%) [11-13,18]. This comparatively lower recurrence may reflect both our center’s early thrombus detection—which enabled timely intervention before clinical events occurred—and our proactive use of carotid revascularization as a secondary prevention strategy. Notably, no recurrence was observed among patients who underwent early carotid intervention, which may indicate a possible benefit of anatomical correction, though this finding should be interpreted with caution due to the limited sample size. These findings reinforce the notion that CW may represent a high-risk condition warranting careful evaluation and management.
Notably, 4 additional patients demonstrated in vivo thrombus formation within the CW, detected via multimodal imaging, despite the absence of clinical symptoms. When considering both clinical recurrences and imaging-detected thrombi, the overall rate of recurrent or potentially high-risk events rises to 26%, suggesting that focusing solely on clinical strokes may underestimate the true burden of recurrence in this population.
A novel and clinically relevant finding of our study is the detection of acute thrombus formation within CW during the early post-EVT phase, within 48 hours from reperfusion. Wang et al. [19] reported a case in which carotid ultrasound 60 hours post-thrombolysis revealed a CW with a hyperechoic mass, prompting emergent endarterectomy. Histology confirmed a mixed thrombus. Our series extends these findings beyond an isolated case and identifies an asymptomatic thrombus formation rate of 9.1%, emphasizing that silent thrombosis is not rare and may go undetected without targeted imaging.
Routine duplex ultrasound enabled early detection of thrombus, even in asymptomatic patients, facilitating timely intervention. In 1 case, ultrasound identified a thrombus not seen on CTA, underscoring its complementary diagnostic value. Current guidelines recommend combining duplex and CTA, with ultrasound offering advantages like portability, real-time assessment, and accessibility [20]. Despite some debate over its standalone use, ultrasound remains a sensitive tool for early surveillance [21]. Detecting silent thrombosis, as in this study, may help prevent embolic strokes. Emerging technologies like microfluidic imaging may further enhance CW detection [22]. These observations suggest that post-EVT patients with CW should be considered for routine early duplex surveillance, as part of a structured monitoring protocol. The ability to detect preclinical thrombus formation may offer a critical window for preventive intervention.
Our observations are consistent with prior reports suggesting that carotid stenting and endarterectomy may be effective treatment strategies. All 6 patients with either recurrent stroke or thrombus underwent intervention (4 with stenting and 2 with endarterectomy), and none experienced further events during the follow-up period. Moreover, the procedures were technically straightforward and free of complications, further reinforcing their potential safety profile. These outcomes suggest a potential role for anatomical correction in mitigating recurrence risk, consistent with prior reports where no recurrences were observed post-treatment [7,11,12].
While both stenting and endarterectomy were effective, the choice of treatment was individualized, based on anatomical, clinical, and procedural considerations. Stenting was more commonly utilized in our cohort, possibly reflecting its minimally invasive nature and institutional expertise. However, the comparative long-term efficacy and safety of these approaches remain unknown, and randomized prospective studies are warranted to guide clinical decision-making between surgical and medical options.
Despite its strengths, this study has limitations. The small sample size and retrospective design limit the generalizability of the findings. Additionally, follow-up protocols and imaging techniques were not standardized across all cases, which may have influenced the sensitivity for detecting thrombus or lesion morphology as well as the consistency of event identification. Nonetheless, the consistent pattern of recurrence and post-treatment stability supports the relevance of the results.
This study contributes to the growing evidence that CW may represent a modifiable contributor to stroke recurrence. The detection of thrombus formation within CW lesions opens the possibility of intervening before clinical events occur. Incorporating regular imaging surveillance—particularly with sonography—may help identify high-risk patients and guide timely revascularization strategies. Based on our findings, we advocate for a structured early imaging protocol in hospitalized CW patients post-stroke, including duplex sonography within 48 hours and CTA within 24–72 hours. This may represent a turning point for early intervention and secondary stroke prevention.
In line with previous reports, we emphasize the need for either early definitive intervention or, at minimum, close imaging surveillance. Given the substantial risk of recurrence, medical therapy alone may be insufficient in many cases. Brinster et al. [7] have similarly advocated for an aggressive treatment approach in symptomatic patients with CW, based on the outcomes in their series.
Future research should focus on defining optimal imaging follow-up intervals, establishing standardized management pathways, and conducting prospective, randomized trials comparing medical management (e.g., antiplatelet therapy) versus surgical strategies (CEA or stenting). Additionally, a key research priority should be evaluating the efficacy of early intervention versus structured, close imaging-based surveillance protocols, particularly in asymptomatic patients. Regardless of the approach, vigilant follow-up remains essential in this high-risk population.
CONCLUSION
CW represents a significant and underappreciated mechanism of recurrent ischemic stroke, particularly in young patients with cryptogenic strokes. Beyond confirming the recurrence risk of CW, we report for the first time the in-hospital reappearance of thrombus within CW post-EVT, which highlights the need for early imaging surveillance for these patients. Importantly, interventions such as carotid stenting or endarterectomy may effectively prevent further strokes, emphasizing the value of addressing the structural abnormality underlying CW. These findings underscore the importance of early recognition, standardized diagnostic approaches, and tailored management strategies to reduce the burden of CW-associated strokes. Prospective studies are essential to refine treatment paradigms and optimize outcomes for this high-risk population.
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