Abstract

Background: The carotid web (CW) is a shelf-like defect located on the posterior wall at the origin of the internal carotid artery. Abnormal blood flow in the CW causes thrombus formation, making it difficult to diagnose. Some reports have indicated that CWs become detectable only after thrombus resolution. We report a case of a patient who underwent carotid artery stenting (CAS) for a previously undetected CW with the resolution of an adherent thrombus resulting in a favorable outcome.

Case Description: A 39-year-old male presented with the left hemiparesis rushed to our hospital. Magnetic resonance imaging and angiography revealed a cerebral infarction caused by occlusion of the right middle cerebral artery. Initial cerebral angiography showed a mobile contrast defect in the posterior wall of the right cervical internal carotid artery. The patient was treated conservatively with medical therapy and rehabilitation. Follow-up angiography 1 month later revealed a shelf-like defect at the posterior wall of the origin of the internal carotid artery, which was different from the initial cerebral angiography. CAS was performed for the CW with a resolution of the adherent thrombus.

Conclusion: A CW may present with varying imaging findings depending on the nature of the adherent thrombus. In cases where such adherent thrombus hamper diagnosis or in the absence of adherent thrombus, the imaging finding of the pooling of the blood flow may help in diagnosing a CW.

Keywords: Carotid artery stenting, Carotid web, Resolution, Thrombus

INTRODUCTION

The carotid web (CW) is one of the causes of occult cerebral infarction in young patients.[ 9 ] It is a shelf-like defect in the posterior wall of the origin of the internal carotid artery[ 4 , 7 , 11 ] and causes thrombus formation and recurrent stroke.[ 1 ] There are several reports of a CW with adherent thrombus, but only a few reports have described the thrombus disappearing over time eventually revealing the CW. Herein, we report a case who underwent carotid artery stenting (CAS) for CW with resolution of adherent thrombus and had a favorable outcome.

CASE DESCRIPTION

A 39-year-old male went to bed at about 0:00 on February 1, 2025, and woke up at around 3:00 am. complaining of left hemiparesis. Initially, he was observed at home; however, as his symptoms did not improve, he was rushed to our hospital at 8:00 pm. the following day. The patient’s medical and family history were unremarkable. On arrival, his Glasgow coma scale score was 14 (E4, V4, M6). Neurological examination revealed left facial nerve palsy, mild dysarthria, left hemiparesis and left hemispatial neglect. His National Institutes of Health Stroke Scale (NIHSS) score was eight. Blood pressure and pulse rate were recorded as 104/56 mm Hg and 76/min, respectively. Head magnetic resonance imaging (MRI) revealed a cerebral infarction in the right middle cerebral artery territory [ Figures 1a and b ]. Head magnetic resonance angiography (MRA) revealed occlusion of the right middle cerebral artery [ Figure 1c ]. Neck MRA (maximum intensity projection [MIP]) revealed no apparent stenosis [ Figure 1d ], and the electrocardiogram revealed no evidence of atrial fibrillation. The patient was hospitalized and treated conservatively.

Figure 1:

(a) Head magnetic resonance imaging showing cerebral infarction in the right middle cerebral artery. (b) Head magnetic resonance imaging showing cerebral infarction in the right middle cerebral artery (black arrow). (c) Head magnetic resonance angiography (MRA) showing occlusion of the right middle cerebral artery (white arrow). (d) Neck MRA (maximum intensity projection) showing no apparent stenosis (white arrow).

Carotid artery ultrasonography revealed a soft and mobile lesion [ Figure 2 ] and cerebral angiography confirmed the presence of a mobile contrast defect in the posterior wall of the right cervical internal carotid artery [ Figure 3a ]; contrast pooling was observed on the rostral side of the lesion [ Figure 3b ]. This defect was also detected on the 3D computed tomography angiography (3D-CTA) of the neck [ Figure 4 ]. Likewise, the MRI plaque image revealed a lesion that was T1 isointensity [ Figure 5a ] and T2 mild high intensity [ Figure 5b ]. The possible differentials – mobile plaque, dissection, or CW – were considered, and medical treatment and rehabilitation were started accordingly.

Figure 2:

Carotid artery ultrasonography revealing a soft and mobile lesion (white arrow). RT-ICA: Right internal carotid artery

Figure 3:

(a) Cerebral angiography showing a mobile contrast defect in the posterior wall of the right cervical internal carotid artery. (b) Pooling of the contrast observed on the rostral side of the lesion (black arrow).

Figure 4:

Neck three-dimensional computed tomography angiography showing a contrast defect in the posterior wall of the cervical internal carotid artery.

Figure 5:

(a) Magnetic resonance imaging plaque image showing isointense lesion on T1 (white arrow). (b) Magnetic resonance imaging plaque image showing isointense lesion on T2 (white arrow).

Argatroban (60 mg/day) was administered for 2 days, followed by 20 mg/day for 5 days. In addition, prasugrel (3.75 mg/day), bayaspirin (100 mg/day) and pitavastatin calcium (2 mg/day) were administered. The patient began to show improvement in dysarthria, left hemiparesis and other neurological symptoms. Repeat 3D-CTA of the neck, MRI plaque image and carotid artery ultrasonography were performed 33 days after symptom onset. Carotid artery ultrasonography showed no obvious abnormal structures [ Figure 6a ], although pooling of the blood flow on the rostral side of the lesion was suggestive [ Figure 6b ]. Neck 3D-CTA revealed a decrease in size in the contrast defect [ Figure 7 ], and MRI plaque image revealed the change of the lesion to T1 isointensity [ Figure 8a ] and T2 strongly high intensity [ Figure 8b ].

Figure 6:

(a) Carotid artery ultrasonography showing no obvious abnormal structures. (b) Carotid artery ultrasonography showing some findings indicative of pooling of blood flow (white arrow).

Figure 7:

Neck three-dimensional computed tomography angiography showing a decrease in the contrast defect.

Figure 8:

(a) Magnetic resonance imaging plaque image showing changes to isointense in T1 (white arrow). (b) Magnetic resonance imaging plaque image showing changes to strongly hyperintense in T2 (white arrow).

Eventually, CAS was performed 37 days after symptom onset, for a CW with an adherent thrombus. An 8 Fr Optimo guidecatheter (Tokai Medical Products, Kasugai, Aichi, Japan) was guided into the right common carotid artery. The right common carotid angiography revealed a shelf-like defect in the posterior wall of the origin of the internal carotid artery, which was different from the imaging findings of the initial cerebral angiography [ Figure 9a ]. A filterwire EZ (Boston Scientific, Natick, MA, USA) was guided and deployed to the rostral side of the lesion. The common carotid artery diameter was recorded as 6.7 mm; accordingly, a CASPER stent (8 mm × 30 mm; Terumo, Tokyo, Japan) was deployed. A percutaneous transluminal angioplasty was performed at eight atm for 30 s using Genity (4.5 mm × 20 mm; Kaneka, Tokyo, Japan). The CW was compressed by CASPER and a good opening was obtained [ Figure 9b ].

Figure 9:

(a) Right common carotid angiography revealed a shelf-like defect in the posterior wall of the origin of the internal carotid artery, which was different from the imaging findings of the initial cerebral angiography. (b) The carotid web was compressed by the stent and a good opening was obtained.

The procedure was completed with no obvious main artery occlusion. Head MRI on the 1^st postoperative day revealed no obvious signs of a new cerebral infarction. The patient’s status improved gradually (NIHSS score = 2; modified Rankin scale score = 2), and he was transferred to a recovery hospital 54 days after symptom onset.

DISCUSSION

CW is a subtype of fibromuscular dysplasia (FMD); however, unlike FMD, its pathology primarily involves fibrotic hyperplasia of the intima, with few changes in the tunica media.[ 2 , 6 ] CW is typically diagnosed through cerebral angiography or computed tomography angiography (CTA). It commonly appears as a shelf-like defect in the posterior wall at the origin of the internal carotid artery, often accompanied by pooling of blood flow on the rostral side.[ 3 , 5 ] Typically, thrombus formation by pooling of blood on the rostral side of the CW is reported as the cause of cerebral infarction.[ 4 ] In our case, the thrombus was adherent to the CW, which obscured the typical shelf-like morphology in the early imaging studies, including 3D-CTA, carotid artery ultrasonography and cerebral angiography.

The differential diagnoses included mobile plaque, arterial dissection, and CW. Because we could not determine whether the thrombus had adhered to a CW, or masked its characteristic structure, and considering the possibility of other etiologies, we initiated treatment with argatroban infusion, dual antiplatelet therapy and statin. One month later, the CTA and endovascular therapy revealed changes at the site of the lesion (posterior wall of the origin of the internal carotid artery) exposing a shelf-like defect and confirming a CW.

As noted above, a CW is typically diagnosed using 3D-CTA, where it commonly appears as a shelf-like defect on the posterior wall at the origin of the internal carotid artery. In the present case, the initial CTA did not show a typical shelf-like defect at that site. However, a follow-up CTA performed 33 days after symptom onset revealed that the lesion had changed in shape, displaying the characteristic shelf-like appearance of a CW. This suggest that even when the initial defect does not appear typical, the possibility of shape alteration due an adherent thrombus should be considered. In this context, CTA may be useful for both the diagnosis and follow-up of CWs with adherent thrombus. Nonetheless, its use for frequent imaging is limited by concerns regarding radiation exposure and contrast agent administration.

Although commonly performed, the detection rate of CW by carotid artery ultrasonography is not high. Joux et al.[ 6 ] reported that CW was not identified in 18 of 21 cases using carotid artery ultrasonography, and the condition was sometimes misdiagnosed as fibrous plaque due to nonspecific findings. Otsuka et al.[ 10 ] reported two cases of CW where carotid artery ultrasonography was performed. In one case, the procedure was performed after a shelf-like defect was identified in the posterior wall at the origin of the internal carotid artery on the cervical MRA plaque image, but no bulge was identified by carotid artery ultrasonography. In another case, the condition was misdiagnosed as an atherothrombotic stroke, even though carotid artery ultrasonography showed a slight elevation with equal brightness. In our case, soft and mobile lesions were initially observed in the posterior wall at the origin of the internal carotid artery; therefore, a definitive diagnosis of CW could not be made at that time due to lack of active suspicion of CW. One month later, carotid artery ultrasonography did not show any obvious abnormal structures, although findings suggestive of the pooling of the blood flow were noted. As mentioned above, the detection rate of CW by carotid artery ultrasonography is low, and in our case as well, CW could not be diagnosed using carotid artery ultrasonography alone. Therefore, carotid artery ultrasonography, including in cases of thrombus adherence to the CW, may misdiagnose the lesion.

To the best of our knowledge, only two cases have been reported in which CW was evaluated using MRI plaque images. Onuki et al.[ 8 ] reported that CW appeared isointense on T1 and hyperintense on T2, findings that did not indicate unstable plaque. Sasaki et al.[ 12 ] reported rapid thrombus formation in CW after stroke onset, and MRI plaque imaging performed 8 days later showed similar findings to those of Onuki et al.[ 8 ] In our case, the initial MRI plaque image also revealed an isointense signal on T1 and mild hyperintensity on T2 in the CW, with thrombus resolution appearing isointense on T1 and strongly hyperintense. MRI plaque images with T1 isointensity and T2 hyperintensity indicate a loose fibrous matrix.[ 14 ] The pathology of CW predominantly involves fibrotic hyperplasia of the intima; therefore, CW may appear as isointense on T1 and hyperintense on T2 MRI plaque images due to the fiber component. In our case, the CW showed mild hyperintensity on T2 when the thrombus was adherent, but changed to strong hyperintensity on T2 when the thrombus disappeared. Thrombus resolution may have rapidly exposed the CW to the blood, resulting in a strong hyperintense signal on the T2 MRI plaque image.

Imaging follow-up methods for CW include carotid artery ultrasonography, neck 3D-CTA, neck MRA (MIP, plaque image) and cerebral angiography. Neck MRA (MIP) is not suitable for imaging follow-up due to its low sensitivity. Likewise, cerebral angiography is not suitable for frequent imaging follow-up due to its high invasiveness. Neck 3D-CTA is also considered unsuitable for frequent imaging follow-up due to the need for contrast media and radiation exposure. In contrast, carotid artery ultrasonography is less invasive and considered appropriate for frequent image follow-up, although it does not have a high CW detection rate. Since our patient had a soft and mobile lesion, we did not perform serial ultrasound arteriography due to the possibility that the pressure of the probe on the neck could cause lesion migration. Although the usefulness of less invasive carotid artery ultrasonography has been reported in a case of rapid thrombus formation in CW,[ 12 ] there is a potential for misdiagnosis when using carotid artery ultrasonography alone diagnosis of CW. Nevertheless, careful carotid artery ultrasonography follow-up may be considered for monitoring lesion changes over time, especially in cases involving taking mobile. To the best of our knowledge, there has been only one report of imaging follow-up with neck MRA plaque image.[ 12 ] In our patient, the shape of the CW clearly changed from the time of onset to the 1 month follow-up on neck MRA plaque image studies, suggesting that neck MRA plaque image may be considered as a less invasive imaging follow-up.

Several cases of CW with adherent thrombus have been reported in the literature,[ 1 , 5 ] with an incidence ranging from 16.2% to 28%.[ 4 , 11 ] The present report describes a rare case in which CW was initially missed due to thrombus adhesion but was eventually detected as the thrombus changed in shape over time. To the best of our knowledge, only one such case has been reported so far. Kimura et al.[ 7 ] reported a case of recurrent ischemic stroke misdiagnosed as atherosclerotic carotid stenosis due to an adherent thrombus obstructing the CW. In this case,[ 7 ] the patient was initially diagnosed with atherosclerotic internal carotid artery stenosis because, unlike our case, the thrombus was not “soft and mobile.” In some cases, like our patient, the thrombus attached to the CW may be soft and mobile; therefore, CWs with a thrombus may present different imaging findings depending on the nature of the thrombus. In the same report,[ 7 ] pooling of the blood flow could be seen on the rostral side of the CW even when the CW had an adherent thrombus. Similar pooling of the blood flow was also seen in our case and may help in the diagnosis of CW.

If the lesion is a CW with an adherent thrombus, there is a risk that the thrombus may disperse and cause a new cerebral infarction. Therefore, early stenting may be desirable in such cases. However, performing stenting too early – before adequate antithrombotic therapy – is associated with the risk of in-stent thrombus formation. In addition, we considered the possibility that the lesion could be an arterial dissection, in which case spontaneous vascular remodeling would be expected, and stenting would not be indicated. Given these considerations, when a CW with adherent thrombus is suspected, it may be prudent to initiate aggressive antithrombotic therapy and proceed with stenting once the CW is confirmed. Our patient was treated with an argatroban infusion and dual-antiplatelet therapy from the onset, and the thrombus adhering to the CW may have disappeared as a result of the medical treatment. Because there were no neurological aggravations, if the thrombus adhering to the CW migrated distally, it may have translocated to the area where the cerebral infarction had already occurred. If a thrombus adhering to the CW migrates to an area where cerebral infarction has not yet occurred and causes new neurological aggravations, emergency treatment, such as mechanical thrombectomy, is warranted.

In terms of treatment, the recurrence rate of CW-associated cerebral infarction is high with medical therapy, whereas carotid endarterectomy or CAS are reported to be highly efficient in preventing recurrent cerebral infarction.[ 15 ] A review of past reports on CAS for CW described that closed stents were used in 70% of cases.[ 5 ] CAS is known to be effective in preventing the recurrence of embolism, and no recurrences have been reported for open-cell and closed-cell stents. In our case, a braided stent (CASPER) was deployed. CASPER is a double-layer micromesh stent with a fine mesh structure. Tachizawa et al.[ 13 ] reported that CASPER may have a flow-diverting effect, which could promote thrombosis in areas of stagnant blood flow, such as residual ulcers, following implantation. In our patient, the CW appeared to be compressed by the stent, although not completely, and slight pooling of contrast was still observed on the rostral side of the lesion. Even if residual blood flow persists outside the stent immediately after implantation, endothelialization occurs over time, and the blood thromboses and disappears through vascular remodeling.[ 5 ] Furthermore, the slight pooling observed on the rostral side of the CW may undergo thrombosis due to the flow-diverting properties of the CASPER stent. Nevertheless, imaging follow-up should be performed to observe if the contrast pooling disappears.

CONCLUSION

The diagnosis of CW may be challenging when an adherent thrombus is present, as it may obscure the lesion. However, resolution of the thrombus with medical treatment over time can reveal the underlying CW, facilitating diagnosis. In such cases, CAS has been shown to be an effective treatment, leading to favorable patient outcomes. Imaging findings can vary depending on the nature of the thrombus and whether it is adhering to the CW. Even when the CW is considered difficult to diagnose due to an adherent thrombus, the imaging finding of pooling of the blood flow may help in the diagnosis.

Ethical approval:

The Institutional Review Board approval is not required.

Declaration of patient consent:

The authors certify that they have obtained all appropriate patient consent.

Financial support and sponsorship:

Nil.

Conflicts of interest:

There are no conflicts of interest

Use of artificial intelligence (AI)-assisted technology for manuscript preparation:

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

Disclaimer

The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Journal or its management. The information contained in this article should not be considered to be medical advice; patients should consult their own physicians for advice as to their specific medical needs.

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