Acute Ischemic Stroke Due to a Mobile Thrombus Adherent to a Carotid Web

Abstract

A 48-year-old man presented with impaired consciousness and aphasia. Magnetic resonance imaging (MRI) of the head revealed acute cerebral infarction in the left temporal and parietal lobes. Carotid ultrasonography revealed a mobile structure at the origin of the left internal carotid artery. Cervical MRI using fat-saturation T1 imaging showed an isointense structure at the origin, with a high-signal structure extending toward the head. Digital subtraction angiography revealed contrast stagnation, suggesting the presence of a carotid web (CaW). The mobile structure was released, indicating thrombus resolution. Carotid artery stenting eliminated contrast stagnation and was well-tolerated. This case highlights the diagnostic challenges associated with a CaW-related stroke.

Introduction

The carotid artery web (CaW) is a non-atherosclerotic, non-inflammatory, shelf-like lesion that occurs along the posterior wall of the internal carotid bulb (1). The CaW disrupts laminar blood flow, leading to endothelial stress, blood stagnation, and downstream platelet aggregation, resulting in artery-to-artery thromboembolism (2-4). It is an under-recognized cause of ischemic stroke in young individuals (5). Although carotid ultrasonography combined with computed tomographic angiography (CTA) or magnetic resonance imaging (MRI) is an effective and reliable method for identifying CaWs, misdiagnoses and oversight remain common (5).

Several studies have suggested that patients with symptomatic CaW treated with antiplatelet or anticoagulation therapy alone are at high risk of recurrent stroke (6). Although the effectiveness of carotid endarterectomy (CEA) and carotid artery stenting (CAS) has been documented, a standard treatment has yet to be established (6).

We herein report a case of a CaW with thrombus adhesion in the acute phase of ischemic stroke, in which CAS was performed after thrombus release, leading to a favorable outcome.

Case Report

A 48-year-old man presented to our emergency department with impaired consciousness and aphasia. The patient had a history of hypertensive brain hemorrhaging 16 years previously and had a mild sensory disturbance on the left side of his body as an aftereffect. He was also taking medications for hypertension and hyperlipidemia. The patient had no history of smoking.

At admission, the patient's clinical characteristics and vital signs were as follows: height, 176 cm; weight, 73.7 kg; body mass index, 23.7 kg/m²; blood pressure, 127/54 mmHg; heart rate, 76 beats/min; body temperature, 36.5°C; respiratory rate, 18 breaths/min; and oxygen saturation, 98% on room air. The patient had a Glasgow Coma Scale score of E4V4M6. No abnormalities were observed in his heart or breath sounds. A neurological examination on admission revealed aphasia and dysarthria. His National Institutes of Health Stroke Scale score was 11. Laboratory test results revealed no significant abnormalities.

MRI of the head indicated acute ischemic stroke involving the distribution of the left middle cerebral artery (MCA), and magnetic resonance angiography confirmed occlusion of the left MCA M3 (Fig. 1). Intravenous thrombolysis was contraindicated because of his history of cerebral hemorrhaging, and mechanical thrombectomy was not initiated because of the distal location of the occluded vessel. Treatment for embolic stroke of an undetermined source was initiated with aspirin. Carotid ultrasonography performed on day 4 after admission revealed a mobile structure at the origin of the left internal carotid artery (ICA) without any evidence of carotid intimal disruption. (Fig. 2A-C). Transcranial Doppler (TCD) showed no high-intensity transient signals (HITSs).

Figure 1.

DWI and MRA imaging findings. A: DWI on admission reveals a hyperintense lesion extending from the left insular cortex to the parietal lobe. B: MRA showed occlusion of left MCA M3 (yellow arrow). DWI: diffusion-weighted imaging, MCA: middle cerebral artery, MRA: magnetic resonance angiography

Figure 2.

Ultrasound findings of the internal carotid artery before and after DSA. A, B: Ultrasound B-mode and color Doppler imaging show an isoechoic structure at the origin of the left internal carotid artery. C: Power Doppler imaging reveals a blood flow signal at the far wall of the origin of the left internal carotid artery. D-F: After DSA, B-mode ultrasound, color Doppler, and power Doppler imaging show the disappearance of the previously observed isoechoic structure, revealing a shelf-like formation at the origin of the left internal carotid artery. DSA: digital subtraction angiography

The patient's symptoms remained stable, and no recurrence was observed on imaging. Clopidogrel was administered because of suspicion of an atherosclerotic plaque with rupture or a carotid artery dissection with a mobile thrombus. CTA and cervical MRI were performed on day 7. CTA confirmed a vertically elongated filling defect (Fig. 3A). Cervical MRI using fat-saturation T1 imaging showed an isointense structure at the origin and a high-signal structure extending toward the head (Fig. 3B, C). Digital subtraction angiography (DSA) was performed on day 13 and showed a shelf-like filling defect in the left ICA bulb. Contrast agent retention was observed during the late venous phase, suggesting CaW (Fig. 4A, B). 3D rotational DSA revealed a CaW projecting perpendicular to the arterial wall, measuring 2.5 mm in length. Conversely, the mobile structure observed on ultrasonography was resolved using DSA.

Figure 3.

Findings of cervical internal carotid artery on CTA and MRI. A: CTA confirmed a vertically elongated filling defect (yellow arrow). B: Coronal view of cervical MRI fat-saturation T1 imaging showed an isointense structure at the origin and a high-signal structure extending toward the head (yellow arrow). C: Axial view of cervical MRI fat-saturation T1 imaging shows findings consistent with those observed in the coronal view (yellow arrow). CTA: computed tomographic angiography, MRI: magnetic resonance imaging

Figure 4.

DSA findings before and after CAS. A: Arterial phase DSA before CAS demonstrated a shelf-like filling defect in the left ICA bulb (yellow arrow). B: Venous phase DSA before CAS showed contrast agent retention (red arrow). C: 3D rotational DSA revealed a carotid web projecting perpendicularly from the arterial wall. D: Arterial phase DSA after CAS showed resolution of the shelf-like filling defect in the left ICA bulb. E: Arterial phase DSA after CAS demonstrated the disappearance of contrast agent retention. DSA: digital subtraction angiography, CAS: carotid artery stenting, ICA: internal carotid artery

A reexamination of carotid ultrasonography on day 14 revealed findings indicative of a CaW but did not confirm the mobile structure observed on day 4 (Fig. 3D-F). Comprehensive thrombophilia screening, including coagulation studies, antithrombin III, protein C, protein S, antiphospholipid antibodies (lupus anticoagulant and anticardiolipin), and homocysteine levels, showed no abnormal findings. Based on the above, a diagnosis of ischemic stroke was made because of the adhesion and release of a mobile thrombus on the CaW. A left CAS procedure was performed on day 29 as secondary prevention, using a 9×40-mm Protégé stent (Medtronic, Dublin, Ireland) to cover the CaW. After CAS, the contrast pooling in the left ICA improved (Fig. 4C, D).

There were no post-CAS complications, and the patient was transferred for rehabilitation on day 36 after admission.

Discussion

In the present case, the CaW and adherent thrombi were observed using ultrasonography, CTA, and MRI. CAS was performed in the acute phase of cerebral infarction with favorable outcomes. Although several reports have identified the CaW as a cause of cerebral infarction, cases in which thrombus adherent to the CaW has directly caused infarction are rare (7,8). Furthermore, to our knowledge, there have been no previous reports describing the corresponding MRI findings, constituting a noteworthy imaging feature of thrombus-adherent CaWs.

In the treatment of stroke caused by a CaW, the key factors are the early diagnosis and appropriate treatment strategies. Although CaWs have been increasingly frequently recognized in recent years, their early diagnosis is challenging (5). Radiological differentials of CaWs include atherosclerotic plaques with rupture and carotid artery dissection. Differentiating these conditions from a CaW is particularly challenging when a thrombus adheres to the CaW, as was observed in the present case. Previous reports have suggested that thrombus formation in CaWs may result from turbulent flow at the lesion site and blood stasis within a pocket located on the dorsal side of the CaW (9). Thrombus formation is considered more likely when the lesion is large and forms a sharp angle with the vessel wall, i.e. when the pocket is deep (10). In contrast, in the present case, as demonstrated by ultrasonography and DSA, the CaW extended vertically relative to the course of the ICA, and DSA showed flow stagnation distal to the lesion. This flow disturbance may have contributed to the thrombus directly adhering to the CaW. Similarly, in previously reported cases of cerebral infarction caused by a thrombus directly attached to a CaW, the CaW also ran perpendicular to the ICA without forming a pocket, and the thrombus extended from the CaW in the direction of blood flow (7,8).

A CaW is a non-atherosclerotic and non-inflammatory lesion that has been reported to appear isointense on T1-weighted MRI (11,12). In the present case, the MRI findings - an isointense signal at the base of the lesion and a high-intensity signal in the mobile portion - suggested the potential presence of a thrombus attached to the CaW.

While diagnostic accuracy has improved with the reporting of several ischemic strokes caused by CaWs, standard treatment has not yet been established. It has been reported that medical treatment alone for CaW-caused ischemic stroke has a high recurrence rate, and the current prevailing view is that surgical intervention is preferable (6). No large-scale studies have compared the efficacies of CEA and CAS. Although CEA has long been reported as a revascularization procedure for CaW, recent reports suggest that CAS is equally effective and safe (13-15). As with ICA stenosis treatment, it is advisable to select the appropriate treatment based on the respective advantages and disadvantages of each option. To date, no study has investigated the optimal treatment timing. Although intervention should be performed before recurrence, treatment during the acute phase of ischemic stroke may increase the risk of perioperative complications. A particularly challenging issue is whether or not to proceed with revascularization when a thrombus is present, as CAS in such cases carries the risk of distal embolization during lesion crossing. In addition, the diagnosis of a CaW can be challenging when a thrombus is attached; the risk of misdiagnosing a dissection as a CaW and proceeding with CEA is increased. There have been case reports of CEA and CAS performed in patients with thrombus adhesion (7,16), and early intervention may be advisable in the event of recurrence after medical treatment. In the present case, upon identifying a mobile structure within the ICA on ultrasonography, we considered initiating anticoagulation therapy or performing an invasive intervention, such as CEA or CAS. However, as the patient's symptoms were stable, and no HITS were detected on TCD monitoring, we proceeded with a further evaluation while initiating dual antiplatelet therapy (DAPT) with aspirin and clopidogrel. By the time the CaW was diagnosed on DSA, the thrombus had already detached, and both CAS and CEA were considered safe treatment options. Based on previous studies that demonstrated comparable efficacy and safety between CEA and CAS for the treatment of CaW, we adopted CAS as our first-line approach because of its minimally invasive nature. However, CEA has the advantage of providing macroscopic and pathological information about CaW lesions, which can be valuable for diagnostic and research purposes. Regarding antiplatelet management, our standard postoperative antiplatelet regimen consists of lifelong single antiplatelet therapy after CEA and DAPT for three months followed by lifelong single antiplatelet therapy after CAS. Although the patient had a history of intracerebral hemorrhaging, his blood pressure had been well-controlled over the years, and we judged that he could tolerate a short course of DAPT. After providing a detailed explanation of both treatment options, the patient chose CAS as a strategy to prevent recurrence. Accordingly, we proceeded with CAS without initiating anticoagulation therapy, continuing aspirin and clopidogrel throughout, and achieved favorable outcomes.

Conclusion

We herein report a case of CaW with thrombus adherence in the acute phase of ischemic stroke for which MRI, CTA, and ultrasonography findings were documented. CAS was performed during hospitalization, and the patient had a favorable outcome. This report may contribute to the improvement of the accuracy of CaW diagnoses. Further studies are needed to determine the appropriate treatment strategies.

The authors state that they have no Conflict of Interest (COI).