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Updated: Apr 21, 2026

A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
[Pathogenesis of in-stent thrombosis after carotid artery stenting]
Saya Ozaki1, Masahiko Tagawa, Shirabe Matsumoto
1Department of Neurosurgery, Ehime University Graduation School of Medicine.
Insights
In-stent thrombosis (IST) after carotid artery stenting (CAS) is rare. This study found low echoic plaque and open cell stents were associated with IST, but no definitive risk factors were identified. Further research is needed.
Area of Science:
- Vascular Surgery
- Interventional Cardiology
- Neurology
Context:
- In-stent thrombosis (IST) is a rare but serious complication following carotid artery stenting (CAS).
- Understanding the pathogenesis of IST is crucial for preventing severe thromboembolic events.
- This study investigated potential factors contributing to IST after CAS.
Purpose:
- To investigate the pathogenesis of in-stent thrombosis (IST) after carotid artery stenting (CAS).
- To compare clinical parameters between patients who developed IST and those who did not.
- To identify potential risk factors associated with IST after CAS.
Summary:
- A retrospective review of 101 CAS patients identified 5 cases of IST.
- IST cases were associated with low echoic plaque and open cell stent design.
- No significant differences in baseline characteristics were found between IST and non-IST groups.
- While anticoagulant therapy led to resolution in most cases, one patient experienced symptomatic thromboembolism.
Impact:
- This study highlights the association of low echoic plaque and open cell stents with IST.
- It suggests a potential mechanism involving plaque protrusion and turbulent flow at stent flexions.
- The findings underscore the need for larger studies to definitively identify IST risk factors and inform preventative strategies.
Background And Purpose:
In-stent thrombosis (IST) after carotid artery stenting (CAS) is a rare complication that can lead to severe thromboembolic events. The purpose of this study was to investigate the pathogenesis of IST after CAS.
Patients And Methods:
A total of 101 patients underwent CAS from January 2006 to September 2013 at our hospital. Five of these patients experienced IST. We reviewed their clinical course and treatment. In addition, we compared various parameters, including basal disease, preceding anti-platelet therapy, rate of stenosis, length of stenosis, preoperative examination, type of stent, length of stent, post dilatation, and postoperative examination, between the IST and the non-IST groups.
Outcome:
All cases in the IST group had low echoic plaque and open cell stent, and all thrombi were located at the dorsal side of the internal carotid artery and the distal side of the stent flexion. Four cases without neurological symptoms were found to have resolution of IST at 3-6 weeks after CAS with anticoagulant therapy. One case had symptomatic thromboembolism at 1 month after CAS, and the thrombus was removed along with the stent due to growth of the thrombus despite anticoagulant therapy. No significant differences were observed between the IST and non-IST groups with regard to the factors described in the methods section.
Conclusions:
This study did not identify factors related to IST. We hypothesize that soft plaque can easily protuberate in the context of a stent with a large cell and that protrusion plaque may increase the risk of thrombus formation in combination with turbulent flow at the site of stent flexion. Further investigation in a larger number of patients is needed to clarify the risk factors related to IST.
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