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A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
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A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis

Published on: May 14, 2013

Stent thrombosis is not always stent thrombosis: de novo atherosclerosis in a stented coronary segment

Pierfrancesco Agostoni, Paul Vermeersch, Michiel Knaapen

    International Journal of Cardiology
    |January 24, 2009
    PubMed

    Insights

    Late stent thrombosis occurred 9 years after bare metal stent implantation due to new plaque formation. This rare event caused myocardial infarction, highlighting the risk of de novo atherosclerosis within stents.

    Area of Science:

    • Cardiology
    • Interventional Cardiology
    • Pathology

    Background:

    • Late stent thrombosis (LST) is a rare but serious complication following percutaneous coronary intervention.
    • Bare metal stents (BMS) have a lower risk of LST compared to early drug-eluting stents, but it can still occur years after implantation.

    Observation:

    • A case of LST 9 years post-overlapping BMS implantation in the circumflex artery is presented.
    • The patient experienced acute ST-segment elevation infero-lateral myocardial infarction.
    • Coronary angiography showed a sub-occlusive thrombus within the stent boundaries.

    Findings:

    • Pathological analysis of aspirated material revealed fibrin thrombus, platelet aggregates, and atherosclerotic plaque fragments.
    • The plaque fragments contained necrotic core, cholesterol clefts, inflammatory cells (macrophages), and iron deposition, indicative of plaque rupture.
    • The findings suggest de novo formation of a vulnerable, rupture-prone atherosclerotic plaque within the stent.

    Implications:

    • This case highlights the potential for de novo atherosclerosis development within BMS, leading to late thrombotic events.
    • Understanding the mechanisms of LST is crucial for optimizing long-term management of patients with coronary stents.
    • Further research into the biological processes driving intra-stent plaque formation and rupture is warranted.

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