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Updated: Jun 19, 2026

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

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

Published on: May 14, 2013

Drug-eluting stent thrombosis.

T Pilgrim¹, S Windecker

¹Department of Cardiology, Bern University Hospital, Bern, Switzerland.

Minerva Cardioangiologica

|October 20, 2009

Summary

Drug-eluting stents (DES) significantly reduce repeat procedures but carry a risk of stent thrombosis. Newer DES aim to improve healing and reduce this rare but serious complication.

Area of Science:

Cardiovascular Medicine
Biomedical Engineering
Interventional Cardiology

Background:

Drug-eluting stents (DES) offer significant benefits over bare metal stents, reducing repeat revascularization by 50-70%.
Stent thrombosis (ST), though rare, is a severe adverse event associated with coronary stents.
Very late stent thrombosis (VLST), occurring >1 year post-implantation, is a complicating factor specifically with DES.

Purpose of the Study:

To investigate the mechanisms underlying very late stent thrombosis (VLST) in drug-eluting stents (DES).
To identify factors contributing to VLST, particularly polymer components in DES.
To highlight the development of newer generation DES focused on enhanced vascular healing and neointimal suppression.

Main Methods:

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Ferromagnetic Bare Metal Stent for Endothelial Cell Capture and Retention

Ferromagnetic Bare Metal Stent for Endothelial Cell Capture and Retention

Published on: September 18, 2015

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Last Updated: Jun 19, 2026

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

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

Published on: May 14, 2013

Ferromagnetic Bare Metal Stent for Endothelial Cell Capture and Retention

Ferromagnetic Bare Metal Stent for Endothelial Cell Capture and Retention

Published on: September 18, 2015

Review of autopsy studies examining mechanisms of VLST.

Analysis of stent components, focusing on polymers in DES.

Evaluation of newer generation DES designs targeting improved vascular healing.

Main Results:

Delayed healing and incomplete re-endothelialization are identified as primary mechanisms for VLST.
Polymer components of DES are implicated as a significant factor in VLST.
Autopsy studies provide critical insights into the pathophysiology of VLST.

Conclusions:

VLST is a complex complication of DES, with delayed healing and incomplete re-endothelialization being key contributors.
The materials used in DES, especially polymers, play a role in the occurrence of VLST.
Next-generation DES are being developed to mitigate VLST risk by promoting better vascular healing and drug delivery.