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Related Experiment Video

Updated: Jul 5, 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.

D H Steinberg¹, L F Satler

¹Division of Cardiology, Washington Hospital Center, Washington, DC 20010, USA. daniel.h.steinberg@medstar.net

Minerva Cardioangiologica

|April 25, 2008

Summary

Drug-eluting stents (DES) reduce restenosis but not death or heart attack. Concerns about late stent thrombosis (LST) and very late stent thrombosis (VLST) after stopping antiplatelet therapy warrant careful review.

Area of Science:

Cardiology
Interventional Cardiology
Biomaterials

Background:

Drug-eluting stents (DES) significantly reduce restenosis and target lesion revascularization compared to bare metal stents (BMS).
Despite restenosis benefits, DES do not decrease rates of death or myocardial infarction.
Long-term safety concerns include a potential increase in late stent thrombosis (LST) and very late stent thrombosis (VLST), especially after antiplatelet therapy cessation.

Purpose of the Study:

To critically appraise drug-eluting stents (DES) and their role in percutaneous coronary intervention.
To focus on the definitions, incidence, mechanisms, and clinical implications of DES thrombosis.
To address concerns regarding late and very late stent thrombosis associated with DES.

Main Methods:

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Ferromagnetic Bare Metal Stent for Endothelial Cell Capture and Retention

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Published on: September 18, 2015

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Last Updated: Jul 5, 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 existing literature on drug-eluting stent thrombosis.

Analysis of factors contributing to DES thrombosis, including patient, lesion, stent, and physician-related elements.

Examination of the debated incidence and definitions of DES thrombosis.

Main Results:

DES are effective in reducing restenosis but offer no survival benefit over BMS.
A small but significant risk of LST and VLST exists with DES, particularly after antiplatelet therapy discontinuation.
The multifactorial nature of DES thrombosis involves modifiable and non-modifiable factors.

Conclusions:

The benefits of DES are primarily limited to reducing restenosis.
Concerns about LST and VLST necessitate a critical evaluation of DES use in percutaneous coronary intervention.
Understanding the mechanisms and contributing factors is crucial for managing DES thrombosis.