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Updated: Jun 5, 2026

A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
Proximal atherosclerotic lesion as a cause of very late stent thrombosis
Sainath Gaddam1, Muniba Rizvi, Krishna Chaitanya Nimmagadda
1Department of Internal Medicine, Staten Island University Hospital, New York, United States. gaddamsainath@gmail.com
Insights
Very late stent thrombosis, occurring over a year after coronary artery stent placement, may be caused by new atherosclerotic lesions. These lesions can impede blood flow and create a prothrombotic state, leading to thrombosis.
Area of Science:
- Cardiology
- Vascular Biology
- Medical Device Research
Background:
- Very late stent thrombosis (VLST) is a serious complication occurring >1 year after coronary stent implantation.
- Drug-eluting stents (DES) have faced scrutiny due to reported increases in VLST.
- The precise mechanisms underlying VLST remain incompletely understood.
Purpose of the Study:
- To propose a novel hypothesis for the etiology of very late stent thrombosis.
- To investigate the role of de novo atherosclerotic lesions in VLST development.
- To link the natural progression of atherosclerosis to stent thrombosis risk.
Main Methods:
- Literature review and theoretical modeling based on Virchow's triad.
- Analysis of blood flow dynamics and endothelial environment.
- Hypothesizing the impact of proximal de novo lesions on distal stent patency.
Main Results:
- Proposed that de novo atherosclerotic lesions proximal to stents cause distal blood flow stasis.
- Hypothesized that these lesions induce myocardial ischemia, creating a prothrombotic milieu.
- Linked stasis and prothrombotic conditions to the formation of very late stent thrombosis.
Conclusions:
- De novo atherosclerotic lesion formation in the proximal stented artery segment is a potential cause of VLST.
- The aging process of atherosclerosis may predispose individuals to VLST through proximal lesion development.
- Understanding this mechanism could inform future prevention and treatment strategies for VLST.
Abstract:
Very late stent thrombosis is defined as in-stent thrombosis occurring after 1 year of an intra-coronary artery stent placement. Drug eluting stents have lately been criticized for increased reports of very late stent thrombosis. The exact cause of these very late stent thromboses is not clearly understood. Virchow's triad describes the three main factors of thrombus formation to be stasis of blood flow, endothelial injury and hypercoagulability. Based on Virchow's triad, we propose the cause of very late stent thrombosis to be formation of a de novo atherosclerotic lesion in the proximal segment of a stented artery. The de novo atherosclerotic lesion narrows the vessel lumen and causes stasis of blood flow in the distal stent. The de novo lesion can also cause myocardial ischemia creating a prothrombotic environment in the stented region. Stasis of blood flow and prothrombotic environment in the stented region can lead to the formation of very late stent thrombosis. Since atherosclerosis is a dynamic aging process in humans, we propose de novo proximal lesions in the coronary arteries can predispose to very late stent thrombosis.
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