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Updated: Apr 20, 2026
Experimental Investigation of Secondary Flow Structures Downstream of a Model Type IV Stent Failure in a 180° Curved Artery Test Section
Published on: July 19, 2016
Simulation of the microscopic process during initiation of stent thrombosis
Jennifer K W Chesnutt1, Hai-Chao Han2
1Cardiovascular Biomechanics Laboratory, Department of Mechanical Engineering, The University of Texas at San Antonio, San Antonio, TX, USA.
Objective:
Coronary stenting is one of the most commonly used approaches to open coronary arteries blocked due to atherosclerosis. However, stent struts can induce stent thrombosis due to altered hemodynamics and endothelial dysfunction, and the microscopic process is poorly understood. The objective of this study was to determine the microscale processes during the initiation of stent thrombosis.
Methods:
We utilized a discrete element computational model to simulate the transport, collision, adhesion, and activation of thousands of individual platelets and red blood cells in thrombus formation around struts and dysfunctional endothelium.
Results:
As strut height increased, the area of endothelium activated by low shear stress increased, which increased the number of platelets in mural thrombi. These thrombi were generally outside regions of recirculation for shorter struts. For the tallest strut, wall shear stress was sufficiently low to activate the entire endothelium. With the entire endothelium activated by injury or denudation, the number of platelets in mural thrombi was largest for the shortest strut. The type of platelet activation (by high shear stress or contact with activated endothelium) did not greatly affect results.
Conclusions:
During the initiation of stent thrombosis, platelets do not necessarily enter recirculation regions or deposit on endothelium near struts, as suggested by previous computational fluid dynamics simulations. Rather, platelets are more likely to deposit on activated endothelium outside recirculation regions and deposit directly on struts. Our study elucidated the effects of different mechanical factors on the roles of platelets and endothelium in stent thrombosis.
Insights
Platelet activation and thrombosis initiation around coronary stents are complex. This study reveals platelets deposit on activated endothelium outside recirculation zones and directly on struts, influenced by strut height and shear stress.
Area of Science:
- Cardiovascular research
- Biomedical engineering
- Computational fluid dynamics
Background:
- Coronary stenting is vital for atherosclerosis treatment.
- Stent struts can cause stent thrombosis via altered hemodynamics and endothelial dysfunction.
- Microscale processes of stent thrombosis initiation are not well understood.
Purpose of the Study:
- To determine microscale processes during stent thrombosis initiation.
- Investigate the role of platelet and endothelial interactions.
- Analyze the impact of stent strut geometry on thrombosis.
Main Methods:
- Utilized a discrete element computational model.
- Simulated transport, collision, adhesion, and activation of platelets and red blood cells.
- Modeled thrombus formation around stent struts and dysfunctional endothelium.
Main Results:
- Increased strut height correlated with greater endothelium activation by low shear stress, increasing mural thrombi.
- Thrombi were typically outside recirculation regions for shorter struts.
- Platelet deposition was highest on activated endothelium outside recirculation zones and directly on struts, influenced by strut height and shear stress.
Conclusions:
- Platelets initiate stent thrombosis by depositing on activated endothelium outside recirculation regions and directly on struts.
- Contrary to previous models, platelets do not necessarily enter recirculation zones.
- Mechanical factors significantly influence platelet and endothelial roles in stent thrombosis initiation.
