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Vascular stent intervention is a pivotal treatment for coronary atherosclerosis, though in-stent thrombosis remains a significant postoperative complication with an unclear underlying mechanism. This study utilized dissipated particle dynamics analysis to investigate the impact of stent and its injury on platelet behavior. The findings suggest that thrombus formation upstream of the stent is mainly initiated by upstream arterial injury, which leads to increased platelet accumulation and activation in that area. While thrombosis downstream of the stent is more directly influenced by the stent itself. The morphology and size of in-stent thrombosis can vary significantly due to the different contributions of the stent and underlying injuries. Additionally, the volume of in-stent thrombosis is affected by the extent of the injury and the viscosity of platelets, showing a notable increase in volume with the lengthening of the injury area and rise in platelet viscosity. This study provides a novel theoretical framework for optimizing stent placement strategies and structural designs by examining the effects of stent struts and associated injuries on thrombus formation., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Background: Stent implantation is a highly efficacious intervention for the treatment of coronary atherosclerosis. Nevertheless, stent thrombosis and other post-operative complications persist, and the underlying mechanism of adverse event remains elusive., Methods: In the present study, a dissipative particle dynamics model was formulated to simulate the motion, adhesion, activation, and aggregation of platelets, with the aim of elucidating the mechanisms of in-stent thrombosis., Findings: The findings suggest that stent thrombosis arises from a complex interplay of multiple factors, including endothelial injury resulting from stent implantation and alterations in the hemodynamic milieu. Furthermore, the results suggest a noteworthy association between in-stent thrombosis and both the length of the endothelial injured site and the degree of stent malposition. Specifically, the incidence of stent thrombosis appears to rise in tandem with the extent of the injured site, while moderate stent malposition is more likely to result in in-stent thrombosis compared to severe or minor malposition., Interpretation: This study offers novel research avenues for investigating the plasticity mechanism of stent thrombosis, while also facilitating the clinical prediction of stent thrombosis formation and the development of more precise treatment strategies., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

A high in-stent restenosis rate and thrombosis have compromised clinical benefits after vascular stent placement. Exercise rehabilitation after stenting emerges as a promising and practical therapeutic strategy to improve the clinical performance of this therapy, although it remains controversial. The present study aimed to explore the impact of exercise training on hemodynamic performance after vascular stent implantation. Different 3-dimensional computational models based on the patient-specific carotids were constructed to calculate hemodynamic parameters, including flow velocity, time-averaged wall shear (TAWSS), oscillatory shear index (OSI) and relative residence time (RRT). The results demonstrated that exercise training increased TAWSS but decreased OSI and RRT in some cases after the intervention, and high-intensity exercise further suppressed the adverse blood flow. However, exercise training remarkably reduced TAWSS and elevated OSI and RRT in patients with mild stenosis at upstream of stented segment. Additionally, we discovered that the hemodynamic environment change induced by exercise training was not significant compared to the stent position in some cases. Exercise had a less beneficial impact on the disturbed blood flow after the distal common carotid artery (CCA) stenting. These findings highlighted that exercise-induced hemodynamic changes differ under different conditions. The exercise training for the intervention patients should only be performed after a comprehensive vascular function assessment.