Why the study?
Stent restenosis and late thrombosis compromise clinical benefit through unclear mechanisms, and stenting may affect nitric oxide concentration in the host artery.
Does stent implantation affect nitric oxide concentration in patient-specific carotid artery models?
Does stent implantation affect nitric oxide concentration in patient-specific carotid artery models?
Numerical simulations demonstrate that carotid stenting decreases local nitric oxide concentration, potentially explaining the mechanisms behind stent restenosis and late thrombosis.
Answers are grounded in this paper and cite their sources.
Stent-induced NO disruption may heighten restenosis risk; leaves open whether NO-targeted interventions warrant prospective validation.
Stent restenosis and late thrombosis compromise endovascular stent implantation clinical benefit, and the mechanism is unclear. Since nitric oxide (NO) plays a pivotal role in maintaining vascular homeostasis, we believe that stenting can affect NO concentration in the host artery, thereby contributing to postoperative adverse events. We numerically investigated NO concentration after stenting based on the patient-specific carotid to verify this hypothesis. The simulation revealed that stent implantation caused blood flow disturbance, a low wall shear stress, and a significant decrease in NO on the luminal surface, especially in the region of the stented segment. Moreover, severe damage to the artery wall or low blood flow, leading to a low NO generation rate, would induce relatively low NO level in the stented segment. Additionally, we demonstrated that NO distribution might be affected by the combination of stent struts and carotid bifurcation geometry, while the host arterial configuration might play a leading role in the distribution of NO concentration. In conclusion, the carotid artery had a relatively low NO concentration level near stent struts, especially at the severely injured artery, low blood flow, long stenting, and complex host artery which might lead to a genesis/development of adverse events after that intervention.
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Fan et al. (2023) studied this question.
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