Background: Atherosclerosis is associated with disturbed blood flow characterized by low and oscillatory shear stress (SS), however, few study directly links SS to neointimal hyperplasia in animal model. This study was focused on the effects of changed SS upon the neointimal hyperplasia which responded to balloon injury in a novel rabbit model with partially-constricted abdominal aorta.
Methods: We established a rabbit model subjected to partial abdominal aortic constriction with a cylinder-shaped cannula as a model of disturbed flow, which was similar to the hemodynamic features of stenosis caused by atherosclerosis plaque. Further, balloon injury was performed to investigate the relationship between SS and neointimal hyperplasia. Four weeks later, the abdominal aorta was assessed with digital subtraction angiography (DSA) and intravascular ultrasound (IVUS). The vascular sections were embedded in paraffin blocks for morphometric analysis to evaluate neointimal hyperplasia, and anti-CD31 immunohistochemical staining was for endothelialization ratio.
Results: In upstream the stenosis, the changed SS leads to neointimal hyperplasia compared with normal SS (11,729 ± 1205 vs 8418 ± 737, P = 0.023). However, the upstream SS of the stenosis can promote vascular re-endothelialization after balloon injury compared with normal SS, verified by endothelialization ratio (0.36 ± 0.03 vs 0.32 ± 0.03, P = 0.017), thereby attenuate neointimal hyperplasia (64,851 ± 3995 vs 68,335 ± 3867, P = 0.018).
Conclusion: The upstream SS of stenosis, not downstream SS, inhibits the neointimal hyperplasia after balloon injury by promoting vascular re-endothelializtion.
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http://dx.doi.org/10.1186/s12872-017-0690-3 | DOI Listing |
J Mater Sci Mater Med
January 2025
Department of Neurology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, PR China.
In-stent restenosis (ISR) following interventional therapy is a fatal clinical complication. Current evidence indicates that neointimal hyperplasia driven by uncontrolled proliferation of vascular smooth muscle cells (VSMC) is a major cause of restenosis. This implies that inhibiting VSMC proliferation may be an attractive approach for preventing in-stent restenosis.
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December 2024
Institute of Biomedical Engineering, College of Medicine, Southwest Jiaotong University, Chengdu, Sichuan 610031, China.
Modification of polylactic acid (PLA) is a promising strategy for the next generation of bioresorbable vascular stent biomaterials. With this focus, FeMOFs nanoparticles was incorporated in PLA, and then post loading of carbon monoxide (CO) was performed by pressurization. It showed FeMOFs incorporation increased hydrophilicity of the surface and CO loading, and CO release was sustained at least for 3 days.
View Article and Find Full Text PDFProg Cardiovasc Dis
January 2025
Division of Cardiovascular Medicine, Department of Medicine, University of Virginia Health System, 1215 Lee Street, Charlottesville, VA 22909, United States of America. Electronic address:
Coronary artery in-stent restenosis (ISR) is driven by neointimal hyperplasia and neo-atherosclerosis in previously placed stents. Drug eluting stents (DES) have been adopted as first line therapy for the initial episode of ISR. However, recurrent ISR has limited durable salvage options.
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Aging and Metabolism Research Group, Korea Food Research Institute, Wanju‑gun, 55365, Republic of Korea.
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View Article and Find Full Text PDFRev Cardiovasc Med
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Department of Cardiology, University Clinical Center of Serbia, 11000 Belgrade, Serbia.
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