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CHEM Biomedical Applications
Published in Witold M. Sokolowski, Cold Hibernated Elastic Memory Structure, 2018
Witold M. Sokolowski, Naziha Chirani, L’Hocine Yahia
Recently, Wache et al. [17] have conducted a feasibility study and preliminary development on a polymer vascular stent with shape memory as a drug delivery system. Presently, most commercially available stents are made of metallic materials. A common aftereffect of stent implantation is restenosis. Restenosis occurs as a result of the response of the vascular tissue to the injury caused by coronary angioplasty. In the case of in-stent restenosis, it is the result of vascular injury that occurs after stenting. The injury caused by the insertion of a stent is different from the injury caused by the angioplasty alone. This results in differences in the pathophysiological mechanisms that lead to restenosis in response to injury. In this research, a team presented a new concept for a vascular stent and the possibility to use the stent as a drug delivery system was described. The shape-memory properties of thermoplastic polyurethane allowed for the design of a new fully polymeric self-expandable stent.
Investigator-driven randomized trials
Published in Yoshinobu Onuma, Patrick W.J.C. Serruys, Bioresorbable Scaffolds, 2017
Daniele Giacoppo, Roisin Colleran, Adnan Kastrati
Patients aged between 18 and 80 years are deemed eligible when at least one of the following risk factors for restenosis are present: diabetes; multi-vessel disease with more than one de novo target lesion; and/or patients must have at least one complex de novo lesion satisfying one or more of the following criteria: lesion length >28 mm, reference vessel diameter 2.25–2.75 mm (“small vessel”), lesion with pre-existing total occlusion (TIMI-flow grade 0), or bifurcation lesion requiring a single-stent strategy. Randomization sequence is stratified for STEMI and diabetes. Exclusion criteria include the following: left ventricular ejection fraction <30%, renal insufficiency with eGFR <45 mL/min; known comorbidities making it unlikely for patients to complete 5-year follow-up; known nonadherence to dual antiplatelet therapy; patients on oral anticoagulation; cardiogenic shock; reference vessel diameter <2.25 mm and >4.0 mm or >3.5 mm in the setting of STEMI; target lesion located in a graft, ostial left main lesion, bifurcation requiring a two-scaffold/-stent strategy; in-scaffold/stent thrombosis; in-scaffold/stent restenosis; and severe target-vessel tortuosity.
st Century
Published in Tatiana G. Volova, Yuri S. Vinnik, Ekaterina I. Shishatskaya, Nadejda M. Markelova, Gennady E. Zaikov, Natural-Based Polymers for Biomedical Applications, 2017
Tatiana G. Volova, Yuri S. Vinnik, Ekaterina I. Shishatskaya, Nadejda M. Markelova, Gennady E. Zaikov
In recent years, attempts have been made to enhance biocompatibility of vascular stents by adding biological agents inhibiting hyperplasia of a neointima (dexamethasone, rapamycin, paclitaxel, sirolimus etc.) to stent coatings. Coronary stents Hercules III (Intek, Switzerland) are metallic constructs coated with the drug that contains paclitaxel – the active substance preventing restenosis [data found at the sites of Intek – http://intek/koronarnye_stenty_intek; ROSSLYN Medical®http://rosslynmedical.com]. Hercules III was based on the Hercules II stent. The polymer coating of the stent is biologically stable and bio- and hemocompatible, enabling controlled release of paclitaxel. The active component is concentrated on the outer surface and is directly delivered to the restenosis initiation site. Therefore, Hercules III coronary stents not only mechanically widen the artery but also suppress cell growth in its tissues, thus perceptibly increasing the effect of angioplasty. The active component – paclitaxel – interrupts the cascade development of restenosis; the service life of the drug coating is 18 months. The material used to fabricate Hercules III stents is both mechanically strong and highly pliable. Thanks to this combination, coronary stents are capable of assuming the natural shape of the problem region of the artery and effectively maintaining the width of the lumen sufficient for the normal blood flow. Drug-eluting stents reduce the incidence of restenosis by over 90%, making unnecessary repeated transluminal angioplasty.
Modification of hexachiral unit cell to enhance auxetic stent performance
Published in Mechanics of Advanced Materials and Structures, 2023
Amir Asadi, Dorna Hedayat, Sadegh Ghofrani, Ali Abouei Mehrizi, Ghasem Shadalooyi, Javad Kadkhodapour, Ali Pourkamali Anaraki
Despite the medical and beneficial application of stents, they display many disadvantages which are mentioned accordingly. Foreshortening [22], defined as axial shrinkage during radial expansion. Dogboning [3, 22–24], which is more expansion of both ends of the stent compared to its middle, resulting in a bone-shaped configuration. Stent migration [2, 3, 6, 23], known as the movement of the stent after deployment. Restenosis, that is re-narrowing of the lesion post-stenting. Thrombosis [2, 3, 25], stent collapse [2, 6], isotropic property [2, 24], and finally, permanent nature of the primary BMS stents [3, 25, 26] are also included. To overcome and excel these disadvantages, stents have evolved from BMS [27] to DES [25] and from permanent to biodegradable [28]. Moreover, many advancements have been made in their design and geometries. However, there is still a debate about the ideal stent. Theoretically, an ideal stent better be biodegradable [3, 12], biocompatible [16], have high radial strength [16, 23, 29, 30] and adequate flexibility [16, 23, 29, 30], provide good arterial support [30], and cause minimal injury to the artery in its expanded state [30]. Plus, compromising between radial strength and bending flexibility is inevitable in stent design [30]. In addition to the material of the stent, the geometry also affects its expansion method. Overall, balloon expandable stents should be able to undergo plastic deformation and self-expanding stents should have adequate elasticity to be in crimped state during delivery and expand in the target region [9, 13].
The role of nanomaterials and nanostructured surfaces for improvement of biomaterial peculiarities in vascular surgery: a review
Published in Particulate Science and Technology, 2021
Marius Fodor, Lucian Fodor, Olimpiu Bota
During balloon angioplasty, the endothelial lining of the vessel is interrupted, the atherosclerotic plaque (Figure 4) is ruptured and the vascular smooth muscle is disrupted. This results in a highly thrombogenic area. The formation of a clot in this area is prevented by the administration of antithrombotic agents. After balloon angioplasty, the elastic recoil of the vessel tends to re-occlude the lumen. Stents are used to maintain the vessel open, but these are also prone to restenosis and thrombosis. The injury to the vessel wall promotes the recruitment of vascular smooth muscle and mesenchymal cells, which proliferate and form an extracellular matrix. The cells migrate through the stent struts and occlude the vessel lumen (Bassous, Cooke, and Webster 2016). When the restenosis occurs, the treatment is stent replacement or surgical by-pass. Drug-eluting stents have been developed to inhibit the proliferation of vascular smooth muscle cells and the development of an extracellular matrix. At the same time, these drugs inhibit the proliferation of the natural endothelium, leaving the stent uncovered and prone to life-threatening thrombosis (Nageh and Meier 2005; Joner et al. 2006).
A fully coupled framework for in silico investigation of in-stent restenosis
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2019
Shibo Li, Long Lei, Ying Hu, Yanfang Zhang, Shijia Zhao, Jianwei Zhang
From biological perspectives, various studies have shown that restenosis is caused by neointimal hyperplasia (Dussaillant et al. 1995; Shah 2003; Kleinedler et al. 2012), which is characterized by the proliferation and migration of vascular smooth muscle cells (VSMCs) in the tunica intima of the artery wall. This process is illustrated in Figure 1. The restenosis process starts with tissue damage and inflammation resulted from stent implantation or angioplasty procedure, followed by extracellular matrix (ECM) degradation and VSMC phenotype switches (Thyberg et al. 1997), which would result in neointimal formation. Moreover, increasing evidences have shown that the proliferation, migration and apoptosis behaviors of VSMCs are regulated by matrix-degrading metalloproteinases (MMPs) (Zempo et al. 1996; Newby 2006). Despite the complexity of the biological processes, mathematical models for computational purposes have been built for various problems (Garzón-Alvarado et al. 2012; Prokharau et al. 2014; Boyle et al. 2011).