engleski

Electrochemically-assisted Functionalization of 316L Stainless Steel, NiTi and CoCr Surfaces: Towards the Minimization of In-stent Restenosis

Occlusive coronary artery disease (CAD) is reported to be the single largest cause of death in developed countries, such as Canada and United States. The disease is characterized mostly by the formation of a plaque, resulting in considerable narrowing and hardening of the vessels. Approximately one third of CAD patients are treated by angioplasty and stenting. A stent, which is a tiny wire-mesh predominantly made from stainless steel (316L) , is inserted into an artery at the place of the blockage, then it is expanded thus widening the blocked/narrowed artery and enabling increased blood flow . The aim of this work was to develop a new method for the stent surface modification, in an attempt to decrease the in-stent restenosis rate. The ultimate aim of the project was to functionalize surfaces of most common stent materials, 316L stainless steel (SS), NiTi and CoCr, with a chemically-bound extracellular matrix protein fibronectin (FN), and thus to control endothelial and smooth muscle cells / surface(FN) interactions. However, in order to irreversibly immobilize a monolayer of FN on these surfaces, one needs first to form a stable and durable chemical “linking” monolayer on the surface, which was the major aim of the project to be presented. Forming a stable (irreversibly attached) ‘linking’ chemical monolayer on SS, NiTi and CoCr surfaces is a very challenging task, due to the high topographical, morphological, chemical and charge-distribution heterogeneity of the surface and its high susceptibility to get passivated. However, we developed a novel electrochemistry-based method for the modification of these surfaces by an alkanethiol self-assembled monolayer (SAM) of choice. To evaluate the biocompability of FN-modified SS, endothelial and smooth muscle cells attachment and proliferation was done. The results revealed that the rate of endothelial cells attachment and proliferation has remarkably increased on the FN-modified surface, in comparison to the bare metal surface, which consequently may decrease the rate of restenosis. Moreover, platelet adhesion experiments demonstrated that the FN-modified surface is less thrombogenic than the naked SS surface. Furthermore, preliminary in-vivo results with an animal model revealed that the FN-modified SS stent showed a considerable higher biocompatibility than the commercial bare metal stent (control).

cardiovascular stents; 316 L; NiTi; CoCr; fibronectin modified surface; biocompatibility

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