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Conclusions
We have developed a self-actuating, self-sensing device for detecting the presence of endothelial cells on a surface. The device is biocompatible and functions reliably in ionic liquids, making it appropriate for implantable applications. This sensor can be placed along the struts of a coronary stent to detect when the struts have been covered with a layer of endothelial cells and are no longer available surfaces for clot formation. Anti-platelet therapy can be adjusted in real-time with respect to a patient's level of healing and hemorrhaging risks.
Currently, the greatest limitation of this technology is the inability to differentiate between the various cell types or any object with mass that may deposit on the surface of a stent. The possibilities for adhered masses include fibrin, clots, neointima, and endothelial cells. It has been shown that a higher ratio of stent struts covered with either neointima or endothelial cells to total stent struts is correlated with a lower incidence of late stent thrombosis [6]. In contrast, an increasing amount of fibrin on the stent surface is correlated with an increased risk [6]. Thus, the sensor must differentiate between stent coverage associated with lower incidence of thrombosis (neointima and endothelialization) and stent coverage associated with higher incidence of thrombosis (fibrin). One test that could provide this differentiation is application of a fibrinolytic drug. The sensors would be monitored as the drug was administered, if the frequency peaks indicating strut coverage persist, this would indicate that the surface is covered with substances other than fibrin or clots and thus anti-platelet therapy can be safely terminated. If the frequency peaks return to the uncoated state, the physician will be alerted that the patient is still at an increased risk of clotting and preventative measures should be continued. Future versions of this device could be designed to exploit the differences (i.e. density) of different types of biological coatings to more sophisticatedly detect stent healing.
Currently, the struts on a drug-eluting stent range from 81 to 140-μm wide [19,20]. The cantilever used in this paper is 262-μm wide. Ideally, the sensor should be thinner than the stent strut, so that it does not provide a greater surface area for potential clot formation. A similar, thinner cantilever should be developed for the final device to remedy this issue.

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