Abstract

A drug-eluting stent with rhombic-shaped drug reservoirs is proposed, aimed at providing long-term drug delivery and enhanced fatigue life. Unique rhombic-shaped reservoirs or channels on the stent struts can increase the total drug capacity and improve the stress distribution for longer fatigue life, without compromising other important clinical attributes. Our rhombic-shaped channel stent increases the total drug capacity by multiple times. Its fatigue safety factor, even with the large rhombic cutouts on the stent struts, could be 50% higher than that of the conventional drug-eluting stent. A pulsed fiber-optic laser and a series of expansions and heat treatments were used to make the first prototype of our rhombic-shaped channel stent. This new concept may open up a wide variety of new treatment options and opportunities for the medical industry in the future.

Highlights

  • A stent is a tiny, coiled wire-mesh tube that can be deployed into an artery and expanded percutaneously with a catheter during angioplasty

  • The same phenomenon was observed for the conventional depot stent, at the crown regions and around the reservoirs

  • The total drug capacity was several times greater, and the fatigue safety factor was 50% higher, than those of the conventional drug-eluting stent (DES) stent

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Summary

Introduction

A stent is a tiny, coiled wire-mesh tube that can be deployed into an artery and expanded percutaneously with a catheter during angioplasty. Due to artery wall injury during stenting, intimal cells could proliferate, often leading to excessive neo-intimal hyperplasia and restenosis. Since 2003, stent technology has evolved from the bare metal stent to the drug-eluting stent (DES). A drug-eluting stent is a bare metal stent coated with a drug (e.g., Sirolimus and its analogues, Paclitaxel) that is known to intervene in the cell cycle and the restenosis process. Sirolimus and Paclitaxel inhibit the cell cycle via different mechanisms. Sirolimus has a cytostatic effect and induces cell cycle arrest in the late G1 phase, which has been shown to inhibit all phases of the restenosis cascade, inflammation, neointimal hyperplasia formation, and smooth muscle cell migration [4,5,6]

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