The implantation of a balloon expandable stent induces chronic stent-induced stresses on the artery wall. These highly non-physiologic stresses can provoke inflammation and smooth muscle cell proliferation. Ultimately, this cascade of events leads to restenosis, or the development of a new blockage in the stented artery. Since the initial human implantation of balloon expandable stents, technological advances in stent design, material properties, and deliverability have expanded the application and success rate of the procedure. More recently, anti-restenotic strategies such as drug-eluting stents have aimed to counteract the restenosis process. While clinical trials have demonstrated the success of drug eluting stents in coronary arteries [1], risk of late thrombosis [2] and failure to prevent restenosis in peripheral arteries [3] has limited this technology. A further investigation into the artery wall stresses induced by stent implantation, and the pursuit of strategies to minimize them could reduce the restenosis rates for both bare metal and drug-eluting stents.

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