Abstract

Stents are tubular meshed devices implanted to restore the perviety of an occluded vessel owing to the presence of an atherosclerotic plaque. These devices were introduced in to clinical practice from 1980. The first stent implanted in a human coronary artery was the Wallstent [1], a self-expandable metallic device. The use of a stent to expand the vessel was introduced to overcome the greater limit of angioplasty, the elastic recoil of the vessel wall, yet also caused the onset of another, different pathology: intra-stent restenosis. This pathology results from injuries on the vessel wall after balloon inflation as well as the different fluid dynamic regime established after stent implantation [2]. Intra-stent restenosis is caused by the abnormal growth of tissues within stent meshes, leading to the implant failure. The common therapeutic approach to limit hyperplasia is the systemic administration of antimitotic and anti-inflammatory drugs. This treatment generally fails because effective dosing levels have toxic effects on patients. Since 2000, a new and emerging class of stents was introduced to redress this problem. We are referring to drug-eluting stents (DES), new devices loaded with one or more active principles for the local administration of the drug, avoiding the systemic administration of massive doses. DES are metallic devices impregnated with a drug on their surface or coated with a polymeric thin layer containing the active principle.

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