Recent advances in drug eluting stents - PubMed (original) (raw)

Review

Recent advances in drug eluting stents

Amey S Puranik et al. Int J Pharm. 2013.

Abstract

One of the most common medical interventions to reopen an occluded vessel is the implantation of a coronary stent. While this method of treatment is effective initially, restenosis, or the re-narrowing of the artery frequently occurs largely due to neointimal hyperplasia of smooth muscle cells. Drug eluting stents were developed in order to provide local, site-specific, controlled release of drugs that can inhibit neointima formation. By implementing a controlled release delivery system it may be possible to control the time release of the pharmacological factors and thus be able to bypass some of the critical events associated with stent hyperplasia and prevent the need for subsequent intervention. However, since the advent of first-generation drug eluting stents, long-term adverse effects have raised concerns regarding their safety. These limitations in safety and efficacy have triggered considerable research in developing biodegradable stents and more potent drug delivery systems. In this review, we shed light on the current state-of-the-art in drug eluting stents, problems related to them and highlight some of the ongoing research in this area.

Copyright © 2012 Elsevier B.V. All rights reserved.

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Figures

Fig. 1

Fig. 1

Illustration of the mechanisms leading to (A) Atherosclerosis, (B) Restenosis due to angioplasty and (C) in-stent restenosis. (A) Dysfunction of endothelial cells triggers a response-to-injury mechanism increasing monocyte and lymphocyte adherence to the endothelium. Interaction of these cells with the endothelium leads to recruitment of more monocytes/macrophages, lymphocytes, platelets, and smooth muscle cells. Lipid accumulation produces foam cells, which along with lymphocytes and smooth muscle cells drives plaque/lesion formation. (B) Angioplasty causes intimal and medial tears which attract platelets and result in thrombi formation. Smooth muscle cells and collagen then synthesized as a result of the response-to-injury mechanism lead to vessel remodeling. (C) Stent implantation causes endothelial denudation and crushing of the plaque triggering an inflammatory response. Eventually, smooth muscle cell migration and proliferation leads to formation of neointima.

Fig. 1

Fig. 1

Illustration of the mechanisms leading to (A) Atherosclerosis, (B) Restenosis due to angioplasty and (C) in-stent restenosis. (A) Dysfunction of endothelial cells triggers a response-to-injury mechanism increasing monocyte and lymphocyte adherence to the endothelium. Interaction of these cells with the endothelium leads to recruitment of more monocytes/macrophages, lymphocytes, platelets, and smooth muscle cells. Lipid accumulation produces foam cells, which along with lymphocytes and smooth muscle cells drives plaque/lesion formation. (B) Angioplasty causes intimal and medial tears which attract platelets and result in thrombi formation. Smooth muscle cells and collagen then synthesized as a result of the response-to-injury mechanism lead to vessel remodeling. (C) Stent implantation causes endothelial denudation and crushing of the plaque triggering an inflammatory response. Eventually, smooth muscle cell migration and proliferation leads to formation of neointima.

Fig. 1

Fig. 1

Illustration of the mechanisms leading to (A) Atherosclerosis, (B) Restenosis due to angioplasty and (C) in-stent restenosis. (A) Dysfunction of endothelial cells triggers a response-to-injury mechanism increasing monocyte and lymphocyte adherence to the endothelium. Interaction of these cells with the endothelium leads to recruitment of more monocytes/macrophages, lymphocytes, platelets, and smooth muscle cells. Lipid accumulation produces foam cells, which along with lymphocytes and smooth muscle cells drives plaque/lesion formation. (B) Angioplasty causes intimal and medial tears which attract platelets and result in thrombi formation. Smooth muscle cells and collagen then synthesized as a result of the response-to-injury mechanism lead to vessel remodeling. (C) Stent implantation causes endothelial denudation and crushing of the plaque triggering an inflammatory response. Eventually, smooth muscle cell migration and proliferation leads to formation of neointima.

Fig. 2

Fig. 2

Schematic of sirolimus eluting Cypher stent: (A) cross-sectional and side views (B) in vitro sirolimus release profile Adapted from Acharya and Park (2006) by permission.

Figure 3

Figure 3

Schematic of paclitaxel eluting Taxus stent: (A) cross-sectional and side views (B) in vitro paclitaxel release profile Adapted from Acharya and Park, 2006 by permission.

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