doi: 10.1161/01.CIR.0000069331.67148.2F
(Circulation. 2003;107:2383.)
© 2003 American Heart Association, Inc.
Clinical Cardiology: New Frontiers |
New Frontiers in Cardiology
Drug-Eluting Stents: Part II
From the Institute Dante Pazzanese of Cardiology, São Paulo, Brazil (J.E.S.); Thoraxcenter, Dijkzigt University Hospital, Rotterdam, the Netherlands (P.W.S.); and University of Florida Health Science Center, Shands Jacksonville, Jacksonville, Fla (M.A.C.).
Correspondence to Prof. J. Eduardo Sousa, MD, PhD, Director of the Institute Dante Pazzanese of Cardiology, Av. Dr Dante Pazzanese, 500 – Ibirapuera, 04012180, São Paulo, Brazil. E-mail jesousa@uol.com.br
Key Words: stents • drugs • restenosis • trials
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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In this second part of the article, we will complete the review of drug-eluting stent technologies (Table 1) and discuss methodological and technical aspects of drug-eluting stents.
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Biological Agents (Continued)
(1) Stents Eluting Antiproliferative Agents
A number of antineoplastic medications have been considered for the prevention of restenosis. Paclitaxel and its derivatives have been the most investigated compounds of this group.
(a) Paclitaxel-Eluting Stents
Paclitaxel (Taxol; Bristol-Myers Squibb) is a microtubule-stabilizing agent with potent antitumor activity.1 Many different platforms that use polymer coating or surface modifications to adhere paclitaxel onto the stents have been utilized over the past 2 years.
Preclinical Data
Unlike other antimitotic agents, paclitaxel shifts the cytoskeleton equilibrium toward assembly, leading to reduced vascular cell proliferation, migration, and signal transduction.2 Paclitaxel is highly lipophilic, resulting in a rapid cellular uptake and a long-lasting effect in the cell.3
NIR stents (Boston Scientific Corp) coated with poly(lactide-co-
-caprolactone) copolymer and paclitaxel (200 µg/stent) were placed in porcine coronary arteries. Paclitaxel-eluting stents showed a marked reduction in neointimal and medial cell proliferation at all time points (7, 28, 56, and 180 days).4 However, arteries treated with paclitaxel showed incomplete healing, late persistence of a large number of macrophages, and fibrin deposition. Similar findings were observed with a stent platform coated with cross-linked biodegradable polymer (chondroitin sulfate and gelatin) and 42.0, 20.2, 8.6, or 1.5 µg of paclitaxel in rabbit iliac arteries.5 These studies indicate the need for a more controlled drug release of paclitaxel due to the narrow toxic-therapeutic window and high
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