Impact of polymer hydrophilicity on biocompatibility: Implication for DES polymer design

✍ Scribed by Ayala Hezi-Yamit; Carol Sullivan; Jennifer Wong; Laura David; Mingfei Chen; Peiwen Cheng; David Shumaker; Josiah N. Wilcox; Kishore Udipi

• Book ID: 102295400
• Publisher: John Wiley and Sons
• Year: 2009
• Tongue: English
• Weight: 364 KB
• Volume: 90A
• Category: Article
• ISSN: 1549-3296
• DOI: 10.1002/jbm.a.32057

✦ Synopsis

Abstract

Polymer coatings are essential for local delivery of drug from the stent platform. In designing a DES, it is critical to balance the hydrophilic and hydrophobic components of the polymer system to obtain optimal biocompatibility, while maintaining controlled drug elution. This study investigates the impact of polymer composition of the BioLinx™ polymer blend on in vitro biocompatibility, as measured by monocytic adhesion. Comparable evaluation was performed with polymers similar to those utilized in various DES that are currently being marketed. Relative hydrophilicities of polymer surfaces were determined through contact angle measurements and surface analyses. Polymer biocompatibility was evaluated in a novel in vitro assay system in which activated monocyte cells were exposed to polymer coated on 96‐well plates. Enhanced monocyte adhesion was observed with polymers of a more hydrophobic nature, whereas those which were more hydrophilic did not induce activated monocyte adhesion. Our data supports the hypothesis that polymer composition is a feature that dictates in vitro biocompatibility as measured by monocyte driven inflammation. Monocyte adhesion has been shown to induce local inflammation as well as promote vascular cell proliferation factors contributing to in stent restenosis (Rogers et al., Arterioscler Thromb Vasc Biol 1996;16:1312–1318). Observed results suggest hydrophobic but not hydrophilic polymer surfaces support adhesion of activated monoctyes to the polymer scaffold. The proprietary DES polymer blend BioLinx has a hydrophilic surface architecture and does not induce an inflammatory response as measured by these in vitro assays. © 2008 Wiley Periodicals, Inc. J Biomed Mater Res, 2009