Biocompatibility of cardiovascular devices - Biomaterials and Devices for the Circulatory System - page 65

those processes which improve it. These strategies range from the induction
of endothelialization by EC seeding of biomaterials or by promoting angio-
genic mechanisms, to the passivation of surfaces with ECM coatings for the
purposes of minimizing protein adsorption. This section will focus on a few
of the most widely studied strategies. Owing to the high volume of research
activity in the coronary stent literature, much of the discussion refers to
strategies focused on stent and bypass conduit durability. However, the
concepts and strategies apply to most cardiovascular devices as they induce
similar host responses.

3.4.1 Passivation/inert biomaterials

Early attempts to passivate biomaterial surfaces with albumin, polyethylene
oxide (PEO), heparin, phosphorylcholine, and other agents to limit protein
and cell adhesion, had provided encouraging successes (Cziperle et al. , 1992;
Laredo et al. , 2004; Jordan and Chaikof, 2007). These strategies alter bio-
material surface active binding sites, as well as the electrochemical and
hydrophobic properties that contribute to protein and cell adhesion to
biomaterial surfaces. While entirely inert biomaterials have yet to be
discovered (van der Giessen et al. , 1996), recent attempts to utilize more
relatively inert biomaterials as coatings can minimize the surface-blood
interfacial processes which limit device biocompatibilities. This remains a
common and evolving strategy for almost all cardiovascular devices. Spe-
cifi c semiconductive properties of amorphous silicon carbide and magne-
sium alloy, novel biomaterials utilized to coat metallic stent surfaces, have
been shown to be associated with lower rates of platelet adhesion, platelet
activation, and fi brin formation compared with uncoated stainless steel
stents (Hansi et al. , 2009).
Poly(L-lysine)-graft-poly(ethyleneglycol) (PLL-g-PEG) coated on metal-
lic stent surfaces reduces stent intimal hyperplasia in a porcine coronary
artery restenosis model compared with uncoated stents, and does not induce
noticeable increases in infl ammation or thrombosis (Billinger et al. , 2006).
Cytotoxicity analysis of poly(propylene fumarate-co-ethylene glycol)
[P(PF-co-EG)]copolymer hydrogels has demonstrated acceptable biocom-
patibility in terms of EC viability correlative to an increasing weight percent
of PEG, favorable rates of infl ammatory and leukocyte infi ltration in vivo ,
and decreased platelet adhesion under both fl ow and static conditions rela-
tive to PPF homopolymer (Suggs et al. , 1999a, b). PEG has also demon-
strated relatively low levels of complement activation and is associated with
less calcifi cation when grafted to bovine pericardium compared with
untreated GA fi xed bovine pericardium, making it potentially useful as a
valve coating (Aravind et al. , 1998).

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