Biocompatibility of cardiovascular devices - Biomaterials and Devices for the Circulatory System - page 63

disease, is limited by Ni dissolution during metal corrosion (Trepanier et al. ,
1999). Allergic responses to nickel released from Ni-containing devices
constructed of nitinol or from stainless steel stents can have signifi cant
consequences in patients (Rigatelli et al. , 2007; Diaz et al. , 2008). In a study
utilizing a Ni-containing nitinol device used to close an intracardiac shunt,
eight of nine patients with nickel allergies receiving a nitino-based device
for shunt closure developed chest discomfort, exertional dyspnea, and
asthenia, along with leukocytosis, two or three days post-procedure. No
patients without predetermined nickel allergy demonstrated these symp-
toms (Rigatelli et al. , 2007). Nitinol corrosive products and nitinol condi-
tioned supernatants have been found to be toxic to SMCs and inhibit the
proliferation of SMCs (Shih et al. , 2000). These effects on SMC viability
could have the effect of inducing stromal cell death in the coronary vascu-
lature which could perpetuate the infl ammatory and injury response after
device implantation.

3.3.2 Biologic and tissue devices

Biocompatibility of fi xatives

Most tissue devices require fi xation processes with glutaraldehyde (GA),
sodium dodecyl sulfate (SDS), or glycerol, among others, which ideally
preserve the structural and biomechanical integrity of the tissue while erad-
icating the cellular and immunogenic components within the tissue. While
effective as fi xative methods, these have potential drawbacks in their vas-
cular cell (and surrounding stromal cell) cytotoxicity if they leach out of
the device, and are associated with device calcifi cations (Grabenwoger et
al. , 1996, Isenburg et al. , 2006; Rodas et al. , 2008; Caamano et al. , 2009). This
issue is especially pertinent to the biocompatibility of valvular replacement
devices and for the development of acellular scaffolds for tissue engineer-
ing. In the case of heart valves, while tissue devices do not require long-term
anticoagulation as do mechanical valves, they are prone to failure and
replacement within approximately 15 years, in part due to the progressive
calcifi cation which develops on the valves. This is thought to be initiated by
residual devitalized cells that remain in the tissue, and appears to be sig-
nifi cantly associated with fi xation methods, primarily with GA (Schoen and
Levy, 2005; Rapoport et al. , 2007). Specifi c protocols and fi xative methods
utilized may affect these processes to various extents. Evidence has dem-
onstrated decreased calcifi cation and improved endothelialization of bovine
pericardial valves fi xed with glycerol with or without formaldehyde in com-
parison to GA fi xation. These improvements were tempered, however,
by an apparent increase in infl ammation and more severe histologic degen-
eration (Liao et al. , 1993). Superior biomechanical properties, improved

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