Biocompatibility of cardiovascular devices - Biomaterials and Devices for the Circulatory System - page 56

growing on the device (Lackie and de Bono, 1977; Tonnesen et al. , 1984;
Bevilacqua et al. , 1985).
Macrophages, which are either resident in the tissues or are derived from
circulating monocytes, also make up part of the early response to cardio-
vascular devices. Monocytes are recruited to implanted devices by numer-
ous chemokines and macrophage recruiting mediators from various sources
including the regenerating endothelium, platelets and other macrophages,
as well by the fi brin coagulum and complement products (Kay et al. , 1973;
Deuel et al. , 1982; Bar-Shavit et al. , 1983; Bevilacqua et al. , 1985; DiCorleto
and de la Motte, 1985; Marder et al. , 1985; Greisler, 1988, 1990; Greisler et
al. , 1989a). These activated macrophages produce infl ammatory mediators
such as IL-1, TNF, and others which propagate the host response to wound
healing, the reaction to foreign materials, and the remodeling of myointimal
and atherosclerotic plaques on the surface of devices. Interestingly, the role
of diet as a mediator of macrophage activity may be suggested by studies
which have demonstrated that media conditioned by macrophages taken
from rabbits given atherogenic diets are more mitogenic for fi broblasts,
smooth muscle cells (SMCs), and ECs compared with macrophages taken
from rabbits fed normal diets. Further, atherogenic diets have been shown
to affect macrophage/biomaterial interactions, as the mitogenic profi le of
macrophage conditioned media was signifi cantly altered by the addition of
biomaterials in a material and diet-specifi c manner (Greisler et al. , 1991).
Dendritic cells and other antigen presenting cells link the innate immu-
nologic response to the antigen specifi c and T-cell mediated adaptive
response. The role of specifi c T-cell responses to implanted biomaterials is
still unclear (Rodriguez et al. , 2008). Emerging literature, however, has
explored the role of biomaterial surfaces as enhancers of adaptive immu-
nity, and has investigated the role of biomaterials on dendritic cell matura-
tion and phenotype (Babensee, 2008). Similarly, the role of regulatory T
cells in cardiovascular device biocompatibility remains largely a mystery.

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3.2.4 Endothelialization
The vessel intima and the endothelium and endocardium of heart valves
and cardiac tissue is believed to be a signifi cant inhibitor of thrombosis and
to attenuate the myointimal hyperplastic response. This effect is partially
dependent on the phenotypic characterization of the endothelium, however,
as an endothelium activated by injury may function to promote thrombosis
or myointimal hyperplasia by the upregulation and release of adhesion
receptors, vWF, tissue factor, endothelin-1, PDGF, and other EC products
(McGuigan and Sefton, 2007; Anggrahini et al. , 2009).
It is likely that the inability of humans to promptly generate a functional
endothelium and establish normal histological archeology in the coronary