Biomedical Engineering Reference
In-Depth Information
Trans-anastomotic endothelialisation (TAE) appears to be very difficult in humans. Early
studies on synthetic prostheses report that they cannot be longer than 0.5 cm, even after
prolonged implantation. In spite of a long period of observation, internal endothelialisation
has not been observed in humans, except in sites of anastomosis (Berger K et al 1972).
Several factors have been observed to influence this, such as species, senescence, anatomic
dimensions of the vessel, and prosthetic materials (Zilla P et al 2004), but even in animals
TAE is limited (Zhang Z et al 2004).
Study of endothelial cells, both human and canine, compared in vitro, suggest that human
cells have a greater potential for migration but a lower capacity for adhesion, which may
explain the lack of re-endothelialisation in vivo, when blood flow may obstruct cell adhesion
(Dixit P et al 2001).
Instead, the transmural pathway seems to enhance rapid endothelialisation, according to
recent studies on materials with sufficient porosity. Pore size takes on importance in these
studies, since the prosthesis must be sufficiently large to allow cell growth, but not too large
to cause loss of intercellular adhesion (Mooney DJ et al 1996; Kim BS et al 1998; Wake MC et
al 1996). Materials with differently sized pores inside and outside the conduit have even
been experimented, in order to obtain an ecocompatible surface internally and a colonisable
one externally (Mooney DJ et al 1996; Kim BS et al 1998; Wake MC et al 1996).
Pore size also alters the haemocompatibility of biomaterials, as well as their compliance and
degradation time. An optimal pore size for vascular engineering has been hypothesised,
ranging from 30 to 50 microns. It appears that smaller pores would not allow growth of
endothelial cells, and larger ones would cause excessive leakage of blood (Matsuda T et al
1996). Pores in the walls of prosthetic materials can also avoid intimal hyperplasia. It has
been hypothesised that a thrombus initially deposited on the walls of the prothesis later
organises itself into muscle-like tissue, which then gives rise to intimal hyperplasia. The
precocious growth of endothelial tissue would avoid thrombosis and thus the consequent
cascade of events leading to intimal hyperplasia (Mooney DJ et al 1996; Kim BS et al 1998;
Wake MC et al 1996). Increased pore size causes increased radial compliance of the material.
Several studies have shown that vascular implants with fibers organised in a circular
fashion do not cause dilation (Mooney DJ et al 1996; Kim BS et al 1998; Wake MC et al 1996).
This is local, since cells undergo mechanical stress and are thus conditioned in their spatial
orientation.
''Fall-out healing'' leads to the formation of endothelial islands, with no connection with the
formation of trans-anastomotic or transmural tissue. This is a late phenomenon, not of great
importance in materials such as Dacron and e-PTFE grafts, and thus it does not play a
central role in present-day prostheses (Zilla PD et al 2007), but it appears to be the
mechanism for repairing small vascular lesions (Roberts NM et al 2005). However, recent
studies show how this mechanism may be enhanced, by attracting EPC cells to participate
(Avci-Adali MG et al 2010).
3. Mechanical properties of biomaterials
Before describing the mechanical properties of vascular replacements, we must digress to
describe those of vessels. Arteries are mechanically anisotropic, i.e., their elasticity and
resistance (maximum pressure tolerated before bursting) varies according to the direction
along which they are measured. The capacity for distension of the arterial wall is generally
called compliance (radial elasticity), or the difference in diameter obtained by varying
