Biomedical Engineering Reference
In-Depth Information
2.6 Biocompatibility and the Substrate-Blood and
Platelet Interaction: A Comment on Long-term
Effects
The huge importance of the biochemistry of interaction of cells with substrate
surfaces in terms of biocompatibility has figured significantly in the
summarizing material presented above. Here we address, as a final comment,
the damaging effects that the interaction of biological elements, including cells,
suffers as a result of this type of process. The subsequent cascade of events can
lead to serious medical problems. Blood interactions with bio-active surfaces
are of course ubiquitous in medicine with respect to both intra- and extra-
corporeal devices. Included are a host of implantables such as artificial hips
and stents placed inside the body and extracorporeal structures such cardio-
pulmonary bypass circuitry, oxygenators, and dialysis and hemoperfusion
membranes. To fabricate these systems a very wide variety of materials are
employed which include many polymers and metals such titanium and steel.
A key issue with regard to blood-surface interactions, whatever the substrate, is
the possibility of increased thrombogenicity. For the non-biologist this means
the increased risk of clot formation in the vasculature. The foreign body can
result in the accumulation of circulating platelets at its surface. These in turn
are activated, culminating in thrombus formation via an aggregation of
thrombin and fibrin. Of course there are many possible biological causes for
thrombus formation, which is now well-understood through research in cellular
and molecular biology. However, the role of foreign substrates is perhaps less
well characterized.
With respect to cardiopulmonary systems such as dialysis, hemoperfusion
and bypass membranes, there is evidence for a persistent and debilitating effect
on the brain function which is manifested as cognitive deficit. It has been shown
by Stroobant and Van Nooten
99
that many patients who undergo cardiopul-
monary bypass surgery present post-surgical cognitive defects. The mechanism
of this process is thought to involve cerebral micro-strokes caused by thrombi
release from, for example, perfusion apparatus due to platelet activation and
protein coagulation. In a similar vein, it has also been shown that patients who
receive continual hemodialysis treatment for renal failure exhibit a progressive
decline in cognitive function.
100
Again, at least part of this decline is thought to
involve foreign surface instigation of inflammatory effects.
Coronary artery disease can be treated by bypass surgery (and balloon
angioplasty). An alternative to this approach was introduced by Sigwart et al.
25
in terms of the first coronary stent, a medical device designed to serve as a
temporary or permanent mechanical support within the artery. Stents are
meshed cylindrical scaffolds, usually constructed from metals or polymers.
The stent is typically inserted via balloon- or self-expandable technology into
the vascular lumen and expanded into contact with the diseased portion of the
arterial wall, restoring adequate blood supply to the heart muscle. However,
neointimal hyperplasia (NIH) has remained the principal cause of in-stent
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