Principles of Clinical and Engineering Integration in Hemocompatibility - Biomaterials Science: An Integrated Clinical and Engineering Approach - page 9

validity of the biomaterial. It is therefore critical that when designing bioma-
terials, we take into account various considerations that focus on the patient
[1, 27, 60]. There are enormous individual differences, yet we can attempt
to better characterize and classify certain similarities among patients that
may explain the successes and failures of a biomaterial once implanted into
a patient [1, 3, 9, 17-23].
Stratifying patients can allow us to achieve several important objec-
tives with respect to the biomaterial being implemented in a particular
medical technology. First, better patient selection, according to relevant
risk factors inherent to the patients, can allow a higher success rate in
a targeted patient population in terms of the hemocompatibility of the
biomaterial. Such factors can include predispositions to thrombogenesis
due to inherent biological factors such as polymorphisms of inflammatory
factors and genetic resistance to anticoagulation adjunct therapy [2, 22-24].
Second, by distinguishing the factors that do or do not contribute to the
success of the biomaterial, we can achieve additional targets for future
surface modification of the biomaterial. This would allow us to enlarge the
targeted patient population. Yet we must be aware that while the attempts
must continue to better stratify patients, individual patient differences can
still occur [2].
Genetic Polymorphism and Individual
Variability: Focus on Cardiac Stents
Genetic polymorphism has a critical influence on the development of
thrombosis as well as on the specific treatment response, in that it affects
the efficacy and safety of drugs used in the treatment and prevention of
thrombosis. Genetic polymorphism may impact the systemic and local
response to the surface modification of a biomaterial [2, 6, 22-24]. Cardiac
stents are an example where the impact of genetic polymorphism and
individual variability can be seen [4, 6, 22-24]. The characterization of
inflammation as an important factor of stent restenosis has assisted in
identifying several culprit genes that may impact thrombosis [4, 6]. Much
effort is continuously being allocated to preventing thrombosis by mini-
mizing local inflammation and, the proliferation of particular cells, such
as smooth cells, by the use of drug-eluting stents that carry agents that
prevent smooth-cell proliferation. At the same time, a confluent layer of
endothelial cells is needed within the lumen of the stent to prevent throm-
bosis [1, 6, 8, 16-21, 27, 50, 60]. In this section, we will discuss the multiple
targets of genetic polymorphisms that have demonstrated predisposition
to thrombosis with respect to cardiac stents.