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The therapeutic efficacy of a cardiovascular device after implantation is highly dependent on the host-initiated complement and coagulation cascade. Both can eventually trigger thrombosis and inflammation. Therefore, understanding these initial responses of the body is of great importance for newly developed biomaterials. Subtle modulation of the associated biological processes could optimize clinical outcomes. However, our failure to produce truly blood compatible materials may reflect our inability to properly understand the mechanisms of thrombosis and inflammation associated with biomaterials. In vitro models mimicking these processes provide valuable insights into the mechanisms of biomaterial-induced complement activation and coagulation. Here, we review (i) the influence of biomaterials on complement and coagulation cascades, (ii) the significance of complement-coagulation interactions for the clinical success of cardiovascular implants, (iii) the modulation of complement activation by surface modifications, and (iv) in vitro testing strategies.
Abstract: The main purpose of new stent technologies is to overcome unfavorable material-related
incompatibilities by producing bio- and hemo-compatible polymers with anti-inflammatory and antithrombogenic properties. In this context, wettability is an important surface property, which has a
major impact on the biological response of blood cells. However, the influence of local hemodynamic
changes also influences blood cell activation. Therefore, we investigated biodegradable polymers
with different wettability to identify possible aspects for a better prediction of blood compatibility.
We applied shear rates of 100 s−1 and 1500 s−1 and assessed platelet and monocyte activation as
well as the formation of CD62P+ monocyte-bound platelets via flow cytometry. Aggregation of
circulating platelets induced by collagen was assessed by light transmission aggregometry. Via
live cell imaging, leukocytes were tracked on biomaterial surfaces to assess their average velocity.
Monocyte adhesion on biomaterials was determined by fluorescence microscopy. In response to
low shear rates of 100 s−1
, activation of circulating platelets and monocytes as well as the formation
of CD62P+ monocyte-bound platelets corresponded to the wettability of the underlying material
with the most favorable conditions on more hydrophilic surfaces. Under high shear rates, however,
blood compatibility cannot only be predicted by the concept of wettability. We assume that the
mechanisms of blood cell-polymer interactions do not allow for a rule-of-thumb prediction of the
blood compatibility of a material, which makes extensive in vitro testing mandatory.