Long-Term Alterations in Large-Caliber Arterial Prostheses Used for Aortic Repair

Large-caliber prostheses used for aortic replacement initiate blood–material interfacial processes that begin almost immediately upon establishment of circulatory flow. These processes lead to prosthetic encapsulation and structural alteration, occasionally a degree of degradation of synthetic polymers, and ultimately these events contribute to the long-term development of thrombosis, intimal hyperplasia, tissue incorporation, and dilatation of aortic prostheses.

Early Host Responses to Implanted Materials

Protein Deposition

Almost immediately after circulatory flow is established, protein adsorbs to the biomaterial surface and provides the initial scaffold upon which host coagulation and healing responses will build. Initially, the most abundant and mobile proteins such as albumin, immunoglobulin G (IgG), low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, fibrinogen, and others are adsorbed to the prosthetic surfaces. Over the next several minutes to hours, protein adsorption continues on the biomaterial surface as determined by the Vroman effect. This is characterized by the dynamic interchange between proteins initially adsorbed on the biomaterial surface and proteins with higher affinity whose binding properties depend on their intrinsic three-dimensional conformational and electrochemical properties, as well as the structural irregularity and electrochemical activity of the biomaterial itself.

Platelet Deposition and Coagulation

The tendency of biomaterials to adhere platelets and promote their aggregation and activation before fibrin coagulum forms is a critical component to the host’s response to prosthetic material. Clearly, thrombus formation not only leads to acute graft failures but also serves as a scaffold for mesenchymal and inflammatory cell infiltration before the formation of atherosclerotic plaques and intimal hyperplastic lesions. Platelet adherence occurs by way of binding of the platelet surface glycoprotein (GP) receptor complexes to exposed subendothelial extracellular matrix (ECM) proteins like collagen or to von Willebrand factor (vWF) bound to collagen. The interaction between these glycoproteins and vWF bound to the exposed subendothelium or to endothelial cell (EC) surfaces activates platelets and causes the release of α-granule products, and it increases the local concentrations of serotonin, epinephrine, and adenosine diphosphate (ADP), among others. This degranulation serves to propagate platelet aggregation and activation. The formation of the prothrombinase complex on activated platelets mediated by the extrinsic coagulation pathway facilitates thrombin formation and subsequent fibrin generation.

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