Nonspecific protein adsorption is the initial event at the interface between the surface of the implant and human blood, wherein the dynamics of protein adsorptions are governed by kinetic and thermodynamic principles. Although the blood contains over 300 proteins of varying shape, size, and concentration, the main contributors to the formation of the non-specific protein adsorbed layer are fibrinogen, albumin, and immunoglobulins. Typically, the first plasma protein to be adsorbed to the surface is fibrinogen following other contact factors, and adsorption of even small amounts of fibrinogen can initiate a cascade of events including platelet adhesion and activation of coagulation (Figure ). Locally generated thrombin converts fibrinogen to fibrin and the fibrin monomers then polymerize to form fibrin. Thrombin also serves as a potent platelet agonist, which activates ambient platelets that adhere and aggregate on the graft surface. Formation of plateletrich thrombi on the graft surface fouls the device and can provide a nidus for infection, or can reduce graft patency and lead to embolic complications (Figure ). Complement activation by synthetic vascular grafts could also lead to the prevention of endothelial cell seeding, resulting in the aggregation of platelets and the in situ production of tissue thromboplastin by polymorphonuclear leukocytes. Aside from thrombosis, fibrosis and calcification are other long term complications of synthetic vascular grafts.