Thrombogenicity

Thrombogenicity refers to the tendency of a material, surface, biological environment, or medical device to promote thrombosis—the formation of a blood clot—when it contacts blood. It is a major concern in cardiovascular medicine and biomaterials because clots can occlude vessels or devices.

The underlying mechanisms involve protein adsorption that precedes cellular events: plasma proteins such as fibrinogen, von Willebrand factor, and others rapidly coat a surface, influencing platelet adhesion and activation. Activated platelets release agonists and provide a scaffold for thrombin generation, leading to fibrin formation. On artificial or nonendothelial surfaces, contact activation of factor XII can initiate the intrinsic coagulation pathway, amplifying thrombogenicity, especially under low shear or turbulent flow. Shear rate and flow patterns strongly modulate thrombus growth.

Thrombogenicity depends on material properties (roughness, hydrophobicity, charge), chemical composition, and the presence of adsorbed proteins. Host factors such as coagulation status, antithrombotic therapy, and comorbidities also influence risk.

Assessment combines in vitro tests of hemocompatibility, such as platelet adhesion and aggregation assays or thrombin generation measurements, with in vivo animal studies and standardized biocompatibility protocols. In medical device development, reducing thrombogenicity is a central design goal.

Mitigation strategies include surface coatings (e.g., heparin, zwitterionic or PEG-like polymers), endothelialization, and material choices that reduce protein adsorption or promote antithrombotic signaling. Understanding thrombogenicity supports safer device design and patient management.