Thromboresistance

Thromboresistance is a term used to describe a reduced tendency for blood to form clots, either in living tissue or on artificial surfaces, under conditions that would normally promote thrombosis. It can refer to a physiological phenotype in individuals or to the design and properties of biomaterials and medical devices that resist thrombus formation.

In biological contexts, thromboresistance depends on the balance between prothrombotic and antithrombotic factors. Endothelial cells with intact anticoagulant properties—through mechanisms such as nitric oxide and prostacyclin production, thrombomodulin, and endothelial protein C pathway activity—contribute to a resistant surface within vessels. Platelet reactivity, coagulation factor activity, and fibrinolytic capacity also shape thrombus formation. Genetic, epigenetic, or acquired variations that dampen platelet activation or coagulation can contribute to a thromboresistant state, albeit not constitutively or universally.

In materials science and medical device design, thromboresistance refers to surface properties that minimize protein adsorption, platelet adhesion, and thrombin generation after blood contact. Approaches include heparin coatings, hydrophilic or zwitterionic surfaces, nitric oxide–releasing or endothelialized coatings, and other biocompatible chemistries that reduce clot formation on catheters, vascular grafts, stents, and extracorporeal circuits. Flow conditions and hemodynamics also influence thromboresistance, with laminar, nonstagnant flow reducing clot risk.

Clinical relevance and research use emphasize that thromboresistance is context-dependent and not a universal diagnostic category. It informs device development and antithrombotic strategy, but measurement and interpretation vary by system, assay, and environment.