Figure 2.

Mechanism of thrombosis in heparin-induced thrombocytopenia. Several mechanisms contribute to thrombosis in heparin-induced thrombocytopenia. Platelet factor 4–heparin–immunoglobulin G (IgG) complexes bind to the Fcg receptor IIA on platelets, leading to platelet aggregation, acceleration of soluble clotting reactions (such as the conversion of factor II [prothrombin] to factor IIa [thrombin]), and activation of neighboring endothelial cells. IgG antibodies bind to heparin–platelet factor 4 complexes on the surface of endothelial cells, leading to additional endothelial-cell activation. Endothelial-cell activation in turn may lead to focal changes in the expression of endothelial-derived procoagulants and anticoagulants. Finally, platelet microparticles, which may be increased in heparin-induced thrombocytopenia, have increased procoagulant activity. Reproduced from Aird and Mark⁶⁵ with the permission of the Massachusetts Medical Society.