Clinical Application of Extracorporeal Membrane Oxygenation in the Treatment of Fulminant Myocarditis

Fig. 1.. Pathogenesis of HIT. PF4 is released from alpha granules in platelets. Positively charged PF4 binds with negatively charged heparin to create the PF4-heparin complex. The IgG HIT antibodies produced bond to this complex to form the IgG-PF4-H complex, which then binds to the platelet Fc receptor. This activates the platelets and leads to the release of procoagulant particles that increase thrombin production. Activated platelets release substantial quantities of PF4, which has a positive feedback effect on HIT. This ultimately results in both thrombocytopenia and thrombosis. The involvement of HIT antibodies with endothelial cells and monocytes, as well as the interaction between IgG-PF4-H complexes and neutrophils, is also implicated in this process. HIT, heparin-induced thrombocytopenia; PF4, platelet factor 4; IgG, immuneglobulin G; IgG-PF4-H complexes, IgG-PF4-Heparin complexes. The figure was drawn by Figdraw.