1. HIT: The Consequences of Heparin’s Nonspecific Binding to Platelet Factor 4
Heparin is neutralized by platelet factor 4, (PF4), which is present in high concentrations near vascular injury.
Thrombin continues activating platelets.
PF4/heparin complex antibodies activate platelets, causing thrombocytopenia as well as heparin-induced thrombocytopenia thrombosis syndrome (HIT/TS).
Angiomax® (bivalirudin) does not bind to PF4, and remains fully active.
There is no risk of HIT/TS or other thrombotic events associated with PF4/heparin antibodies.
Key Message: Angiomax does not cause HIT/TS.
This slide presents information on the consequences associated with nonspecific binding by heparin.
Heparin is neutralized by platelet factor 4, or PF4, which is present in high concentrations near areas of vascular injury. Therefore thrombin continues activating platelets.
PF4 and heparin antibodies activate platelets, causing thrombocytopenia as well as heparin-induced thrombocytopenia thrombosis syndrome.
In contrast, Angiomax does not bind to PF4 and remains fully active. There is no risk of heparin-induced thrombocytopenia thrombosis syndrome or any of the other thrombotic events associated with PF4 and heparin antibodies because there is no binding to PF4.
Weitz JI et al. Thromb Res. 2002;106:V275-V284.
Williams RT et al. Circulation. 2003;107:
Weitz JI et al. Thromb Res. 2002;106:V275-V284.
CM Gibson 2006