Anticoagulation during Cardiopulmonary bypass in Patients with Heparin-Induced Thrombocytopenia using Heparin and the Platelet Glycoprotein IIb-IIIa Antagonist

Heparin induced thrombocytopenia (HIT) is a potentially devastating prothrombotic disease associated with heparin therapy usually occurring after five days or more of therapy [1]. When heparin binds to platelet factor 4 (PF4), a heparin-binding protein stored on platelets, an epitope is exposed by a conformational change in PF4. Susceptible patients develop an Immunoglobulin G (IgG) along with IgA and IgM antibody to the heparinPF4 epitope and upon binding to the heparin-PF4 epitope the antibody forms an immune complex on the surface of platelets. The fragment c (Fc) portion of the IgG then activates the platelet, which cause microparticle release that promotes thrombin formation. Furthermore, thrombin enhances further platelet activation, release of PF4, and perpetuation of a prothrombotic state. After a patient has formed HIT antibodies, they are susceptible to HIT until they become antibody negative. Fortunately, this time is relatively short, as the average half-life of these antibodies is three months. However, urgent surgery with cardiopulmonary bypass (CPB) for patients with acute HIT is very challenging.