Injected heparin binds with normally occurring low levels of PF4 in plasma to form a macromolecular complex. This complex binds to the surface of platelets. Platelet activation releases procoagulants including additional PF4. Release of the latter in the presence of heparin further increases platelet activation. The activated platelets either join in forming a clot or are removed by the spleen.
Platelet activation ceases when heparin is removed.
However the antibody usually remains detectable for four to six weeks. Clinically, patients with HIT typically present with a decrease in platelet count often occurring five to eleven days after heparin therapy is initiated. This thrombocytopenia is associated with thrombosis rather than purpura or bleeding. Deep vein thromboses and pulmonary emboli are the most common complication. Arterial thrombosis occurs less often and usually involves large limb vessels, cerebral arteries, and visceral arteries.