1. The identification and management of heparin-induced thrombocytopenia in the vascular patient 
Glenn M. LaMuraglia, MD, Rabih Houbballah, MD, Michael Laposata, MD, PhD 
Journal of Vascular Surgery 
Volume 55, Issue 2, Pages (February 2012)
DOI: /j.jvs
Copyright © 2012 Society for Vascular Surgery Terms and Conditions

2. Fig 1
Pathogenesis of heparin-induced thrombocytopenia (HIT). A, Upon activation, platelets release platelet factor 4 (PF4), which can rebind to negatively charged glycosaminoglycan (GAG) on the platelet surface or on the endothelial cell surface, or with much higher affinity to circulating heparin, resulting in circulating large multimolecular complexes of PF4/heparin (unfractionated heparin [UFF] or low-molecular-weight heparin [LMWH]). B, In 1% to 5% of patients, multimolecular complexes of PF4/heparin elicit antibody (HIT-Ab) are produced. C, The HIT antibodies are capable of binding Fc receptors on platelets or other cells. D, Binding of HIT immune complexes triggers platelet activation and release of procoagulant microparticles.
Journal of Vascular Surgery  , DOI: ( /j.jvs )
Copyright © 2012 Society for Vascular Surgery Terms and Conditions

3. Fig 2
Outcome groups in patients with positive platelet factor 4 (PF4) antibodies. Group A has thrombosis and heparin-induced thrombocytopenia (HIT). Group B has positive PF4 antibodies with HIT but without thrombosis. Group C has positive PF4 antibodies but does not have HIT.
Journal of Vascular Surgery  , DOI: ( /j.jvs )
Copyright © 2012 Society for Vascular Surgery Terms and Conditions