Platelet adhesion and thrombus stability are provided by very large polymers. One such material, von Willebrand factor (VWF), is prone to oxidation, particularly by the neutrophil-derived oxidant hypochlorous acid. Oxidation of VWF amino acid methionine1606 (the ADAMTS13 cleavage site) renders VWF resistant to cleavage, while oxidation of other residues in the A1-A2-A3 region of VWF produces a molecule capable of spontaneously aggregating platelets. Alternatively, in the innate immune response, neutrophils can release DNA fibers with histones to form neutrophil extracellular traps (NETS). NETS support platelet adhesion, aggregation and thrombus formation. This session will focus on recent observations that suggest that oxidative stress and neutrophil response are important pathogenic contributors to the prothrombotic state, providing yet another set of links between inflammation and thrombosis. By elucidating these processes of disease, new avenues to interrupt pathogenic mechanisms become possible.

This session was originally selected for Self-Assessment Module (SAM) credit. Unfortunately, test questions have not been received from all of the speakers. SAM credit is no longer being offered for this session.