Management of the Thrombocytopenic Cardiac Surgical Patient???A Role for Aprotinin?

Abstract

The use of aprotinin in this setting can be justified on a number of grounds. Van Oeveren et al.2 showed that aprotinin prevents decrease in the platelet receptor for von Willebrand factor, which mediates platelet adhesion to endothelial cells during cardiopulmonary bypass (CPB). In addition, aprotinin inhibits the hyperfibrinolysis associated with CPB. This hyperfibrinolysis may be of particular concern in the thrombocytopenic patient, as platelet-derived plasmino-gen-activator inhibitor is particularly critical to protecting the clot from plasmin-induced lysis. Indeed, platelet-rich clots are notoriously more difficult than platelet-poor clots for the cardiologist to lyse with fibrinolytic therapy. Thus, treatment of the thrombocytopenic cardiac surgical patient with an inhibitor of fibrinolysis is a sound strategy and, as in this case, may significantly contribute to a better outcome.