The vulnerable endothelium: Priming the vascular endothelium for thrombosis with unfractionated heparin: Biologic plausibility for observations from the Superior Yield of the New Strategy of Enoxaparin, Revascularization and GlYcoprotein IIb/IIIa Inhibitors (SYNERGY) trial

Atherosclerotic coronary artery disease is characterized by impaired inflammoresistance and thromboresistance. Heparin compounds, particularly long-chain saccharides with high endothelial cell binding capacity, may provoke inflammatory/immune responses and have been shown to deplete TFPI storage pools, as well as surface ATIII activity. A sudden cessation of heparin, in an existing proinflammatory and prothrombotic environment, shifts the balance further, augmenting the risk for coronary arterial thrombotic events. TF, Tissue factor; ATIII, antithrombin III).