Thrombosis is an obligatory consequence of all percutaneous vascular interventions. Balloon angioplasty, intravascular stents and other devices routinely used to facilitate dilatation of critical vascular stenoses result in fracture of the intima and exposure of the thrombogenic subendothelium with initiation and perpetuation of platelet activation and aggregation. This not uncommonly results in thrombus formation that may lead to abrupt vessel closure, distal ischemia and tissue infarction, and target organ dysfunction. Fortunately, advances in our understanding of the mechanisms that underlie vascular thrombosis have led to advances in the use of adjunctive pharmacological agents that modulate this pathophysiological response and have led to important reductions in the incidence and severity of thrombotic complications of percutaneous transluminal interventions.