Thrombin as a common downstream target blocking both platelet and monocyte activation

Thromb Haemost 2009; 101: 220–221 Platelets play a pivotal role in the pathogenesis of thrombotic complications after percutaneous coronary interventions (PCI) (1). The use of optimal antiplatelet therapy is critical in reducing adverse events in this setting. Despite the efficacy of dual antiplatelet therapy in patients undergoing PCI, thrombo-ischaemic events and, in particular, stent thrombosis are frequent complications (2). High post-treatment platelet reactivity is associated with cardiovascular outcome after PCI (3) and coronary stent implantation (4). Different agents are currently in use for adjunctive anticoagulant treatment on top of adequate antiplatelet regimen during PCI. Traditionally, unfractionated heparin (UFH) has been the standard anticoagulant administered during coronary intervention. Enhanced platelet activation in vivo and ex vivo has been shown after UFH treatment (5, 6). Moreover, heparin does not suppress the transient increase in thromboxane biosynthesis associated with coronary angioplasty (7). Low-molecular-weight heparin (LMWH), in contrast, does not affect platelet activation in vivo and ex vivo after PCI (5, 8). Recently bivalirudin, a short-acting direct thrombin inhibitor, has been shown to be effective and safe in patients undergoing PCI (9), with reduced bleeding as compared with heparin. Reduced inhibition of adenosine diphosphate (ADP)-induced platelet aggregation at the time of PCI is associated with an increased risk for adverse thrombotic complications (10). Bivalirudin, given during PCI in patients pretreated with 600 mg of clopidogrel, is unlike UFH associated with further inhibition of platelet aggregation (11). A similar effect by bivalirudin was previously described on platelet P-selectin (12). Moreover, bivalirudin alone or coupled with clopidogrel may significantly down© 2009 Schattauer GmbH, Stuttgart