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Improving outcomes with bivalirudin in primary percutaneous coronary intervention

Gregg W. Stone
DOI: http://dx.doi.org/10.1093/eurheartj/ehu227 2269-2272 First published online: 28 May 2014

This editorial refers to ‘Prasugrel plus bivalirudin vs. clopidogrel plus heparin in patients with ST-segment elevation myocardial infarction’, by S. Schulz et al., on page 2282

Optimal pharmacotherapy is essential to realize the best outcomes in patients undergoing primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI). In this regard, effectively restoring reperfusion and maintaining the patency of the infarct artery after stenting requires a balance between the haemorrhagic risks and the ischaemic benefits of anticoagulant and antiplatelet agents. Over the last three decades, as the principal device used for primary PCI has evolved from balloon angioplasty to bare metal stents to drug-eluting stents, parallel advances have occurred in antithrombotic and antiplatelet regimens, from unfractionated heparin (UFH) alone, to UFH plus a glycoprotein IIb/IIIa inhibitor (GPI), to bivalirudin with provisional (bailout) GPI use, and from ticlopidine and clopidogrel to prasugrel and ticagrelor (on a background of aspirin). Given the time, complexity, and costs of performing appropriately powered randomized trials, clinical practice has progressed faster than the evidence base required to inform optimal drug and device usage for all possible drug and device permutations.

Unfractionated heparin, a heterogeneous mixture of polysaccharides of varying chain lengths, while familiar and inexpensive, has numerous shortcomings,1 which become most clinically apparent in acute coronary syndromes (ACS). Unfractionated heparin has an indirect mechanism of action (binding to and activation of antithrombin III, the amount of which varies in disease states) and has limited activity against clot-bound thrombin. Non-specific protein and cellular binding of UFH results in variable biological activity and can result in heparin-induced thrombocytopenia and thrombosis. Moreover, UFH binds to the glycoprotein IIb/IIIa receptor, thereby paradoxically activating platelets.1 Kastrati and colleagues elegantly demonstrated that, despite pre-treatment with aspirin and clopidogrel, myocardial infarction rates in non-STEMI are substantially reduced after PCI with …

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