Antiplatelet polypharmacy in primary percutaneous coronary intervention: trying to understand when more is better.

Timely and sustained reperfusion in the ST-elevation myocardial infarction setting improves mortality, and primary percutaneous coronary intervention (PCI) is the guideline-favored revascularization strategy.1 Primary PCI requires pharmacological support with antiplatelet and antithrombin therapy, and many drugs and combinations are established for this purpose. Likewise, patients with STelevation myocardial infarction are at risk for subsequent ischemic events in the weeks to months after their index event, and long-term antiplatelet therapy is needed. Aspirin alone provides an inadequate effect on a substantial number of patients with atherosclerotic plaque rupture, whether the vascular disruption occurs as part of an acute coronary syndrome (ACS) or a PCI procedure. Indeed, patients with concomitant spontaneous plaque rupture (ie, troponinpositive ACS) and subsequent disruption from PCI have a particularly high rate of ischemic events with aspirin therapy alone and a notably large risk reduction with antiplatelet adjuncts, such as thienopyridines and glycoprotein IIb/IIIa inhibitors.