ABSTRACT
The degree and duration of platelet inhibition using glycoprotein IIb/IIIa receptor antagonists during percutaneous coronary intervention: clinical implications • Resistance to oral antiplatelet agents: aspirin, clopidogrel, or both • Management of patients with antiplatelet drug resistance undergoing percutaneous coronary intervention • Future directions • Conclusions
Plaque rupture may occur spontaneously, as in patients with acute coronary syndromes (ACS), or may be iatrogenically induced, as in patients undergoing percutaneous coronary interventions (PCI). Antiplatelet therapy is therefore a cornerstone of treatment in these scenarios. Three classes of platelet-inhibiting drugs, aspirin, thienopyridines, and platelet glycoprotein (GP) IIb/IIIa inhibitors are most commonly used for the prevention and treatment of ischemic complications associated with plaque rupture. Given the pivotal role of platelets on the adverse events associated with plaque rupture, all these antiplatelet agents have proved to be clinically effective. Nevertheless, despite their efficacy, patients on these medications may continue to suffer from ischemic complications. This may be, at least in part, attributed to the fact that responsiveness to antiplatelet agents is not uniform in all patients. In particular, there is a growing degree of evidence showing that suboptimal responsiveness or ‘resistance’ to antiplatelet medications may contribute to adverse outcomes. Although the mechanisms of antiplatelet drug resistance remain to be established, there is increasing data to suggest that monitoring and tailoring antiplatelet therapy in the individual patient may help optimize clinical outcomes. In the present chapter we describe the impact of individual response variability to antiplatelet agents on clinical outcomes in patients undergoing PCI, and current and future directions for the treatment of patients with suboptimal responsiveness to antiplatelet agents.
