Intracoronary Administration of Abciximab in ST-Elevation Myocardial Infarction

Primary percutaneous coronary intervention (PCI) is now the preferred method of treating patients with ST-elevation myocardial infarction (STEMI). Despite restoration of epicardial flow, microvascular obstruction may persist after primary PCI as a result of both atheromatous and thrombotic embolization, neutrophil plugging, edema, and vasospasm.1–3 Therefore, studies such as the one by Thiele et al4 in this issue of Circulation that focus on the prevention and treatment of microvascular dysfunction are informative with respect to the means to improve the primary PCI strategy.Article p 49 There have been efforts to identify mechanical and pharmacological strategies to improve myocardial perfusion after primary PCI. Compared with the systemic administration of intravenous pharmacotherapies, highly localized administration of intracoronary pharmacotherapy may be associated with a several-hundred-fold increase in the local concentration of an agent in the epicardial artery and microcirculation. A number of pharmacotherapies, including adenosine,5,6 calcium channel blockers,7 α-blockers,8 β2-receptor activators,9 other vasodilators, antithrombotics,10,11 and antiplatelet agents,12–14 have been used to treat microvascular dysfunction.There are tens of thousands of glycoprotein IIb/IIIa (GPIIb/IIIa) receptors on the platelet surface.15 Platelet receptor occupancy studies have demonstrated that if there are fewer GPIIb/IIIa receptors free and available for cross-linking with fibrinogen, then myocardial perfusion is improved.16 To estimate the number of GPIIb/IIIa receptors available for cross-linking, the absolute platelet count has been multiplied by the percent of receptors available to cross link to calculate an index of the absolute number of GPIIb/IIIa receptors available. The absolute number of GPIIb/IIIa receptors available for cross-linking is reduced among patients with successful restoration of myocardial perfusion and ST-segment resolution in an STEMI population.16 Thus, the hypothesized mechanistic basis for intracoronary administration of GPIIb/IIIa inhibitors is that high …