Platelet inhibition and GP IIb/IIIa receptor occupancy by intracoronary versus intravenous bolus administration of abciximab in patients with ST-elevation myocardial infarction
In patients with ST-elevation myocardial infarction (STEMI), direct intracoronary bolus administration of the glycoprotein (GP) IIb/IIIa receptor antagonist abciximab is associated with a reduction in infarct size, better myocardial salvage, less microvascular obstruction and improved myocardial blush grade as compared to intravenous bolus injection, presumably caused by higher local drug concentrations leading to a more pronounced inhibition of platelet aggregation. We investigated whether there are differences in the degree of GP IIb/IIIa receptor occupancy and platelet inhibition in blood drawn from the coronary sinus (CS) shortly after intracoronary versus intravenous abciximab bolus administration. A total of 16 patients with acute STEMI undergoing primary percutaneous coronary intervention within 12 h of symptom onset underwent blood sampling from the CS before, immediately after and 30 min after abciximab bolus administration (intracoronary bolus: n = 8 patients; intravenous bolus: n = 8 patients). Immediately after bolus application, GP IIb/IIIa receptor occupancy in CS blood was significantly higher in patients who received direct intracoronary bolus injection compared to administration via a peripheral vein (intracoronary bolus: 93.5% [IQR 92.7–95.4]; intravenous bolus: 74.0% [IQR 17.6–94.0], p = 0.04). The degree of platelet inhibition was also markedly higher with intracoronary compared to intravenous dosing. At late sampling after 30 min no significant differences were found between groups for both platelet reactivity and GP IIb/IIIa receptor occupancy. Acutely, direct intracoronary bolus injection resulted in a more pronounced local inhibition of platelet function and a higher degree of GP IIb/IIIa receptor occupancy as compared to standard intravenous bolus injection.