February 2, 2010
View Full PaperIntracoronary Eptifibatide Bolus Administration During Percutaneous Coronary Revascularization for Acute Coronary Syndromes With Evaluation of Platelet Glycoprotein IIb/IIIa Receptor Occupancy and Platelet Function
Key Result
Intracoronary eptifibatide during PCI for acute coronary syndromes yielded greater local glycoprotein IIb/IIIa receptor occupancy than intravenous administration (94% vs 51% after first bolus, P<0.001).
Study Design
Type
RCT
Randomization
randomized
Structured PICO
Does intracoronary eptifibatide bolus administration improve local glycoprotein IIb/IIIa receptor occupancy compared to intravenous administration in patients undergoing PCI for acute coronary syndromes?
P
Population
Patients undergoing percutaneous coronary intervention for an acute coronary syndrome.
I
Intervention
Intracoronary bolus administration of eptifibatide
C
Comparator
Intravenous bolus administration of eptifibatide
O
Outcome
Local glycoprotein IIb/IIIa receptor occupancy measured in the coronary sinussurrogate
Intracoronary bolus administration of eptifibatide during PCI for acute coronary syndromes achieves higher local platelet glycoprotein IIb/IIIa receptor occupancy and better microvascular perfusion compared to standard intravenous administration.
Main Result
Absolute Event Rate: 94% vs 51%
p-value: p=<0.001
Abstract
BACKGROUND: Eptifibatide reduces major adverse cardiac events in patients with acute coronary syndromes undergoing percutaneous coronary intervention (PCI). Intracoronary bolus administration of eptifibatide may result in higher levels of platelet glycoprotein IIb/IIIa receptor occupancy in the local coronary bed, disaggregate thrombus in the epicardial artery and microvasculature, and thereby improve coronary flow. METHODS AND RESULTS: Patients undergoing PCI for an acute coronary syndrome were randomized to either intracoronary or intravenous bolus administration of eptifibatide. The primary end point was the local glycoprotein IIb/IIIa receptor occupancy measured in the coronary sinus. There were no angiographic, electrophysiological, or other adverse findings attributable to intracoronary eptifibatide. Platelet glycoprotein IIb/IIIa receptor occupancy was significantly greater with intracoronary versus intravenous administration: first bolus, 94+/-9% versus 51+/-15% (P<0.001); and second bolus, 99+/-2% versus 91+/-4% (P=0.001), respectively. Microvascular perfusion was significantly improved as measured by the corrected thrombolysis in myocardial infarction frame count (cTFC) with intracoronary versus intravenous administration: pre-PCI, 36 (median) (25th and 75th percentiles, 16 and 64) versus 31 (25th and 75th percentiles, 23 and 45; P=0.8); and post-PCI, 18 (25th and 75th percentiles, 10 and 22) versus 25 (25th and 75th percentiles, 22 and 35; P=0.007), respectively. The only multivariate predictor associated with a post-PCI cTFC rank score was the first bolus glycoprotein IIb/IIIa receptor occupancy (P<0.001). CONCLUSIONS: Intracoronary bolus administration of eptifibatide during PCI in patients with acute coronary syndromes results in higher local platelet glycoprotein IIb/IIIa receptor occupancy, which is associated with improved microvascular perfusion demonstrated by an improved cTFC.