Daniel Soffer, Gurkan Taviloglu, Gishel New, Edward Kreps, Michael Collins, Sriram Iyer, Gary Roubin, Jeffrey Moses, Neil Coplan, Issam Moussa, Lenox Hill, Heart and Vascular Institute, New York, NY
Background
Glycoprotein (GP) IIb/IIIa platelet receptor antagonists have been shown to improve outcomes in acute coronary syndromes (ACS) and percutaneous coronary interventions (PCI). The impact of clinical presentation on the degree of platelet inhibition (PI) with GP IIb/IIIa inhibitors is still controversial. We sought to investigate the extent of variability in PI between pts with ACS and pts with stable angina who undergo PCI requiring GP IIb/IIIa inhibitor.
Methods
We measured platelet inhibition (PI) in 42 pts who underwent PCI and required GP IIb/IIIa inhibitor tirofibin (bolus: 10 μg/kg, infusion: 0.15 μg/kg/min) or abciximab (bolus: 0.25 mg/kg, infusion: 0.125 μg/kg/min). Pts were classified according to the Braunwald unstable angina (UA) classification. Group I included 24 pts with stable of class I UA; Group II included 18 patients with class II or III UA. Platelet inhibition was measured with the ICHOR CBC analyzer (Array Medical), using 20 micromole of ADP. All pts received ASA and clopidogrel prior to procedure. Baseline PI was measured prior to GP IIb/IIIa administration and at 15 min post bolus.
Results
Baseline characteristics and risk factors did not differ between groups. Group I had higher PI compared with Group II at baseline (mean±SE: 26±4% vs 13±4% for Group I and Group II respectively, p<0.05) and at 15 minutes following GPIIb/IIIa administration (74±3% vs. 50±5% for Group I and Group II respectively, p<0.0001). In multivariate regression analysis, angina class was the only predictor of PI of >70%, p<0.0005).
Conclusion
Pts with acute coronary syndromes have lower platelet inhibition than pts with stable angina, both at baseline and following GPIIb/IIIa blockade. Further studies are needed to establish whether dose adjustment is necessary in pts with acute coronary syndromes undergoing coronary intervention.
ABSTRACT PRESENTED AT
AMERICAN COLLEGE OF CARDIOLOGY
MARCH 2000
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