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J Am Coll Cardiol, 2004; 44:1187-1193, doi:10.1016/j.jacc.2004.06.050 © 2004 by the American College of Cardiology Foundation |



* Isala Klinieken, location Weezenlanden, Department of Cardiology, Zwolle, the Netherlands
Isala Klinieken, location Weezenlanden, Department of Clinical Chemistry, Zwolle, the Netherlands
Thorax Centre, Department of Cardiology, Groningen, the Netherlands
Manuscript received March 18, 2004; revised manuscript received May 13, 2004, accepted June 7, 2004.
* Reprint requests and correspondence: Dr. Arnoud W. J. van t Hof, Isala Klinieken, location Weezenlanden, Groot Wezenland 20, 8011 JW Zwolle, the Netherlands (Email: v.r.c.derks{at}isala.nl).
OBJECTIVES: To evaluate the extent of platelet aggregation inhibition in patients with ST-segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI), treated with different antiplatelet agents and dosages.
BACKGROUND: The extent of platelet aggregation inhibition is an independent predictor of major cardiac events after elective PCI. In STEMI patients undergoing PCI, routine dose of antiplatelet agents may be associated with less effective platelet aggregation inhibition.
METHODS: Patients were treated with clopidogrel before angiography and randomized to abciximab, tirofiban, high-dose tirofiban, or no glycoprotein (GP) IIb/IIIa inhibitor; GP IIb/IIIa inhibitor bolus, followed by maintenance infusion, was administered after angiography, but before PCI. Platelet aggregation inhibition was assessed before angiography, immediately after PCI, and 1 and 6 h afterwards.
RESULTS: The total study population consisted of 112 patients. Platelet aggregation inhibition was variable for individuals and suboptimal for all agents, particularly in the periprocedural period. Only with high-dose tirofiban, mean periprocedural platelet aggregation inhibition exceeded 80%. Angiographic parameters after PCI were not different between the groups. No relationship was found between the level of platelet aggregation and parameters of PCI success (Thrombolysis In Myocardial Infarction frame count and myocardial blush grade), after combining the data from all four groups studied.
CONCLUSIONS: Platelet aggregation inhibition in STEMI patients undergoing PCI, treated with antiplatelet agents, is variable and suboptimal for all agents and dosages studied. Only with high-dose tirofiban, mean periprocedural platelet aggregation inhibition exceeded 80%. However, no relationship of platelet aggregation inhibition and angiographic outcome was found in this patient cohort.
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