Automated bedside RPFA agreed closely with LTA for abciximab but overestimated platelet inhibition for small molecules, whereas CSA lacked sensitivity to discriminate between GP IIb-IIIa antagonists.
Observational (n=36)
Platelet inhibition is central to the efficacy of glycoprotein (GP) IIb-IIIa antagonist therapy, but is not routinely measured during percutaneous coronary intervention (PCI). Data directly comparing the antiplatelet effects of these agents are also limited. Therefore, we compared ex vivo platelet function by standard light transmission aggregometry (LTA) and two automated bedside platelet function assays in 36 patients undergoing PCI with GP IIb-IIIa inhibitors. At baseline and 10 min following clinically recommended bolus and infusion of abciximab (0.25 mg/kg, 0.125 microg/kg/min), eptifibatide (180 microg/kg, 2 microg/kg/min), or tirofiban (10 microg/kg, 0.1 microg/kg/min), we measured 20 microM ADP- and 1.9 mg/mL collagen-induced platelet aggregation using LTA. Platelet function was also assessed using the bedside Accumetrics Ultegra-Rapid Platelet Function Assay (RPFA) and the Xylum Clot Signature Analyzer (CSA). The degree of platelet inhibition, as assessed by LTA, varied significantly between the clinically recommended doses of these GP IIb-IIIa antagonists. RPFA measurements agreed closely with LTA for abciximab, but tended to overestimate the degree of platelet inhibition for small molecules. CSA demonstrated profoundly inhibited shear-induced platelet function, but lacked sensitivity to discriminate between agents. These findings may have implications for the results of trials comparing the efficacy of these agents in patients undergoing PCI.
Simon et al. (2001) conducted an observational in percutaneous coronary intervention (n=36). Automated bedside platelet function assays (RPFA and CSA) vs. Light transmission aggregometry (LTA) was evaluated on Degree of platelet inhibition. Automated bedside RPFA agreed closely with LTA for abciximab but overestimated platelet inhibition for small molecules, whereas CSA lacked sensitivity to discriminate between GP IIb-IIIa antagonists.
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