Efficacy of abciximab induced platelet blockade using a rapid point of care assay

Anciximab provides potent, but variable degrees of platelet inhibition both during the duration of intravenous administration and at 12 hours followin g therapy. Platelet function was assessed using the PC-RPFA system in 78 pa tients scheduled for percutaneous coronary revascularization who were admin istered the standard abciximab weight-adjusted bolus and 12-hour infusion. The PC-RPFA system is a cartridge-based, semiautomated point-of-care whole- blood assay that incorporates fibrinogen-coated polystyrene beads, buffers, and a modified thrombin receptor activating peptide (Isotrap) in lyophiliz ed form. The instrument detects the agglutination rate between the stimulat ed platelets and the fibrinogen-coated beads, and provides a quantitative d igital display in less than 2 minutes. No differences in the level of plate let inhibition were observed in these abciximab-treated patients by diabeti c status, gender, smoking, diagnosis (unstable angina, chronic stable angin a, recent myocardial infarction), or abciximab treatment status (first time vs. retreatment). Nocorrelation of the PC-RPFA rate of platelet aggregatio n with clinical demographic factors was observed, with the exception of bas eline hematocrit (r(2) = 0.4556). The relationship between the PC-RPFA rate of aggregation and hematocrit reflects light absorbance by erythrocytes an d is specific to the PC-RPFA system. The absolute rate of platelet aggregat ion (slope) reported by the PC-RPFA is correlated with percent aggregation, thus making it potentially possible to predict the level of aggregation wi thout reference to a baseline (pretreatment) measure of platelet function. This correlation was closest for patients having < 40% baseline aggregation (r(2) = 0.55). Thus, PC-RPFA provides a rapid point-of-care assessment of platelet function that could allow for adjustment of abciximab dosing to ac hieve targeted levels of platelet inhibition. The utility of this device to optimize therapy with platelet glycoprotein IIb/IIIa inhibitors is current ly being evaluated.