title: Efficacy of abciximab induced platelet blockade using a rapid point of care assay.
abstract: Anciximab provides potent, but variable degrees of platelet inhibition both during the duration of intravenous administration and at 12 hours following therapy. Platelet function was assessed using the PC-RPFA system in 78 patients scheduled for percutaneous coronary revascularization who were administered 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 lyophilized form. The instrument detects the agglutination rate between the stimulated platelets and the fibrinogen-coated beads, and provides a quantitative digital display in less than 2 minutes. No differences in the level of platelet inhibition were observed in these abciximab-treated patients by diabetic status, gender, smoking, diagnosis (unstable angina, chronic stable angina, recent myocardial infarction), or abciximab treatment status (first time vs. retreatment). Nocorrelation of the PC-RPFA rate of platelet aggregation with clinical demographic factors was observed, with the exception of baseline hematocrit (r2 = 0.4556). The relationship between the PC-RPFA rate of aggregation and hematocrit reflects light absorbance by erythrocytes and is specific to the PC-RPFA system. The absolute rate of platelet aggregation (slope) reported by the PC-RPFA is correlated with percent aggregation, thus making it potentially possible to predict the level of aggregation without reference to a baseline (pretreatment) measure of platelet function. This correlation was closest for patients having <40% baseline aggregation (r2 = 0.55). Thus, PC-RPFA provides a rapid point-of-care assessment of platelet function that could allow for adjustment of abciximab dosing to achieve targeted levels of platelet inhibition. The utility of this device to optimize therapy with platelet glycoprotein IIb/IIIa inhibitors is currently being evaluated.
authors.affiliation: The Carl and Edyth Lindner Research Center for Clinical Cardiovascular Research, Cincinnati, Ohio 45219, USA. linder@healthall.com
authors.forename: D J
authors.initials: DJ
authors.lastname: Kereiakes
authors.forename: M
authors.initials: M
authors.lastname: Mueller
authors.forename: W
authors.initials: W
authors.lastname: Howard
authors.forename: P
authors.initials: P
authors.lastname: Lacock
authors.forename: L C
authors.initials: LC
authors.lastname: Anderson
authors.forename: T M
authors.initials: TM
authors.lastname: Broderick
authors.forename: E M
authors.initials: EM
authors.lastname: Roth
authors.forename: D D
authors.initials: DD
authors.lastname: Whang
authors.forename: C W
authors.initials: CW
authors.lastname: Abbottsmith
mesh_terms: D000077284:Abciximab; D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D001331:Automation; D015897:Comorbidity; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use*; D008297:Male; D008863:Microspheres; D008875:Middle Aged; D010446:Peptide Fragments / Q000378:metabolism; D010973:Platelet Adhesiveness / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D010979:Platelet Function Tests / Q000295:instrumentation / Q000379:methods*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D016896:Treatment Outcome
chemical_list: D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D010446:Peptide Fragments; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; C076901:thrombin receptor-activating peptide (P508-530); D005340:Fibrinogen; D000077284:Abciximab