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(Circulation. 1997;96:3860-3866.)
© 1997 American Heart Association, Inc.
Articles |
From the Pharmaceutical Division, Centocor Inc, Malvern, Pa (M.A.M., E.L., S.M., T.S., H.F.W., R.J.); Chrono-log Corp, Havertown, Pa (N.J.V.); and the Lancaster Heart Foundation, Lancaster, Pa (S.W.).
Correspondence to Mary Ann Mascelli, PhD, Department of Clinical Pharmacology, Centocor, Inc, Malvern, PA 19355-1307.
Background The glycoprotein (GP) IIb/IIIa receptor antagonist abciximab (c7E3 Fab, ReoPro) is approved for use in high-risk percutaneous transluminal coronary angioplasty (PTCA). At present, no "point of care" exists for measuring pharmacological GP IIb/IIIa blockade. To address this need, the Chrono-log Whole Blood Aggregometer, which measures platelet aggregation by electrical impedance, was adapted to test platelet function at the bedside.
Methods and Results GP IIb/IIIa receptor blockade, impedance (5
µg/mL collagen), and turbidimetric aggregation (5 and 20
µmol/L ADP) measurements were obtained on 14 PTCA patients who
received the standard bolus plus a 12-hour infusion of abciximab.
During abciximab administration, mean GP IIb/IIIa receptor blockade was
>91%, and both impedance and turbidimetric aggregation were inhibited
by
90%. At 12 hours after abciximab treatment, the mean inhibition
of turbidimetric platelet aggregation to 5 and 20 µmol/L ADP
was 65±20% and 49±14%, respectively, and inhibition of impedance
aggregation was 69±12%. GP IIb/IIIa receptor blockade was 67±8%. At
36 hours after abciximab treatment (n=8), the mean inhibition of
turbidimetric platelet aggregation to 5 and 20 µmol/L ADP
was 44±21% and 30±14%, respectively, whereas impedance aggregation
was inhibited by 60±14%. GP IIb/IIIa receptor blockade was
57±7%.
Conclusions During and at 12 hours after abciximab therapy, impedance and turbidimetric platelet aggregation to 5 µmol/L ADP were comparable and closely correlated with GP IIb/IIIa receptor blockade. However, at 36 hours after abciximab treatment, impedance platelet aggregation more closely paralleled GP IIb/IIIa receptor blockade and indicated a slower recovery of platelet function than turbidimetric aggregometry.
Key Words: platelet aggregation inhibitors glycoproteins receptors
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