A. Coiffic et al., Inhibition of platelet aggregation by abciximab but not by aspirin can be detected by a new point-of-care test, the hemostatus, THROMB RES, 95(2), 1999, pp. 83-91
We have investigated the type of platelet defect that can be detected with
the Hemostatus test performed with the Hepcon/HMS instrument (Medtronic) de
signed to investigate platelet function during and after surgery. This assa
y is based on the comparison of the activated clotting time of whole blood
measured in cartridges containing kaolin or kaolin and platelet-activating
factor in different concentrations. Addition of platelet-activating factor
shortened the blood activated clotting time when the platelet counts were n
ormal. However, when platelet counts were below 70000/mu L, the activated c
lotting time was prolonged in all channels including those without platelet
-activating factor showing the influence of platelets in the formation of t
he clot under the conditions tested. Inhibition of platelet aggregation wit
h c7E3 (abciximab, ReoPro) also induced a much-prolonged activated clotting
time, and a similar finding was seen with blood from a patient with Glanzm
ann's thrombasthenia confirming the need for platelet aggregation and/or th
e glycoprotein (GP) Ilb-IIIa complex. In contrast, the interaction of GP Ib
with von Willebrand Factor was not of major importance, since inhibition o
f this interaction with the anti-GP Ib murine monoclonal antibody, ALMA-12,
did not modify the activated clotting time. Furthermore, the activated clo
tting time measured for patients with an acquired defect in von Willebrand
Factor activity were unchanged. Finally, inhibition of thromboxane A2 forma
tion by aspirin did not influence the results of this test. Globally, the H
emostatus test was able to detect major abnormalities of GP IIb-IIIa functi
on in the presence or absence of platelet-activating factor. (C) 1999 Elsev
ier Science Ltd, All rights reserved.