Summary
The study investigated how drug inhibition of the GPIIb/IIIa receptor influences the
interactions between platelets and leukocytes. These interactions are believed to
play an important role in the etiology of the acute coronary syndromes. Thirty patients
with unstable angina or non-Q-wave myocardial infarction were studied before the administration
of tirofiban or placebo and after 4 h and 72 h. Platelet-leukocyte aggregates were
characterized in whole blood using three-colour flow cytometry. The leukocyte population
was isolated by a nucleic acid probe (LDS 751) and platelet-neutrophil coaggregates
identified as particles binding both anti-CD42a-FITC and anti-CD45-PE. Tirofiban decreased
by 25% the density of platelets in circulating platelet-neutrophil coaggregates (p
<0.01), and prevented the increase induced by platelet agonist stimulation (p <0.0001).
The reduction correlated with inhibition of fibrinogen binding to platelet (p <0.0001)
and with inhibition of platelet aggregation (p <0.0001). The percentage of neutrophils
with bound platelets following platelet agonist stimulation was, however, increased
following GPIIb/IIIa inhibition. Thus, inhibition of GPIIb/IIIa receptor promotes
platelet-neutrophil adhesion, but markedly reduces the binding density of platelets
in the coaggregates.