Activation of the platelet glycoprotein (GP IIb/IIIa) receptor on the plate
let surface is the final pathway of platelet aggregation, regardless of the
initiating stimulus. Inhibitors of GP IIb/IIIa receptors include monoclona
l antibodies (abciximab) against this receptor and peptidic and nonpeptidic
synthetic specific receptor blockers. Abciximab exchanges between and bind
s to platelets for as long as 2 weeks, whereas synthetic GP IIb/IIIa inhibi
tors inhibit ex vivo platelet aggregation for only a few hours after the en
d of infusion, but some have the advantage of also being orally active. In
the secondary prevention of atherothrombosis, large-scale trials were succe
ssfully conducted with aspirin, dipyridamole, ticlopidine, and clopidogrel.
In the first large-scale trials with GP IIb/IIIa inhibitors, abciximab was
investigated. Tn aggregate, synthetic GP IIb/IIIa inhibitors, combined wit
h aspirin and heparin, were shown to reduce ischemic events in patients wit
h high- and low-risk coronary intervention, stents, unstable angina, and no
n-Q-wave infarction. With short-term use of synthetic GP IIb/IIIa inhibitor
s, there is no suppression of clinical evident restenosis 6 months after th
e end of treatment. With the doses currently used, bleeding occurs more oft
en with the synthetic GP IIb/IIIa inhibitors (used for 3 days) than with ab
ciximab (used for 12 hours), but there are no direct comparisons between th
ese drugs.