Aspirin is an established therapy for the management of acute myocardi
al infarction (AMI) and unstable angina. Secondary prevention with chr
onic aspirin therapy is also indicated for patients with stable angina
. Aspirin inhibits cyclo-oxygenase-I, a key enzyme in the biosynthetic
pathway leading to the production of thromboxane A(2). It therefore i
nhibits only one of the many activation pathways leading to platelet a
ggregation. Other antiplatelet agents that have also been evaluated in
clinical trials include ticlopidine and clopidogrel, which inhibit ad
enosine diphosphate-mediated platelet aggregation, bur these agents ar
e known to be effective against only one of the 90 known agonists thar
stimulate platelet aggregation. The final common pathway for platelet
aggregation involves the glycoprotein Ilb/IIIa receptor combining wit
h fibrinogen. Several inhibitors of the glycoprotein IIb/IIIa receptor
have been developed and have an important role as adjunctive therapy
in angioplasty. Recent trials have been performed in patients with uns
table angina, and trials of adjunctive therapy are currently underway
in patients receiving thrombolysis for AMI, and for secondary preventi
on. These drugs have various different features, including specificity
for blockade of the glycoprotein IIb/IIIa receptor, half life, durati
on of the haemostatic effect and potential for antigenicity. Recently
concluded and ongoing trials of both intravenous and oral agents are e
xpected to provide further support for the introduction of these agent
s into clinical management of patients with acute coronary syndromes.