The acute coronary syndromes (including unstable angina and non-ST-elevatio
n myocardial infarction) and ST-elevation myocardial infarction(17) are rel
ated pathogenetically, because each represents a different stage of plaque
rupture and thrombosis.(44, 45) These entities involve the coagulation casc
ade at different levels and intensities. Hence, antithrombotic therapy play
s a major role in the management of acute coronary syndromes.
In most patients presenting with acute coronary syndromes, the thrombus is
only partially occlusive. Antithrombotic agents maintain vessel patency by
preventing the progression of a nonocclusive thrombus to an occlusive throm
bus and by inhibiting the generation of new thrombi. In contrast, the infar
ct-related artery in most patients with ST-segment elevation is occluded co
mpletely by thrombus. Therefore, the first goal in these patients is to ach
ieve rapid reperfusion by mechanical dissolution of thrombus or administrat
ion of thrombolytic therapy. Second, it is important to maintain patency of
the infarct-related artery to prevent recurrent thrombosis leading to reoc
clusion and recurrent ischemia. This maintenance is accomplished by anticoa
gulant and antiplatelet therapy.
Recent multicenter clinical trials have led to the introduction of new anti
thrombotic agents in the management of acute coronary syndromes. These incl
ude platelet glycoprotein IIb/IIIa (GP IIb/IIIa) receptor inhibitors, low m
olecular weight heparins (LMWHs), and direct thrombin inhibitors. These inn
ovations promise to improve patient outcomes, but their relatively recent d
evelopment raises questions of how best to use the agents in combination wi
th traditional antianginal agents, each other, and percutaneous interventio
n. Developing strategies of care and critical pathways(7) demand more than
administering every drug to every patient.(27) This article reviews the rap
id expansion in the antithrombotic therapeutic armamentarium for acute coro
nary syndromes in the context of optimal management.