Treatment with oral anti-platelet agents constitutes a cornerstone in the therapy of coronary artery disease.
Coronary angioplasty and stent implantation improved the therapy of coronary artery disease and especially the treatment
of acute myocardial infarction. Implementation of glycoprotein IIb/IIIa inhibition further advanced anti-platelet therapy as
a central component in the treatment of acute coronary syndromes.
Sustained prevention of reocclusion was achieved when dual anti-platelet therapy had been introduced and reduced the
risk of stent thrombosis to 1% following elective stenting in stable coronary artery disease. However, targeting more
complex lesions or performing the intervention in states of increased platelet reactivity such as in acute coronary syndromes
or in diabetic patients is still associated with a higher risk of stent thrombosis. Additionally, incomplete ADP-receptor
inhibition by thienopyridine treatment contributes to increased cardiovascular events and mortality after coronary
This review describes the underlying pathophysiology leading to coronary atherothrombosis and contributing to stent
thrombosis as well as the pharmacological approach to prevent it by dual anti-platelet therapy. It summarizes the assessment
of anti-platelet therapy by different analytical methods such as platelet aggregation, platelet function analyzers, and
the platelet reactivity index. Impaired clopidogrel responsiveness and its implication for adverse cardiovascular events and
stent thrombosis are discussed. Current strategies in improving the efficacy of clopidogrel treatment as well as the next
generation of anti-platelet substances such as novel thienopyridines and non-thienopyridine P2Y12-receptor blocking
agents are addressed. Finally, we discuss the potential of von-Willebrand factor aptamers compared to glycoprotein
IIb/IIIa inhibitors in acute coronary syndromes.