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 intervention.
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.
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