Does prasugrel achieve superior platelet inhibition when compared with clopidogrel in patients with CAD?
Meinrad Gawaz
Correspondence Eberhard Karls Universität Tübingen, Medizinische Klinik III, Otfried-Müller-Stra
e 10, Tübingen D–72076, Germany
Email meinrad.gawaz@med.uni-tuebingen.de
This article has no abstract so we have provided the first paragraph of the full text.
Antiplatelet therapy is a cornerstone in the management of CAD and has a major role during PCI. Antiplatelet drugs such as acetylsalicylic acid (aspirin) and clopidogrel are clinically well established and effective in secondary prevention of cardiovascular events. The thienopyridine derivate clopidogrel is a prodrug that requires metabolism in the liver and inhibits platelet activation by blocking the binding of ADP to its platelet P2Y12 receptor. A substantial degree of interindividual variability of clopidogrel-dependent platelet inhibition is, however, increasingly being recognized. Patients who do not respond to clopidogrel adequately (low responders) seem to have an increased risk of developing subacute stent thrombosis or recurrent cardiovascular events.1, 2
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