Clinical Medicine Reviews in Vascular Health

As aberrant platelet activation underlies intra-arterial thrombus formation, dual antiplatelet therapy- of aspirin and clopidogrel- has become a mainstay of treatment of acute coronary thrombosis. Two complementary yet independent mechanisms of blocking platelet activation and aggregation have proven to be clinically beneficial in preventing atherothrombotic complications, including myocardial infarction (MI), stroke, cardiovascular (CV) death, as well as stent-associated thrombosis. Nonetheless, the combination of aspirin and clopidogrel has its drawbacks, and recurrent atherothrombotic events occur in patients receiving this dual antiplatelet therapy. Of note is the phenomenon of so-called resistance, also known as hyporesponsiveness, to aspirin and/or clopidogrel, as this predisposes to recurrent cardiovascular events. Other limitations of clopidogrel include its modest level platelet inhibition, a wide variability in patient response and delayed onset of action. Prasugrel, which is a new member of the thienopyridine antiplatelet agents, is able to overcome these shortcomings of clopidogrel. It is 10 times more potent, has a rapid onset, and is not as influenced by drug interactions nor genetic polymorphisms of cytochrome enzymes; thus prasugrel results in a faster, higher and more consistent level of platelet inhibition. Clinically this translates into a reduction in thrombo-occlusive events, but also an increased bleeding risk. This paper reviews the available pharmacological and clinical data on prasugrel and clarifies the current place of prasugrel in the management of arterial coronary thrombosis.