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The value of routine upstream administration remains a topic of debate, as it might increase rates of bleeding. In NSTEMI patients, upstream administration is discouraged because the risk of bleeding outweighs the risk of thrombotic complications [51]. However, in STEMI patients, early (prehospital) administration seems to be beneficial, http://www.selleck.cn/products/BIBW2992.html in particular following timely presentation ( http://www.selleckchem.com/products/z-vad-fmk.html and STEMI, are summarized in Tables?1 and 2, respectively. Aspirin inhibits the synthesis of thromboxane A2 by targeting cyclo-oxygenase-1 (COX-1) and thereby diminishes platelet aggregation. It has been shown to reduce mortality rates amongst patients with evolving acute myocardial infarction [56] and is the cornerstone of antiplatelet therapy to which other antiplatelet agents have always been compared. However, blocking other pathways is essential for adequate inhibition of platelet activation and aggregation. Inactivation of the adenosine diphosphate P2Y12 receptor plays an important role and can be achieved by administration of thienopyridines such as the widely used clopidogrel. Aspirin plus clopidogrel was shown to be superior to aspirin alone http://www.selleckchem.com/products/ly2157299.html in the prevention of ischaemic cardiovascular events in STEMI and NSTEMI [57�C59]. Therefore, standard dual antiplatelet therapy (loading and maintenance dose for 1?year) comprised clopidogrel and aspirin for several years. Upstream administration of dual antiplatelet loading doses was shown to have additional benefits in patients eligible for intervention [60�C62]. Although no randomized trial has been conducted to examine exclusively its value in NSTEMI, international guidelines have also incorporated upstream antiplatelet therapy in invasively treated NSTEMI patients as a period of time (at least 30�C90?min) is needed to reach adequate plasma levels and inhibition of platelet aggregation. Unfortunately, there is a wide variability in response to clopidogrel partly because of drug interactions and detrimental genotype polymorphisms, such as the CYP2C19-reduced function alleles. This dose-independent resistance, which is seen in approximately one-fifth of all patients [63], eventually may lead to worse clinical outcomes including stent thrombosis and recurrent myocardial infarction [64�C66]. To overcome these problems, other potential adenosine diphosphate P2Y12 receptor antagonists (e.g. prasugrel and ticagrelor) and platelet thrombin receptor antagonists (e.g.