After an acute coronary syndrome, as many as 1 in 5 patients will have a second ischemic event within 5 years. 1,2 Residual risk is related to several factors that may be mitigated by pharmacologic and nonpharmacologic interventions. 2 Antiplatelet therapy is a cornerstone in the management of acute coronary syndrome. 1,3 Acetylsalicylic acid (ASA) -a cyclooxygenase-1 inhibitor -was introduced as an effective treatment for myocardial infarction almost 5 decades ago and remains the most widely used antiplatelet therapy. 4,5 Although ASA is effective in reducing mortality rates, 6 combining ASA with a second antiplatelet agent, a P2Y 12 receptor inhibitor (known as dual antiplatelet therapy [DAPT]) provides additional benefit and is now the preferred initial strategy for acute coronary syndromes over ASA alone. 7 We review emerging evidence regarding the use of antiplatelet therapy in acute coronary syndromes, as well as updates to the Canad ian and European Society of Cardiology guidelines that highlight adjustments in the choice and duration of antiplatelet therapy, in addition to ASA (Box 1). We particularly focus on strategies to reduce bleeding risk after percutaneous coronary intervention (PCI). 3,8 What are the options for oral antiplatelet therapy?Clopidogrel is a second-generation thienopyridine that has a better safety profile than ticlopidine, a first-generation thienopyridine. 9 Clopidogrel reduces ischemic events by almost 20% when added to ASA for patients presenting with acute coronary syndromes, with or without ST-segment elevation. 7,10,11 It irreversibly antagonizes the receptor for platelet adenosine diphosphate (ADP)-P2Y 12 . The use of clopidogrel may be associated with gastrointestinal symptoms and skin rashes.Prasugrel and ticagrelor are more potent P2Y 12 inhibitors than clopidogrel. Prasugrel is a third-generation thienopyridine that exerts its antiplatelet properties by irreversibly antagonizing the ADP-P 2 Y 12 receptor; similar to clopidogrel, it requires hepatic conversion to its active metabolites. Ticagrelor is part of the cyclopentyltriazolopyrimidine family and does not require hepatic conversion to its active metabolites before reversibly inhibiting the ADP-P 2 Y 12 receptor. Ticagrelor may cause shortness of breath or increased levels of uric acid, which leads to gout.Both prasugrel and ticagrelor provide faster and more consistent inhibition of platelet aggregation and are associated with a further 15%-20% relative risk reduction of ischemic events compared with clopidogrel. 12,13 Ticagrelor also reduces cardiovascular and all-cause mortality rates. 12 Although ticagrelor and prasugrel are associated with greater bleeding risk than clopidogrel, both are recommended over clopidogrel in patients with low bleeding risk. Recently, the