Antiplatelet therapy is a cornerstone in coronary artery disease (CAD) management. Acetylsalicyclic acid (ASA) has been known for many decades to have antithrombotic efficacy. Already in the 1980’s, the ISIS-2 study demonstrated that ASA reduces mortality in acute myocardial infarction (AMI) by 23 %.1 ASA leads to irreversible inactivation of cyclooxygenase 1 and thereby blocks the formation of thromboxane A2, a potent mediator of platelet aggregation. Nevertheless, ASA is a relatively weak antiplatelet agent and only inhibits one of many pathways leading to platelet activation. Patients with acute coronary syndrome (ACS) and/or percutaneous coronary intervention (PCI) remained at a substantial risk of future ischaemic events, despite the treatment with ASA.2 Only the combination of ASA with an additional antiplatelet agent could reduce the rate of cardiovascular events.3 In the 1990’s thienopyridines were introduced. Ticlopidine and clopidogrel inhibit platelet activation by blocking the adenosine diphosphate (ADP) P2Y12 pathway. Ticlopidine, the first generation thienopyridine, was effective in reducing ischaemic events, but was associated with serious haematological toxicity. Clopidogrel, the second generation thienopyridine, replaced ticlopidine owing to its equivalent efficacy and lower haematological toxicity. During the last two decades, the utility of clopidogrel has been evaluated in several common clinical scenarios in a large number of patients. The benefits of clopidogrel in patients with stable CAD undergoing elective PCI and in patients presenting with ACS are well established.4–6 However, there are several limitations of clopidogrel, including delayed onset of action and substantial interpatient variability in platelet inhibition.7,8