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Thrombus formation is a crucial event in acute coronary syndromes,1 bypass occlusion,2 and stent thrombosis.3 In the coronary circulation, platelet activation is an initial event,4 while expression of tissue factor and subsequent activation of the coagulation cascade5 and invading white blood cells6 solidify the evolving clot, an event that often leads to vascular occlusion. Platelets are primarily activated by thromboxane and ADP via thromboxane and P2Y12 receptors on the platelet surface that eventually lead to the expression of the glycoprotein IIB/IIIA receptor that binds fibrin. Twenty-one years ago, the first randomized clinical trial established the superiority of dual antiplatelet therapy over anticoagulant therapy among patients undergoing percutaneous coronary intervention.7 Thus, dual antiplatelet therapy has become a crucial therapeutic intervention in patients with stable or acute coronary artery disease.

However, the duration of dual antiplatelet therapy and its combination with anticoagulants in certain patients remain clinical challenges. Thus, the updated ‘2017 ESC focused update on dual antiplatelet therapy in coronary artery disease developed in collaboration with EACTS: The Task Force for dual antiplatelet therapy in coronary artery disease of the European Society of Cardiology (ESC) and of the European Association for Cardio-Thoracic Surgery (EACTS)’, authored by Marco Valgimigli and colleagues from the European Society of Cardiology, is a timely document.8 The authors remind us that based on population estimates, ∼1.4 and 2 .2 million patients per year may have an indication for dual antiplatelet therapy after coronary intervention or a myocardial infarction, respectively. Based on >35 randomized clinical trials, including >225 000 patients, dual antiplatelet therapy is among the most intensively investigated treatments in cardiovascular medicine. Its progressive refinement involved firstly safer drugs, i.e. the move from ticlopidine to clopidogrel, and then more potent and predictable compounds such as ticagrelor or prasugrel. The need to investigate longer dual antiplatelet therapy regimens arose from concerns over late and very late stent thrombosis occurring after first-generation drug-eluting stent implantation as well as late events after an acute coronary syndrome. Yet, the advent of safer newer generation drug-eluting stents and most recent randomized trials have caused major paradigm shifts. Indeed, late and very late stent thrombosis have declined considerably with newer generation drug-eluting stents.9–11 Hence, the risk of bleeding associated with dual antiplatelet therapy prolongation beyond 1 year does not seem to be justified by the small absolute gain in preventing stent thrombosis. Yet, dual antiplatelet therapy seems to reduce the long-term risk of non-stent-related infarction and stroke.12,13 Hence, after 21 years of research, dual antiplatelet therapy has moved from a local, i.e. stent-related, to a systemic treatment strategy, i.e. capable of preventing thrombotic arterial occlusions, conveying global patient protection.

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