Antiplatelet therapy (APT) represents a major cornerstone in the secondary prevention of coronary artery disease, along with modifying patients’ risk factors. Furthermore, it has been clear, since early unsuccessful regimens, including warfarin and dypiridamole with aspirin, that it is APT that stops coronary stents from clotting off and causing stent thrombosis.1,2 Specifically, the requirement for aspirin plus a second antiplatelet drug (thus, dual-antiplatelet therapy [DAPT]) to minimise the risk of ST was quickly established.3 Initially the second agent was ticlopidine, which despite being effective at its primary task was poorly tolerated and associated with an unwelcome incidence of blood dyscrasia. Subsequently, following randomised trial evidence of beneficial clinical outcome with fewer adverse effects, clopidogrel became the P2Y12 inhibitor of choice to accompany aspirin1. Concerns about inter-individual variations in the response to clopidogrel led to the development of apparently more potent and rapidly acting agents in the form of prasugrel and ticagrelor.4,5 Specifically, the latter agents have been shown to have clinical outcome benefit compared to clopidogrel in terms of reducing some ischaemic events in heterogeneous populations of patients with acute coronary syndromes, albeit at the expense of increased bleeding.6
The concept that DAPT is necessary to prevent ST in coronary stents has been dominant for at least two decades. However, the optimal duration of that DAPT therapy always has been, and remains, uncertain and recently, in particular, has attracted considerable debate. Put simply, the question frontline interventional cardiologists face is this: how much DAPT do you need, and for how long, in order to prevent ST but minimise major bleeding?
In most interventional centres, the default DAPT regimen for most patients receiving stents consists of 12 months followed by aspirin monotherapy for life. A forensic assessment of the basis for this default unearths (perhaps surprisingly) shaky foundations. Studying the evolution of our APT to this default DAPT regimen is valuable to put the most recent challenging trial data into context. In particular, it becomes apparent that several factors have recurrently had an influence on the requirements for DAPT, including stable or acute coronary syndrome presentation, type of stent, and risk of bleeding.