In contrast to primary prevention,1,2 the status of aspirin in the treatment of vascular diseases caused by atherothrombosis is unquestionable and unshakable. In addition to its undeniable efficiency, its affordability is a significant extra benefit. However, preventing thrombosis after iatrogenic disruption of the inner surface of a vessel wall by implantation of an intracoronary stent needs more than the antithrombotic efficacy of aspirin.
Many advances in coronary intervention were made possible by extending single antiplatelet therapy (APT) to dual antiplatelet therapy (DAPT), which was done best by adding a P2Y12 receptor inhibitor. Inhibition of platelet haemostatic function by suppressing the two pathways of platelet activation, subsequent platelet adhesion, and aggregation decreases the risk of thrombotic events but increases simultaneously the risk of bleeding, whether spontaneous or iatrogenic.
The availability of P2Y12 inhibitors with different potency, onset of action, doses, and route of administration allows APT to be adjusted according to the risk profile of individuals and the acuity of the situation. DAPT antithrombotic protection can be modulated, i.e. escalated or de-escalated using different drugs or doses of these drugs but also by extending or reducing the duration of DAPT.
Aspirin has been perceived as the cornerstone antithrombotic therapy. If it is necessary to discontinue DAPT prematurely due to bleeding risk, the most common path forward is to continue with aspirin monotherapy, or switch to clopidogrel monotherapy, which may be associated with a lower bleeding risk.3,4 In the absence of high bleeding risk (HBR), aspirin has reinforced its position with a new possible strategy combining a low dose of rivaroxaban with a low dose of aspirin to better control the ischaemic risk.