Introduction

Rupture or erosion of a coronary artery atheroma exposes flowing blood to the prothrombotic contents of the plaque, resulting in platelet activation and subsequent thrombus formation. If this process results in reduced coronary blood flow, the patient may present with an acute coronary syndrome (ACS). Total thrombotic occlusion generally results in ST-segment elevation myocardial infarction (STEMI), whereas incomplete occlusion (or extensive collateralisation) is more likely to present as non-STEMI or unstable angina without evidence of myonecrosis (collectively non-ST-segment elevation ACS (NSTE-ACS)). Revascularisation, most commonly with percutaneous coronary intervention (PCI) is standard of care in ACS, as it restores myocardial perfusion by addressing both the thrombotic obstruction and the underlying coronary stenosis. However, adjunctive pharmacological treatment after revascularisation, or in patients managed conservatively, may be of equal importance in influencing prognosis.1–3

Contemporary adjunctive antithrombotic therapy in ACS includes potent antiplatelet and anticoagulant agents, each of which carries the risk of bleeding. The frequency and implications of haemorrhagic complications must be factored into the risk-benefit analysis for each patient since PCI is increasingly performed in complex subgroups such as those with renal dysfunction, underlying anaemia and the elderly, cohorts with inherently increased bleeding risk.4 ,5 Furthermore, although the absolute bleeding risk will vary according to individual patient characteristics, the overall relative bleeding risk increases with the number, potency and duration of agents co-administered. For example, those patients with ACS, already taking chronic oral anticoagulation (OAC) for stroke protection in atrial fibrillation, are then treated with dual antiplatelet therapy (DAPT) (so-called ‘triple therapy’).6 ,7

There is extensive evidence in the published literature that demonstrates major bleeding to …