ST-elevation myocardial infarction following de-escalation to aspirin monotherapy: evidence of residual platelet function MRP4 overexpression dependent case report

De-escalation from dual antiplatelet therapy (DAPT) to aspirin monotherapy is commonly performed after percutaneous coronary intervention to reduce bleeding risk. However, interindividual variability in platelet response exists, and high-on-aspirin residual platelet reactivity may predispose to thrombotic events. Platelet overexpression of multidrug resistance protein 4 (MRP4) has been proposed as a molecular mechanism contributing to aspirin low response, and it is a further risk factor for cardiovascular events.

An 82-year-old woman with a history of coronary artery disease presented with ST-elevation myocardial infarction 10 days after de-escalation from dual antiplatelet therapy (aspirin plus clopidogrel) to aspirin monotherapy. Coronary angiography revealed thrombotic occlusion of the proximal left anterior descending artery with in-stent restenosis. Platelet molecular analysis demonstrated increased MRP4 expression compared with aspirin-treated patients without acute coronary syndromes, suggesting impaired aspirin responsiveness consistent with a high-on-aspirin residual platelet reactivity phenotype. The patient was successfully treated with ticagrelor-based antiplatelet therapy and experienced no recurrent ischaemic or bleeding events during follow-up.

This case suggests that MRP4-mediated aspirin residual platelet function may contribute to thrombotic events following de-escalation to aspirin monotherapy. Assessment of platelet reactivity and molecular markers such as MRP4 expression, before switch from dual to single therapy, may help identify individuals at higher risk of aspirin failure and support a personalized approach to antiplatelet therapy.