Dual resistance to ticagrelor and prasugrel caused subacute stent thrombosis in a patient, identified by thromboelastography, despite standard and doubled dosing.
This case demonstrates that rare dual resistance to potent P2Y12 inhibitors (ticagrelor and prasugrel) can cause unexplained subacute stent thrombosis, highlighting the potential utility of TEG platelet mapping for guiding individualized therapy.
Absolute Event Rate: 0% vs 0%
Stent thrombosis (ST) may occur due to variability in platelet response to P2Y12 inhibitors, particularly after excluding common causes such as mechanical complications or medication non-compliance. Although ticagrelor and prasugrel typically provide more potent and consistent platelet inhibition than clopidogrel, some individuals still demonstrate inadequate response due to drug resistance. We describe a healthy, non-smoking male in his mid-60s who developed subacute ST 4 days after drug-eluting stent placement while on dual antiplatelet therapy with aspirin and ticagrelor. After excluding mechanical and clinical aetiologies, ticagrelor resistance was suspected. His regimen was switched to aspirin and prasugrel; however, thromboelastography (TEG) platelet mapping demonstrated persistently high on-treatment platelet reactivity to prasugrel, even after doubling the prasugrel dose. This case highlights rare resistance to newer P2Y12 inhibitors as a cause of unexplained ST and underscores the value of TEG platelet mapping to identify antiplatelet non-responsiveness and guide individualised therapy.
Farouji et al. (Sun,) reported a other. Dual resistance to ticagrelor and prasugrel caused subacute stent thrombosis in a patient, identified by thromboelastography, despite standard and doubled dosing.
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