Background: Glycoprotein (GP) IIb-IIIa inhibitors are antithrombotic drugs used in selected patients during and after percutaneous coronary interventions (PCIs), usually as a bail-out in the setting of no-reflow or thrombotic complications. A notorious life-threatening adverse effect of this drug class is immune-mediated drug-induced thrombocytopenia (DITP). Thrombotic microangiopathy (TMA) induced by GP IIb-IIIa inhibitors has never been reported.
Case summary: A 72-year-old woman admitted for anterior myocardial infarction treated with primary PCI and stent implantation underwent a first tirofiban infusion as a bail-out strategy. After a new procedure for stent thrombosis, she received a second tirofiban infusion and developed sudden severe thrombocytopenia (platelet count <20 000/µL). Tirofiban was stopped but no observed increase in platelet count. Acute kidney injury due to renal ischaemia and left ventricular thrombosis followed. Unexpectedly, evidence for haemolysis and schistocytosis at peripheral blood smear prompted a diagnosis of TMA. Plasma exchange was immediately started with evidence for initial increase in platelet count, but the patient died due to sudden haemodynamic and respiratory deterioration.
Discussion: Tirofiban is known to rarely cause immune-dependent DITP. However, it has never been associated with TMA. This case report not only describes the first case of probable tirofiban-induced TMA, but also highlights the importance of a systematic approach to severe thrombocytopenia, even in the setting of low platelet count from a known DITP-related drug. Treatment of TMA in the difficult context of recent myocardial infarction and stent thrombosis requires a complex interplay between cardiologist, haematologist, transfusionist, and nephrologist, carefully balancing thrombotic and haemorrhagic risk.
Keywords: Acute myocardial infarction; Case report; Glycoprotein IIb–IIIa inhibitors; Stent thrombosis; Thrombocytopenia; Thrombotic microangiopathy; Tirofiban.
© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology.