Abstract
Tirofiban is an intravenous glycoprotein IIb/IIIa inhibitor (GPI) that can be used as a bailout strategy in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI) with high thrombus burden. A rare complication of this agent is severe thrombocytopenia, with an incidence ranging from 0.1 % to 0.5 %. We present a case of a patient who presented with ACS, underwent PCI, and subsequently developed severe thrombocytopenia within 24 h of receiving tirofiban. Tirofiban-induced thrombocytopenia is a rare immune-mediated condition that significantly heightens the risk of bleeding complications. Management involves immediate cessation of the drug, close monitoring of platelet counts, and supportive care. Platelet transfusion is indicated when the count falls below 10,000/μL, or below 50,000/μL with significant bleeding. This case highlights the need for early identification with routine platelet checks and close monitoring in patients receiving GPIs to prevent severe adverse outcomes, such as life-threatening bleeding or thrombotic events.
Learning objectives
Severe thrombocytopenia is an exceptionally rare but serious complication of tirofiban. Gaining a comprehensive understanding of the role of tirofiban and other glycoprotein IIb/IIIa inhibitors in the management of acute coronary syndrome, along with recognizing potential complications and accurately differentiating drug-induced thrombocytopenia from other causes, is essential to prevent life-threatening outcomes.
Introduction
Tirofiban is a non-peptide glycoprotein IIb/IIIa receptor antagonist (GPRA) that blocks fibrinogen and von Willebrand factor from binding to the glycoprotein IIb/IIIa receptor on platelets, thus inhibiting platelet aggregation. It is primarily utilized during the management of acute coronary syndrome (ACS) and for patients undergoing percutaneous coronary intervention (PCI) [ ]. The use of tirofiban, along with other GPRAs such as abciximab and eptifibatide, has been proven to significantly reduce the risk of myocardial infarction (MI) and composite cardiac outcomes (death, MI, and revascularization) [ ]. Although tirofiban has displayed a mortality benefit in patients with ACS and during PCI, it has rarely been associated with thrombocytopenia. Studies have demonstrated that the incidence of tirofiban-induced thrombocytopenia, characterized by a platelet count of less than 100,000/μL within 72 h of tirofiban exposure, ranges from approximately 0.4 % to 5.6 % [ ]. Additionally, clinical trials indicate that the occurrence of severe tirofiban-induced thrombocytopenia, defined as a platelet count below 50,000/μL, ranges from 0.1 % to 0.5 % [ ].
It is important to differentiate tirofiban-induced thrombocytopenia from other similar presentations, such as heparin-induced thrombocytopenia (HIT). A primary distinguishing feature between these two conditions is the timing and onset. While tirofiban-induced thrombocytopenia typically has a more rapid onset within hours to a few days, most cases of HIT occur around 5 to 10 days following exposure to heparin [ ]. Further, HIT primarily manifests as thrombosis rather than bleeding complications.
We report the case of a patient presenting with an ST elevation myocardial infarction (STEMI) who underwent PCI and subsequently developed severe thrombocytopenia within 24 h of tirofiban administration.
Case report
A 71-year-old Caucasian female with a 30-pack-year smoking history presented to the emergency department with sharp, substernal chest pain that awoke her from sleep. Upon arrival, her electrocardiogram revealed ST-segment elevations in leads I and aVL, along with reciprocal changes. Her troponin T levels were markedly elevated, with an initial measurement of 35 ng/L and a peak of 5999 ng/L. The patient was subsequently thought to have STEMI, loaded with heparin, and immediately taken to the catheterization laboratory where she was found to have acute 100 % thrombotic occlusion of the mid-left anterior descending artery (LAD) with 95 % ostial D1 stenosis ( Fig. 1 A ). She underwent successful PCI of the ostial to mid-LAD with a 3.0 × 34 mm Onyx drug-eluting stent (DES; Medtronic, Minneapolis, MN, USA), and PCI of the ostial to proximal D1 with a 2.5 × 15 mm Onyx DES ( Fig. 1 B). At the beginning of the procedure, the patient received a 10 μg/mL bolus of tirofiban, followed by a 5 μg/mL bolus in the middle of treatment. Following her procedure, she was loaded with 60 mg of oral prasugrel and dual antiplatelet therapy with prasugrel and aspirin for one year was initiated. The morning following her procedure, a complete blood count (CBC) revealed a critically low platelet count of 22,000/μL, a significant drop from the 229,000/μL recorded on admission. Over the next two days, repeated CBCs consistently showed critically low platelet counts, ranging from 21,000 to 35,000/μL. She did not receive another bolus of tirofiban following the procedure but continued aspirin and prasugrel despite her thrombocytopenia post-PCI. A peripheral smear was negative for schistocytes, effectively ruling out concerns for hemolytic anemia or microangiopathic processes, including thrombotic thrombocytopenic purpura (TTP) ( Fig. 2 ). Furthermore, since the patient had received a brief course of heparin prior to catheterization, a platelet factor 4 (PF4)/heparin enzyme-linked immunosorbent assay was performed, which returned negative results, effectively ruling out HIT.
