Acute Serious Thrombocytopenia Associated with Intracoronary Tirofiban Use for Primary Angioplasty

Tirofiban, a specific glycoprotein IIb/IIIa inhibitor, may cause extensive thrombocytopenia with an incidence of 0.2% to 0.5%. We report the case of a 50-year-old man who developed thrombocytopenia after tirofiban use (both intracoronary and peripheral) over hours and the successful management of this complication after primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarction. 1. Introduction Glycoprotein IIb/IIIa inhibitors (GPIs) are commonly employed in treating patients who have unstable angina, non-ST, and ST-segment elevation myocardial infarction (STEMI), as well as in combination with angioplasty with or without stent placement [1]. Tirofiban, a specific and nonpeptide GPI, competitively inhibits the platelet fibrinogen receptor and may lead to severe thrombocytopenia with an incidence of 0.2% to 0.5% [2]. In this report, we describe a case of acute serious thrombocytopenia after 4？h of tirofiban administration in a patient in whom primary percutaneous coronary intervention (PCI) was performed for acute anterior STEMI. 2. Case Report A 50-year-old man presented with an acute anterior STEMI. Initial laboratory tests showed a normal complete blood count (CBC) including platelet count (265 109/L) at the emergency department. He reports no history of bleeding disorders, hematologic and renal problems, or heparin exposure. He immediately underwent PCI after pretreatment with 300？mg of aspirin and 600？mg of clopidogrel and 10.000？IU of intravenous unfractionated heparin. Coronary angiography showed the totally occluded left anterior descending artery (LAD). After predilatation, a large and fresh thrombus was seen. We first administered tirofiban via intracoronary route at a dose of 10？μg/kg followed by peripheral intravenous infusion at 0.15？μg/kg/min and then implanted a coronary 4.5 18？mm bare metal stent into LAD. A combination therapy of aspirin, clopidogrel, enoxaparin, and tirofiban infusion was given to the patient. Approximately 4？h after the PCI, areas of petechiae and ecchymoses were observed around the sternum and on both legs. The patient's platelet count was detected to be 5 109/L (Table 1). Checkup on the peripheral smear of a blood sample validated the extensive lack of platelets with no clustering. All antiplatelet drugs including tirofiban were immediately discontinued, and the patient was treated with Ig G infusion in order to achieve a quick recovery. There was a very slight rise on day 1, with improvement beginning after day 2 and counts surpassing 100 109/L on day 4 (Table 1). During this