A 44-year-old Caucasian male with no previous history of cardiovascular disease presented to the emergency department of the hospital with a two-hour history of retrosternal chest pain radiating to the left arm and mandible. He denied any previous history of blood dyscrasia or thrombocytopenia. He had no history of cardiac disease, drug abuse, and he mentioned two cardiovascular risk factors (tobacco abuse and hyperlipidemia). Additionally, he denied any history of a previous hospitalization where he may have received heparin or eptifibatide. His electrocardiogram (ECG) showed sinus rhythm with diffuse ST elevation of the II, III, aVF, V3 to V6 leads and reciprocal changes in I, aVL without any hemodynamic compromise (blood pressure 120/85 mmHg). His early management included treatment with intravenous unfractionated heparin (5000 unit bolus) followed by an infusion of 18 units/kg/hr, aspirin 325 mg, clopidogrel 600 mg, iv nitrates at a constant infusion, b-blockers (metoprolol 50 mg), intravenous morphine (4 mg), and oxygen 2 l/min. The patient had a white blood cell count of 11.000/mm3, a hemoglobin level of 14.0 g/dL, and a platelet count of 220,000/mm3. Values of prothrombin time (PT) and activated partial thromboplastin time (aPTT) were within normal limits. Due to the fact that the hospital was unable to perform percutaneous coronary intervention (PCI) or transfer the patient to a tertiary institute at a time less than 120 minute to PCI (door to needle), fibrinolytic therapy was decided upon and performed (tenecteplase 50 mg iv bolus) in the absence of any contraindications (absolute or relative). The symptoms 60 min after the medical revascularization did not reside, the ST-elevation remained unchanged, and reperfusion arrhythmias were not noticed. Taking into consideration all the above reasons, the patient was immediately transferred to the cardiac catheterization laboratory of our clinic for a rescue PCI. Coronary angiography showed that the left main coronary artery (LMCA) was a wide atheromatic vessel without critical stenoses, the left anterior descending coronary (LAD) artery was a relatively large vessel, with sparse atheromatic plaques and revealed a longitudinal critical stenosis of 70% immediately after the origin of a large diagonal branch. The left circumflex artery (LCx) had a 70% stenosis at the level of the bifurcation with the first obtuse marginal branch. The right coronary artery was totally occluded with a residual thrombus, with a Thrombolysis in Myocardial Infarction (TIMI) flow of 0. Protherapy (class IIa indication) with eptifibatide was decided due to the increased thrombus load of the right coronary artery (RCA) for at least 1 hour as an adjuvant measure before proceeding to the percutaneous transluminal coronary angioplasty (PTCA). The patient received an intravenous double bolus of 180 μg/kg of eptifibatide (10 minutes apart), followed by a 2 μg/kg/min infusion. A 3.0×24 mm PROMUS™ Element™ stent was deployed in the LAD with a very satisfying angiographic result (TIMI 3), the lesion of the LCx was also managed with the use of 3.0×24 mm PROMUS™ Element™ stent achieving an excellent result (TIMI 3). At the right coronary artery, thrombus extraction catheter (Thrombuster II) was used to remove the discrete, intraluminal filling defect that was noted within the infarct-related artery. Multiple passages were carried out in order to restore the flow and an important amount of thrombus load was aspirated using a 6-Fr Thrombuster II. The patient then underwent successful stenting of the right coronary artery with the deployment of a 3.0×32 mm PROMUS™ Element™ distally and 3.0×20 mm PROMUS™ Element™ proximally. Once flow was restored in the RCA, the patient became pain-free and had resolution of ST segment elevation. He was transferred in a stable condition to the coronary care unit. Post-percutaneous coronary intervention medications included aspirin 100 mg po daily, ramipril 5 mg po daily, metoprolol succinate 50 mg per os daily, clopidogrel 75 mg po daily, rosuvastastin 20 mg po daily, and the eptifibatide infusion was to be continued for 18 hours. Approximately four hours post-percutaneous coronary intervention and eptifibatide initiation, the patient developed profound thrombocytopenia, with his platelet count dropping by over 90% from baseline to 15,000/mm3 while the hemoglobin level remained stable. A peripheral blood smear showed no signs of platelet clumping, ruling out pseudothrombocytopenia and no evidence of microangiopathic hemolytic anemia. All antiplatelet products including heparin, eptifibatide as well as dual antiplatelet therapy (DAPT) was discontinued for 48 hours due to the profound thrombocytopenia 15,000/mm3, outweighing the risk of an early stent thrombosis with the risk of a fatal bleeding event such as an intercranial hemorrhage that would suspend the dual antiplatelet therapy for an indefinitive time period. Moreover patient related factors for acute stent thrombosis (<24 h of implantation) such as renal failure, diabetes mellitus and low ejection fraction were not present to our patient []. The patient was thereafter consulted to our hematology department. The patient’s platelet level reached its nadir (5,000/mm3) approximately 6 hours post-eptifibatide initiation. A heparin-induced thrombocytopenia (HIT) [,] platelet factor 4 antibody test was negative [,]. The patient was closely observed for any bleeding events. Platelets (5 packs, total) were transfused in the next 24 hours. After the transfusions, the platelet count increased from 5,000/mm3 to 60,000/mm3. Subsequently, the patient’s platelet count continued to rise (80,000/mm3) 48 hours after the eptifibatide exposure, which enabled us to restart both aspirin and clopidogrel. The patient showed no signs of active bleeding, bruises, ecchymosis, or petechiae during the hospitalization and was discharged on day five having a platelet count of 182,000/mm3, free of symptoms.