Case
A 69-year-old man applied for elective CAG. He had only hyperlipidemia without diabetes or hypertension. In the elective CAG of six years ago, one bare metal stent was implanted into proximal segment of OM1 branch of the LCX without any hematological deterioration. CAG of three years later revealed that the stent was patent without any additional new obstructive lesion. At admission, the patient had been taking acetylsalicylic acid of 100 mg/day, metaprolol of 50 mg/day, atorvastatin of 20 mg/day for the last six years. He had normal hematological parameters (Tab. 1). He was taken to the angiography laboratory after receiving 100 mg of acetylsalicylic acid. The CAG revealed 20% stenosis in the LAD, proximal 90% narrowing in the LCX and 90% stenosis in the rudimentary RCA. One bare metal stent was implanted into the LCX following a loading dose of 300 mg clopidogrel and a bolus administration of 8,000 IU of unfractionated heparin. Three hours later, the patient developed severe chest pain without obvious electrocardiographic deviation. Second CAG showed thrombus material filling stent lumen in proximal LCX creating 99% obtruction in the luminal diameter. Thus, tirofiban was started at a bolus administration of 25 μg/kg over 3 minutes and then 0.15 μg/kg/min continuous infusion intravenously. In the follow-up, we observed progressively decreasing hemoglobin without any thrombocytopenia. Hemoglobin level had fallen from 12.0 g/dl to 8.6 g/dl at the end of 24th hour while platelet counts were stable. Tirofiban was ceased immediately at 24th hour. During 24-hour tirofiban infusion, the patient didn’t reveal any clinical signs or symptoms related to hemorrhage except fever of 38.9 °C started approximately four hours after tirofiban infusion. Neurological examination was normal. Computed tomography with intravenous contrast agent revealed negative result for retroperitoneal hematoma or any other source of internal bleeding (Fig. 1a). Microscopic examination of the blood film showed hemolytic anemia findings with single large thrombocytes implying antiaggregant use (Fig. 1b). Both direct and indirect Coombs tests were negative. 24 hours after stopping tirofiban infusion, anemia started to recover without any other intervention. One week later he had hematocrit of 32.4% and obvious recovery on the blood film examination.
Case
A 69-year-old man applied for elective CAG. He had only hyperlipidemia without diabetes or hypertension. In the elective CAG of six years ago, one bare metal stent was implanted into proximal segment of OM1 branch of the LCX without any hematological deterioration. CAG of three years later revealed that the stent was patent without any additional new obstructive lesion. At admission, the patient had been taking acetylsalicylic acid of 100 mg/day, metaprolol of 50 mg/day, atorvastatin of 20 mg/day for the last six years. He had normal hematological parameters (Tab. 1). He was taken to the angiography laboratory after receiving 100 mg of acetylsalicylic acid. The CAG revealed 20% stenosis in the LAD, proximal 90% narrowing in the LCX and 90% stenosis in the rudimentary RCA. One bare metal stent was implanted into the LCX following a loading dose of 300 mg clopidogrel and a bolus administration of 8,000 IU of unfractionated heparin. Three hours later, the patient developed severe chest pain without obvious electrocardiographic deviation. Second CAG showed thrombus material filling stent lumen in proximal LCX creating 99% obtruction in the luminal diameter. Thus, tirofiban was started at a bolus administration of 25 μg/kg over 3 minutes and then 0.15 μg/kg/min continuous infusion intravenously. In the follow-up, we observed progressively decreasing hemoglobin without any thrombocytopenia. Hemoglobin level had fallen from 12.0 g/dl to 8.6 g/dl at the end of 24th hour while platelet counts were stable. Tirofiban was ceased immediately at 24th hour. During 24-hour tirofiban infusion, the patient didn’t reveal any clinical signs or symptoms related to hemorrhage except fever of 38.9 °C started approximately four hours after tirofiban infusion. Neurological examination was normal. Computed tomography with intravenous contrast agent revealed negative result for retroperitoneal hematoma or any other source of internal bleeding (Fig. 1a). Microscopic examination of the blood film showed hemolytic anemia findings with single large thrombocytes implying antiaggregant use (Fig. 1b). Both direct and indirect Coombs tests were negative. 24 hours after stopping tirofiban infusion, anemia started to recover without any other intervention. One week later he had hematocrit of 32.4% and obvious recovery on the blood film examination.
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