Thrombotic Thrombocytopenic Purpura after Percutaneous Coronary Intervention
A 65-year-old female was admitted with complaints of dyspnea and chest discomfort. She had a 9-month history of dyspnea on exertion prior to her admission and a 20-year history of diabetes. She had no allergies and did not take any illicit drugs. Diagnostic studies included cardiac enzymes, in which the cTn-I was mildly elevated at 0.98 ug/L On a transthoracic echocardiogram, the ejection fraction was 39% and hypokinesia was present in the anteroseptal, anterior, septal and apical regions. Gated myocardial scintigraphy demonstrated a reversible reperfusion defect and hypokinesia in the anterior and inferior cardiac walls. The clinical diagnosis was a non-ST elevation myocardial infarction. A complete blood cell count revealed a hematocrit of 29.9%, a white blood cell count of 6,750/µL, and a platelet count of 226×103/µL. Additional laboratory tests performed at the time of admission revealed a blood ureanitrogen level of 40 mg/dL, a creatinine level of 2.0 mg/dL, and a creatinine clearance of 19 mL/min. Liver function tests were normal.\nAspirin and clopidogrel were started as antiplatelet therapy for 3 days before the coronary procedure. Coronary angiography revealed a 90% diameter stenosis of the proximal left anterior descending artery (LAD) and total occlusion of the proximal right coronary artery (RCA). After a 0.5 mm balloon predilation, a 3.0×28 mm sirolimus-eluting stent (SES) was successfully deployed at the LAD lesion. An attempt was made to open the chronic total occlusion in the proximal RCA. A floppy wire was successfully passed into the lesion. With balloon predilation, a 3.0×28 mm SES was successfully deployed at the proximal RCA. After stent implantation, the patient complained suddenly of dizziness and became agitated. The blood pressure dropped to 80 mmHg systolic and the pulse rate decreased to 40 beats per minute for a few minutes. A temporary pacemaker was immediately implanted. After stabilization of her vital signs, additional SESs (2.75×33 mm, 2.5×33 mm) were implanted at the distal and mid RCA. After the PCI, the patient was transferred to the cardiac intensive care unit. Although thevital signs were stable, her mental status was characterized by fluctuating confusion and irritability without any focal neurological findings. The body temperature was elevated to 38.4℃ at that time. To evaluate the cause of her abnormal mentation, serologic laboratory tests were performed. Arterial blood gas analysis demonstrated a metabolic acidosis. The platelet count was decreased to 147×103/µL. The prothrombin time (PT) was 13.9 seconds, the partial thromboplastin time was 43.6 seconds, and the serum ammonia level was normal. Several hours after the PCI, the platelet count rapidly decreased to 55×103/µL, and the aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels increased to 1516 U/L and 789 U/L, respectively. This was in contrast to the nearly normal level of alkaline phosphatase (ALP). Lactate dehydrogenase (LDH) increased to 3,504 U/L. On the first day after the PCI procedure, the platelet count decreased to 35×103/µL and the hematocrit decreased to 21.9%. The blood urea nitrogen increased to 60 mg/dL, the creatinine to 3.6 mg/dL, the AST and ALT levels peaked at 6,500 U/L and 2,063 U/L, respectively, and the LDH rose to 3,504 U/L. Serum amylase was also increased. The peripheral blood smear was consistent for microangiopathic hemolysis with schistocytes and burr cells. The Coombs direct and indirect tests were negative as were viral markers. An ultrasound study of the abdomen was unremarkable. A chest radiograph demonstrated no abnormality and an abdominal radiograph demonstrated contrast enhancement in both kidneys.\nPacked cells and fresh frozen plasma were transfused immediately. After 3 days, the creatinine rose to 5.5 mg/dL. The amylase and lipase levels had steadily risen to 609 U/Land 1,475 U/L, respectively, for several days with no abdominal pain The patient's general condition and mental status stabilized, and the platelet count s increased to 51×103/µL, 3 days after the procedure; and to 117×103/µL, 1 week later. She was discharged with a platelet count of 178×103/µL, a hematocrit of 28.1%, and a creatinine level of 1.6 mg/dL, with resolution of contrast on the abdominal radiograph. 4 weeks later, the platelet count increased to 275×103/µL and the hematocrit improved to 33.1%. After stabilization of all laboratory findings, the EF improved to 49% on a follow-up transthoracic echocardiogram. The patient experienced no adverse cardiovascular events at the time of her 6-month clinical follow-up.