Heparin has been the standard anticoagulation for percutaneous cardiovascular procedures (PCI). Its low cost and the lack of a better therapeutic alternative have accounted for its widespread adoption in the cardiac catheterization laboratory over the past 50 years. However, heparin has several well known limitations, including the induction of thrombocytopenia.1–4 In addition, severe thrombocytopenia not related to a previous administration of heparin may also be a challenge in patients in need of PCI. Platelet counts below 100,000/µL of any etiology have been statistically correlated with a higher incidence of hematoma (p = 0.002) and platelet counts of Case Report. In November 2002, a 71-year-old white male presented with unstable angina of recent onset. His past medical history was significant for psoriasis, systemic hypertension, type II diabetes mellitus, dyslipidemia and obesity but no previous use of heparin. Admission labwork showed severe thrombocytopenia (platelet count by Coulter T 890 of 47,000 platelets/mm3). Diagnostic angiography showed a critical type B (AHA/ACC) lesion in the mid-left anterior descending artery, and diffuse and mild disease in the remaining coronary arteries with preserved left ventricular contractility. To avoid the risk of lowering the patient’s platelet count further and to minimize the risk of bleeding we performed PCI using bivalirudin, instead of heparin. The patient was premedicated with 300 mg of clopidogrel and 365 mg of ASA two hours before the procedure. He was given a 13.5 mL (0.75 mg/kg) intravenous (IV) bolus of bivalirudin followed by a 32 mL/hr (1.75 mg/kg/min) IV infusion for the duration of the procedure. Baseline activated clotting time (ACT) was 120 seconds. Five minutes after the bivalirudin bolus and infusion, the ACT was 365 seconds. PCI was performed with coronary stent deployment in the mid-left anterior descending artery. The procedure was uncomplicated and lasted 45 minutes. Bivalirudin infusion was discontinued at the end of the procedure. The ACT value obtained 90 minutes later was 160 seconds and allowed for safe sheath removal with no residual hematoma at the femoral access. The patient’s platelet count remained at 47,000/mm3 post-procedure and up to hospital discharge on the next day. Forty days after the procedure, the patient’s platelet count showed no change from baseline and the patient was feeling well. Discussion. This case report describes a patient with severe thrombocytopenia unrelated to previous heparin treatment, who underwent successful PCI with coronary stenting using bivalirudin as an alternative to heparin. Thrombocytopenia can result in alteration of the platelets’ ability to activate and participate in clot formation thereby increasing a patients risk for bleeding complications. Thrombocytopenia has a number of different etiologies, including platelet destruction caused by hereditary, acquired or iatrogenic factors, and pharmacological therapies.5 In the present case, a myelogram and biopsy was performed to assess the patient for potential causes of thrombocytopenia, such as leukemia or myelodysplasia. However, no blood cell alterations were detected and the bone marrow was normal. It was concluded by the consulting hematologists that the patient’s thrombocytopenia was a consequence of immunological depression related to psoriasis. Heparin has been used as an antithrombotic agent since the earliest studies performed by Howell and McLean in 1884 and 1916.8,9 The use of heparin has matched the exponential growth of percutaneous interventional procedures in cardiology. However, heparin has important limitations in the setting of interventional cardiology, including unpredictable dose-response, nonspecific and extensive protein binding, activation of platelets, and the ability to stimulate the immune-mediated disorders heparin-induced thrombocytopenia (HIT) and heparin-induced thrombocytopenia and thrombosis syndrome (HITTS).1–4,10 Despite several recent alternative anti-thrombotic drugs (Danaparoid,® Reo-Pro,® Refludan,® Argatroban®), many are either associated with low rates of thrombocytopenia, or have not demonstrated ischemic or bleeding advantages over heparin in PCI. Danaparoid is a glycosaminoglycan, similar to heparin and is known to cross react with heparin antibodies.11 Glycoprotein IIb/IIIa receptor inhibitors have been associated with thrombocytopenia in up to 7% of patients.5 While lepirudin and argatroban do not cross-react with heparin antibodies and have not been reported to cause thrombocytopenia, they also have not demonstrated any significant benefit over heparin in PCI. The thrombin-specific inhibitor bivalirudin is an attractive alternative anticoagulant, having advantages over heparin including those patients with severe thrombocytopenia.12 Bivalirudin is a 20-amino acid synthetic peptide. Bivalirudin binds directly and specifically to thrombin.13 The predictable dose-response and linear pharmacokinetics associated with bivalirudin lead to consistent levels of anticoagulation during PCI such that frequent ACT monitoring is not required, unlike anticoagulation with heparin. Bivalirudin does not cross-react with heparin antibodies, is not associated with the development of HIT or HITTS, and to date, there are no published reports of immune-mediated thrombocytopenia after anticoagulation with bivalirudin.6,9,14 In addition, the 25-minute half-life of bivalirudin allows for early sheath removal, 90 minutes in our patient, and the potential for early ambulation. The REPLACE-2 trial demonstrated an overall low incidence of thrombocytopenia. Significantly fewer patients treated with bivalirudin had thrombocytopenia compared to patients treated with heparin plus GPIIb/IIIa inhibition. Among bivalirudin-treated patients (n = 2,868), 0.7% had platelet counts of
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