The Successful Use of Enoxaparin in the Lack of Bivalirudin in a Patient with Chronic Lymphocytic Leukemia and Thrombocytopenia who Underwent Percutaneous Coronary Revascularization

We present a patient with chronic lymphocytic leukemia and thrombocytopenia who underwent a percutaneous coronary intervention. Such patients are at increased risk for ischemic and hemorrhagic complications and the choice of anticoagulant therapy should be made very carefully. Unfractionated heparin or glycoprotein IIb/IIIa inhibitors may cause thrombocytopenia and increased bleeding. Bivalirudin therapy is safer in such patients. However, bivalirudin is not always available. We used enoxaparin, a low-molecularweight heparin, as an anticoagulant in a case in which bivalirudin was not available. No ischemic or hemorrhagic complications were seen in the followup period. We suggest that low-molecular-weight heparin may be eff ective and safe as an alternative to bivalirudin in patients with chronic lymphocytic leukemia and thrombocytopenia when bivalirudin is unavailable.


Introduction
Chronic lymphocytic leukemia (CLL) is characterized by the progressive accumulation of small, monoclonal B cells in the blood, bone marrow, lymph nodes and spleen.Abnormal hematopoiesis results in anemia and thrombocytopenia [1].
Ischemic and bleeding complications are seen more frequently in patients with thrombocytopenia and the selection of an anticoagulant therapy should be made carefully [2].Anticoagulant therapy with unfractionated heparin (UFH) or UFH plus glycoprotein IIb/IIIa inhibitor is not appropriate in such patients [2,3].It has been suggested that bivalirudin therapy may be effective and safe in patients with CLL and thrombocytopenia [3].Low-molecular-weight heparin (LMWH) has been demonstrated to be as effective as UFH and it has a predictable dose response.We present a patient with CLL and thrombocytopenia in whom enoxaparin, a low-molecular-weight heparin, was successfully used as an anticoagulant in the absence of bivalirudin during a percutaneous coronary intervention (PCI).

Case Report
A 56-year-old male patient who demonstrated angina pectoris for two days was examined in our department.He had a CLL diag-nosis and had been followed up in the hematology department.An ECG demonstrated a biphasic T wave in V 3 derivation.His cardiac biomarkers were within the normal limits (CK-MB: 13 U/L, troponin-I: 0.01 ng/mL).An echocardiogram displayed hypokinesia in the anterior wall and the ejection fraction was measured as 50%.The patient was hospitalized with a diagnosis of unstable angina.His hematologic values were as follows: hemoglobin, 11.1 g/dL; hematocrit, 33.5%; platelets, 47×10 3 /μL; and leukocyte count, 92.9×10 3 / μL with 70% lymphocytes, 7% neutrophils, 18% monocytes and 3% basophils.The patient was treated with acetylsalicylic acid 1×100 mg, clopidogrel 1×75 mg, metoprolol 1×100 mg, ramipril 1×2.5 mg, atorvastatin 1×40 mg, enoxaparin 2×0.6 cc subcutaneous and intravenous nitrate.Rest angina occurred despite continuing medical therapy.His cardiac biomarkers were retested and troponin-I became positive (0.5 ng/mL).
The patient was scheduled to undergo diagnostic cardiac catheterization.He received a consultation in the hematology department.He was administrated one unit of platelets prior to the procedure.Informed consent was received from the patient and he was transferred to our catheter laboratory.The mid-portion of the left anterior descending (LAD) artery showed 95% stenosis (Figure1).The left circumflex artery and the right coronary artery were normal.A decision was made to perform angioplasty to the LAD artery.Prior

Discussion
Thrombocytopenia is associated with bleeding, recurrent ischemia, urgent revascularization and death in patients undergoing a PCI [2].Care must be taken in choosing an anticoagulant therapy for thrombocytopenic patients.
UFH is the most commonly used anticoagulant during a PCI.However, UFH therapy cannot inactivate fibrin-bound thrombin and it is associated with heparin-mediated platelet activation, a risk factor for heparin-induced thrombocytopenia [4].UFH plus glycoprotein IIb/IIIa inhibitor therapy increases the efficacy of UFH.However, therapy with UFH or UFH plus glycoprotein IIb/IIIa inhibitors may cause thrombocytopenia and has the increased risk of post-procedural hemorrhagic complications [5].LMWH has been demonstrated to be as effective as UFH as well as safer.Additionally, it does not require laboratory monitoring [4].
Bivalirudin has been suggested as an alternative to heparin and it has been successfully used in PCIs in patients with thrombocytopenia and at increased risk for bleeding without any significant adverse events [6].In addition, it has been reported that bivalirudin therapy was successfully used in a PCI in a patient with CLL and thrombocytopenia [3].However, there are no data concerning which anticoagulant therapy should be used for such patients in PCIs when bivalirudin is unavailable.
This case suggests that enoxaparin therapy together with acetylsalicylic acid and clopidogrel may be effective and safe in PCIs in patients with CLL and thrombocytopenia if bivalirudin is unavailable.As an anticoagulant, LMWH may be used in such patients when bivalirudin is not available.