Elective Coronary Stent Implantation in a Patient with Unstable Angina and Thrombocytopenia

Myelodysplastic syndrome is a clonal hematopoietic stem-cell disorder characterized by cytopenia caused by inadequate proliferation and differentiation of blood cells due to dysmorphic or abnormal cellular bone marrow. When the megakaryocytic series is affected, the predisposition to hemorrhage becomes an important factor for clinical aggravation.¹ The association of thrombocytopenia caused by myelodysplastic syndrome with coronary disease is a challenge to interventional cardiologists, since percutaneous coronary interventions require the administration of antiplatelet aggregators to avoid intracoronary thrombosis, while at the same time there is a need to avoid bleeding after the procedure. Case Report. A retired 61-year-old male patient was admitted to the hospital with oppressive precordial pain. The symptoms started to occur 8 months before during heavy exertion, and 1 month before hospital admission, they started to occur during mild exertion. The patient’s only risk factor for coronary disease was systemic hypertension. He had been making irregular use of 200 mg/day of acetylsalicylic acid (ASA), 40 mg of propanolol each 12 hours, 20 mg/day of omeprazol, 5 mg/day of folic acid, and vitamin B complex. One year prior, the patient presented with spontaneous gengival hemorrhage and petechiae. On that occasion, the hemogram showed thrombocytopenia with 20,000 platelets/mm3. The patient underwent a myelogram and a immuno-histochemical test of bone marrow, which led to the diagnosis of myelodysplastic syndrome involving both granulocytic and megakaryocytic series, with preservation of the erythroid series. The patient was then medicated with folic acid, pyridoxin, and cyanocobalamin. The number of platelets was maintained at approximately 40,000/mm3, and no further hemorrhagic events were observed. Physical examination evidenced hypoplasia of the upper limbs (phocomelia), a blood pressure of 180/110 mmHg, and a heart rate of 96 bpm. Cardiopulmonary auscultation was normal. An electrocardiogram at rest showed sinus rhythm with unspecific alterations of repolarization in the lower wall. During the occurrence of pain, the ECG showed ST-segment depression and T-wave inversion (plus-minus) in the lower wall. Thoracic radiography exhibited a cardiothoracic index of 0.5 and normal pleuropulmonary fields. Transthoracic echocardiography revealed moderate left ventricular dysfunction due to hypokinesia of the lower dorsolateral wall, with an ejection fraction of 40%. Laboratory tests showed 40,000 platelets/mm3, 1,850 leucocytes/mm3, and hemoglobin 13.2 g/dl. Coagulogram results were within normal values: INR (International Normalized Index) was 1.09 (normal range = 0.90–1.26), and the APTT (Activated Partial Thromboplastin Time) was 28 seconds (normal range = 25–45 seconds). Serologic tests for B and C hepatitis, HIV, HTLV, CMV, and VDRL were all negative. The patient underwent coronary angiography 2 hours after transfusion of 10 units of platelets. The examination was performed by right femoral artery (RFA) puncture according to the Judkins’s technique, using 6 French (Fr) introducer and catheters. Immediately after the procedure, the introducer was removed from the RFA and local compression was performed for 20 minutes. Neither bleeding nor hematoma occurred after compression. The examination showed an obstruction of 80% in the right coronary artery (RCA) ostium and 30% in the anterior descending artery (Figure 1). Six days after administration of 75 mg/day of clopidogrel and 2 hours after new transfusion of 10 units of platelets, the patient underwent successful direct implantation of a Lekton® 3.0 x 10 mm stent (Biotronik, GmbH & Co., Berlin, Germany) in the RCA ostium. The hemogram and coagulogram done on the day of the procedure showed thrombocytopenia 40,000/mm3, leukopenia 1,620/mm3, an APTT of 31 seconds, and an INR of 1.03. The approach was made through the left femoral artery (LFA) using a 6 Fr introducer and catheter JR 3.5. During the procedure, the patient received 20 mg of intracoronary isosorbide mononitrate and 6,000 IU (100 IU/kg) of intravenous heparin. The stent release pressure was 14 atm, and post-dilatation was performed using the same balloon catheter as the stent at 18 atm. Laboratory tests post-procedure exhibited 71,000 platelets/mm3, 2,370 leukocytes/mm3, an APTT of 28.9 seconds, and an INR of 1.03. The introducer was removed 4 hours after the procedure and local manual compression was performed for 30 minutes. Neither bleeding nor hematoma were observed after compression (Figure 2). No complications occurred after the procedure. After the administration of 75 mg/day of clopidogrel for 2 weeks, the platelet count remained stable at 40,000/mm3 and 7 days after stent implantation, the patient was prescribed continuous use of 75 mg/day of clopidogrel without ASA, and was discharged from the hospital. Discussion. The association of thrombocytopenia caused by myelodysplastic syndrome with coronary disease is a rare situation. The literature present 2 case reports of patients with idiopathic thrombocytopenic purpura who underwent coronary transluminal angioplasty to treat acute myocardial infarction,^2,3 and in one of them, a coronary stent was implanted to treat an angioplasty complication (dissection).² Since these procedures were performed emergently, there was no previous preparation and the patients presented hemorrhagic complications at the site of arterial puncture. There are some case reports of patients with idiopathic thrombocytopenic purpura who underwent myocardial revascularization surgery with prophylactic treatment using steroids, immunosuppressors, or platelet transfusion to increase the number of platelets,⁴ however, there are no case reports of prophylactic treatment previous to coronary angioplasty and elective coronary stent implantation in patients with thrombocytopenia caused by myelodysplastic syndrome. TAR syndrome (Thrombocytopenia with Absent Radius), a rare congenital anomaly that involves the association of phocomelia with thrombocytopenia and the reduction of megakaryocytes in the myelogram, and differs from the myelodysplastic syndrome in that the latter also exhibits reduction of the granulocytic and erythroid series.⁵ The patient presented phocomelia of upper limbs, however, the myelogram showed marked reduction of both granulocytic and megakaryocytic series. According to the America’s Blood Centers, prophylactic platelet transfusion should be performed in patients with platelet counts lower than 50,000/mm3 who will be undergoing surgery or invasive procedure in which the operative site can be visualized, or where external pressure can be used to maintain hemostasis.⁶ In the present case, the patient’s platelet count was 40,000/mm3 and the transfusion of 10 units of platelets was performed 2 hours before the procedures in order to increase the number of platelets to above 50,000/mm3. This conduct proved to be safe both for coronary angiography and for stent placement. Heparin use in the dosage of 100 IU/kg during the procedure also proved to be safe, since the introducer was removed from the femoral artery 4 hours after the procedure, without bleeding or hematoma formation. The use of small diameter introducers and catheters is recommended to facilitate post-procedure hemostasis. In the present case 6 Fr material was used, since this is the smallest diameter available. There are new stent implantation case reports using 5 Fr guiding catheter with success rates comparable to those obtained with 6 Fr.⁷ Unstable angina is stimulated by cellular mechanisms that convert the atherosclerotic lesion from the stable to the activated state, making it prone to fracture or rupture with subsequent platelet adhesion and aggregation and thrombus formation.⁸ The reduction of the coronary lumen diameter resulting from mural thrombus formation is probably responsible for the decrease in the angina threshold during exertion. Despite presenting thrombocytopenia, this patient progressed from stable to progressivly unstable angina, which suggests that the platelets’ function remained normal, regardless of the reduced number of platelets. This is a rationale for the use of antiplatelet aggregators as a means of preventing acute or subacute thrombosis after stent implantation. Among the thienopyridinic derivatives, clopidogrel — a potent antiplatelet aggregator — was the drug of choice because it presents lower rates of hemorrhagic and vascular complications, neutropenia and thrombocytopenia.⁹ During the 2 weeks of clopidogrel administration, no complications were reported. This case description suggests that percutaneous coronary interventions, angiography, and stent implantation in patients with thrombocytopenia are safe procedures, as long as prophylactic platelet transfusion is performed 2 hours beforehand. george@tre-sp.gov.br

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