- Email: [email protected]
Acute Profound Thrombocytopenia After Treatment With Tirofiban and Off-Pump Coronary Artery Bypass Grafting
Ann Thorac Surg 2009;87:629 –31
CASE REPORT BEIRAS-FERNANDEZ ET AL DRUG-INDUCED THROMBOCYTOPENIA AFTER CORONARY SURGERY
629
Comment
References 1. Naito Y, Nakajima M, Inoue H, et al. Unexpected durability of Smeloff-Cutter aortic ball valve prosthesis. Ann Thorac Surg 2003;75:1633–5. 2. Stormer B, Mendling W, Kohler J, et al. Comparative study of in vitro flow characteristics between a human aortic valve and a designed aortic valve and six corresponding types of prosthetic heart valves. Eur Surg Res 1976;8:117–31. 3. Lund O, Pilegaard HK, Ilkjaer LB, et al. Performance profile of the Starr-Edwards aortic cloth covered valve, track valve, and silastic ball valve. Eur J Cardiothorac Surg 1999;16:403–13. 4. Godje O, Fischlein T, Adelhard K, et al. 25 years follow-up of patients after replacement of the aortic valve with a SmeloffCutter prosthesis. Thorac Cardiovasc Surg 1996;44:234 – 8. 5. Gometza B, Duran CM. Ball valve (Smeloff-Cutter) aortic valve replacement without anticoagulation. Ann Thorac Surg 1995;60:1312– 6. 6. Rao PS, Solymar L, Mardini MK, et al. Anticoagulant therapy in children with prosthetic valves. Ann Thorac Surg 1989;47: 589 –92. 7. Starr DS, Lawrie GM, Howell JF, et al. Clinical experience with the Smeloff-Cutter prosthesis: 1- to 12-year follow-up. Ann Thorac Surg 1980;30:448 –54. 8. Hsi DH, Ryan GF, Taft H, et al. A 29-year-old Harken disk mitral valve: long-term follow-up by echocardiographic and cineradiographic imaging. Tex Heart Inst J 2003;30:319 –21. © 2009 by The Society of Thoracic Surgeons Published by Elsevier Inc
Acute Profound Thrombocytopenia After Treatment With Tirofiban and Off-Pump Coronary Artery Bypass Grafting Andres Beiras-Fernandez, MD,* Anke Kowert, MD,* Pascale Jiru, MD, Marion Weis, MD, Michael Spannagl, MD, Bruno Reichart, MD, and Michael Schmoeckel, MD Departments of Cardiac Surgery, Anesthesiology, and Transfusion Medicine, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany
The glycoprotein IIb/IIIa (GP IIb/IIIa) receptor antagonists prevent platelet aggregation and thrombus formation, improving outcomes of patients with acute coronary syndrome. Therapy with these agents may lead to bleeding complications and thrombocytopenia, challenging the perioperative management of patients undergoing coronary surgery. We report the successful management of an acute profound thrombocytopenia after urgent off-pump coronary surgery in a patient treated with tirofiban for unstable angina and acute coronary syndrome. (Ann Thorac Surg 2009;87:629 –31) © 2009 by The Society of Thoracic Surgeons
G
PIIb/IIIa receptor antagonists prevent platelet aggregation and thrombus formation, improving outcomes after acute coronary syndrome [1]. However, they may lead to bleeding complications and thrombocytopenia [2], challenging the management of patients after coronary surgery.
A 63-year-old man patient presented with acute coronary syndrome (anterior ST-segment elevation depression; negative myocardial laboratory markers) after a 6-day period of unstable angina. Cardiac catheterization showed a two-vessel coronary disease involving the left main, the left anterior descending, and the left circumflex coronary arteries. The patient was scheduled for coronary artery bypass grafting and infusion with heparin (1,000 IU/h) and tirofiban (initial infusion of 0.4 mg/h for 30 minutes followed by 0.1 mg/h) was started. Initial laboratory results revealed no remarkable findings (Table 1). The baseline platelet count was 223 ⫻ 109/L. Treatment with tirofiban and heparin was continued until surgery, which occurred 8 hours later. At this time, the platelet count was 226 ⫻ 109/L. The patient underwent off-pump coronary artery bypass Accepted for publication June 10, 2008. *Both authors contributed equally to this work. Address correspondence to Dr Beiras-Fernandez, Department of Cardiac Surgery, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, 81377, Germany; e-mail: [email protected].
0003-4975/09/$36.00 doi:10.1016/j.athoracsur.2008.06.040
FEATURE ARTICLES
The Smeloff-Cutter valve was designed and has been demonstrated to have mild regurgitation [2]. This regurgitant flow prevents thrombus formation on the ball and cage of the prosthesis. Indeed, as compared with the Starr-Edwards ball-cage prosthesis (Edwards Laboratories), the Smeloff Cutter valve has a lower thromboembolism rate at 25 years (1.41% vs 2.01% per patient year) [3, 4]. Furthermore, Gometza and Duran [5] described a subset of young patients (n ⫽ 29) with an isolated Smeloff-Cutter aortic valve taking dipyridamole and aspirin, but no anticoagulants, at a thromboembolism rate of 0.9% per patient year in their series. Rao and colleagues [6] demonstrated a 2.5% per patient year thromboembolism rate in young patients taking dipyridamole and aspirin, but no anticoagulants. Several groups have published their long-term follow-up of patients with the Smeloff-Cutter aortic prosthesis. In the largest published experience of 358 patients, Starr and colleagues [7] demonstrated a 5.4%, 2.9%, and 2.6% per patient year thromboembolism rate in patients, respectively, taking no anticoagulation, antiplatelet agents, and warfarin. We believe that our patient has the oldest, functionally normal aortic mechanical valve described. Previously, a 29-year-old Harken disk mitral valve (Surgitools Inc, Woodvale, WA) has been described [8]. Although preoperative and intraoperative findings showed that in our patient the Smeloff-Cutter valve (Cutter Laboratories) was normal and functioning well, we decided to replace this 37-year-old valve because of the uncertainty of how much longer it would continue to function well.
630
CASE REPORT BEIRAS-FERNANDEZ ET AL DRUG-INDUCED THROMBOCYTOPENIA AFTER CORONARY SURGERY
Ann Thorac Surg 2009;87:629 –31
Table 1. Laboratory Values of the Patient After Tirofiban Infusion and Transfusion of Thrombocytes
A ⫽ angiography;
h ⫽ hours;
Hb ⫽ hemoglobin;
O ⫽ surgical procedure.
FEATURE ARTICLES
grafting by using the left internal thoracic artery to the left anterior descending artery and a single saphenous vein graft to the medial portion of the left circumflex artery. Anticoagulation was initially performed with 10,000 IU of unfractioned heparin and was carefully monitored with activated clotting time (⬎300 sec). Heparin was conventionally antagonized with protamine after the aortic anastomosis. However, the patient showed a severe diffuse bleeding. Intraoperative blood loss was 1,700 mL. Nine units of frozen fresh plasma, 1 unit of erythrocytes, and 1 unit of platelets were administered. The patient was transferred to the intensive care unit in stable condition with low pharmacologic support with norepinephrine (0.2 mg/h) and milrinone (0.4 mg/h). At admission, the platelet count was 77 ⫻ 109/L. The myocardial laboratory measurements were slightly increased, and the plasmatic coagulation laboratory findings were unremarkable (Table 1). Postoperative blood loss was less than 50 mL/h in the first 8 hours and less than 20 mL/h after that time. Six hours after intervention, the laboratory analyses showed a platelet count of 1 ⫻ 109/L. No clinical signs of bleeding were observed. Severe thrombocytopenia (1 ⫻ 109/L) was reconfirmed 30 minutes later, and pseudothrombocytopenia was excluded by using an alternate anticoagulant (citrate). Heparin-induced thrombocytopenia could be also excluded after negative enzyme-linked immunosorbent assay test for antibodies to platelet factor 4/heparin. The patient was transfused with 3 units of platelets with a rise in the platelet count from 1 ⫻ 109/L to 16 ⫻ 109/L after the first unit and 52 ⫻ 109/L after all of them. No thromboembolic or bleeding phenomena were observed. Six hours later (12 hours postoperatively) the platelet count was again severely reduced to 18 ⫻ 109/L, and a new transfusion of 2 thrombocyte units was necessary. The plasmatic coagulation laboratory values were not remarkable. Two hours later, the platelet count increased to 56 ⫻ 109/L and another thrombocyte unit was transfused. In the following 12 hours, the count of platelets increased slowly without transfusion and remained stable (Table 1). The patient
was discharged from the intensive care unit 4 days after surgery without thromboembolic or bleeding complications with a platelet count of 179 ⫻ 109/L.
Comment Different GPIIb/IIIa receptor inhibitors, abciximab, tirofiban, and eptifibatide, have been approved for clinical use in patients with acute coronary syndrome [3]. Abciximab has been reported to increase the incidence of thrombocytopenia in comparison with placebo, tirofiban, and eptifibatide [4]. In the RESTORE trial [5], severe thrombocytopenia (⬍ 50 ⫻ 109/L) was observed in 0.2% of the patients treated with tirofiban. Druginduced acute thrombocytopenia is defined as a decrease of the thrombocyte count to less than 20 ⫻ 109/L within 24 hours of exposure [6]. In our patient, the platelet counts were lower than 1 ⫻ 109/L at 6 hours after an exposure time of 14 hours. Differential diagnosis with other entities in patients receiving GPIIb/IIIa receptor inhibitors and heparin is mandatory. Pseudo-thrombocytopenia is defined as an artifactual miscalculation of platelets because of clumping platelets in blood samples anti-coagulated with ethylenediaminetetraacetic acid (EDTA). In our case, pseudothrombocytopenia could be excluded after repeated platelet counts in blood anti-coagulated with citrate. Heparin-induced thrombocytopenia could be excluded after a negative enzyme-linked immunosorbent assay test for antibodies to platelet factor 4/heparin. Furthermore, heparin-induced thrombocytopenia type I is associated with mild thrombocytopenia, and heparininduced thrombocytopenia type II typically occurs 4 to 10 days after starting a therapy with heparin. The profound thrombocytopenia observed in our patient was then most likely associated with tirofiban, considering the duration of the therapy (less than 24 h), the severity of the thrombocytopenia (1 ⫻ 109/L 6 hours after exposure), and the negative enzyme-linked immunosorbent assay heparin-induced thrombocytopenia test. However, the mechanism of GPIIb/IIIa recep-
tor antagonists associated with severe thrombocytopenia is not fully understood. One hypothesis suggests the induction of conformational changes in the thrombocyte receptors after therapy, which could react with pre-existing circulating antibodies [7]. Shanmugam and colleagues [8] reported that surgical revascularization could be safely performed in patients within a few hours of receiving tirofiban with little bleeding risk. However, acute profound thrombocytopenia after tirofiban can be life threatening in patients who will undergo coronary surgery, as it may increase the incidence of perioperative bleeding, thus potentially leading to reintervention. In our patient, acute thrombocytopenia presented 6 hours after offpump coronary artery bypass grafting, and increased thrombocyte substitution therapy was needed to obtain sufficient hemostasis. We believe that no data regarding acute profound thrombocytopenia after offpump coronary artery bypass grafting have been published. In our opinion, the thrombocyte count should be strictly monitored in patients presenting with an acute coronary syndrome needing coronary surgery, especially after administration of a GPIIb/IIIa receptor inhibitor. Furthermore, platelet’s transfusion should be considered if presentation of the thrombocytopenia occurs in the early postoperative period, to reduce the bleeding risk.
References 1. Boersma E, Harrington RA, Moliterno DJ, et al. Platelet glycoprotein IIb/IIIa inhibitors in acute coronary syndromes: a meta-analysis of all major randomised clinical trials. Lancet 2002;359:189 –98. 2. Demirkan B, Guray Y, Guray U, Korkmaz S. Differential diagnosis and management of acute profound thrombocytopenia by tirofiban: a case report. J Thromb Thrombolysis 2006;22:77– 8. 3. Karvouni E, Katritsis DG, Ioannidis JP. Intravenous glycoprotein IIb/IIIa receptor antagonists reduce mortality after percutaneous coronary interventions. J Am Coll Cardiol 2003; 41:26 –32. 4. Dasgupta H, Blankenship JC, Wood GC, Frey CM, Demko SL, Menapace FJ. Thrombocytopenia complicating treatment with intravenous glycoprotein IIb/IIIa receptor inhibitors: a pooled analysis. Am Heart J 2000;140:206 –1. 5. RESTORE Investigators. Effects of platelet glycoprotein IIb/ IIIa blockade with tirofiban on adverse cardiac events in patients with unstable angina or acute myocardial infarction undergoing coronary angioplasty. Randomized Efficacy Study of Tirofiban for Outcomes and REstenosis. Circulation 1997; 96:1445–53. 6. Berkowitz SD, Harrington RA, Rund MM, Tcheng JE. Acute profound thrombocytopenia after C7E3 Fab (abciximab) therapy. Circulation 1997;95:809 –13. 7. Bougie DW, Wilker PR, Wuitschick ED, et al. Acute thrombocytopenia after treatment with tirofiban or eptifibatide is associated with antibodies specific for ligand-occupied GPIIb/IIIa. Blood 2002;100:2071– 6. 8. Shanmugam G. Tirofiban and emergency coronary surgery. Eur J Cardiothorac Surg 2005;28:546 –50. © 2009 by The Society of Thoracic Surgeons Published by Elsevier Inc
CASE REPORT ATIK ET AL CATHETER ABLATION FOR POSTOPERATIVE ARRHYTHMIA
631
Recurrent Ventricular Arrhythmia After Coronary Artery Bypass Grafting Treated With Radiofrequency Catheter Ablation Fernando A. Atik, MD, Maria Fernanda M. Garcia, MD, Jose Mario Baggio, Jr, MD, Cristiano N. Faber, MD, Ricardo B. Corso, MD, Luiz Fernando Caneo, MD, and Alvaro V. Sarabanda, MD Departments of Cardiovascular Surgery, Cardiology, and Clinical Arrhythmia and Pacemaker Unit, Heart Institute of Federal District, Zerbini Foundation, Brasilia, Brazil
A 63-year-old diabetic woman was emergently submitted to coronary artery bypass grafting in the setting of acute myocardial infarction. Recurrent, drug-refractory episodes of ventricular arrhythmia occurred for 2 weeks postoperatively, despite no documentation of ongoing myocardial ischemia and optimum medical treatment. Ventricular arrhythmia was initiated by premature ventricular contractions originating from the Purkinje system within the infarct border zone. Radiofrequency catheter ablation was performed at sites where Purkinje potentials were recorded, leading to arrhythmia cessation. A week later, an implantable cardioverter defibrillator was inserted and she was discharged home a few days later. At 15-month follow-up, there were no further episodes of arrhythmia and ventricular function had improved. (Ann Thorac Surg 2009;87:631–3) © 2009 by The Society of Thoracic Surgeons
R
ecurrent, drug-refractory, new onset ventricular tachycardia (VT) and ventricular fibrillation (VF) after coronary artery bypass grafting (CABG) is uncommon, but may be associated with increased morbidity and mortality. The most likely mechanism is residual myocardial ischemia that usually relates to suboptimal anastomosis or incomplete revascularization. However, other factors may be implicated [1], including inadequate myocardial protection, myocardial reperfusion, metabolic imbalance, and anti-arrhythmic drug pro-arrhythmia. We herein report a patient who had drug-refractory, recurrent VT/VF early after CABG, and we discuss the possible mechanisms and the successful use of radiofrequency catheter ablation. A 63-year-old diabetic woman was admitted in the emergency room with a 3-hour history of sudden onset chest discomfort irradiated to the left arm and the back. On physical examination, she was found hemodynamically unstable, with early signs of pulmonary edema. Admis-
Accepted for publication June 19, 2008. Address correspondence to Dr Atik, Heart Institute of Federal District, Zerbini Foundation, Estrada Parque Contorno do Bosque s/n, 1 Andar, Sala 13, Brasília-DF, 70658-700, Brazil; e-mail: [email protected]. org.br.
0003-4975/09/$36.00 doi:10.1016/j.athoracsur.2008.06.065
FEATURE ARTICLES
Ann Thorac Surg 2009;87:631–3
CASE REPORT BEIRAS-FERNANDEZ ET AL DRUG-INDUCED THROMBOCYTOPENIA AFTER CORONARY SURGERY
629
Comment
References 1. Naito Y, Nakajima M, Inoue H, et al. Unexpected durability of Smeloff-Cutter aortic ball valve prosthesis. Ann Thorac Surg 2003;75:1633–5. 2. Stormer B, Mendling W, Kohler J, et al. Comparative study of in vitro flow characteristics between a human aortic valve and a designed aortic valve and six corresponding types of prosthetic heart valves. Eur Surg Res 1976;8:117–31. 3. Lund O, Pilegaard HK, Ilkjaer LB, et al. Performance profile of the Starr-Edwards aortic cloth covered valve, track valve, and silastic ball valve. Eur J Cardiothorac Surg 1999;16:403–13. 4. Godje O, Fischlein T, Adelhard K, et al. 25 years follow-up of patients after replacement of the aortic valve with a SmeloffCutter prosthesis. Thorac Cardiovasc Surg 1996;44:234 – 8. 5. Gometza B, Duran CM. Ball valve (Smeloff-Cutter) aortic valve replacement without anticoagulation. Ann Thorac Surg 1995;60:1312– 6. 6. Rao PS, Solymar L, Mardini MK, et al. Anticoagulant therapy in children with prosthetic valves. Ann Thorac Surg 1989;47: 589 –92. 7. Starr DS, Lawrie GM, Howell JF, et al. Clinical experience with the Smeloff-Cutter prosthesis: 1- to 12-year follow-up. Ann Thorac Surg 1980;30:448 –54. 8. Hsi DH, Ryan GF, Taft H, et al. A 29-year-old Harken disk mitral valve: long-term follow-up by echocardiographic and cineradiographic imaging. Tex Heart Inst J 2003;30:319 –21. © 2009 by The Society of Thoracic Surgeons Published by Elsevier Inc
Acute Profound Thrombocytopenia After Treatment With Tirofiban and Off-Pump Coronary Artery Bypass Grafting Andres Beiras-Fernandez, MD,* Anke Kowert, MD,* Pascale Jiru, MD, Marion Weis, MD, Michael Spannagl, MD, Bruno Reichart, MD, and Michael Schmoeckel, MD Departments of Cardiac Surgery, Anesthesiology, and Transfusion Medicine, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany
The glycoprotein IIb/IIIa (GP IIb/IIIa) receptor antagonists prevent platelet aggregation and thrombus formation, improving outcomes of patients with acute coronary syndrome. Therapy with these agents may lead to bleeding complications and thrombocytopenia, challenging the perioperative management of patients undergoing coronary surgery. We report the successful management of an acute profound thrombocytopenia after urgent off-pump coronary surgery in a patient treated with tirofiban for unstable angina and acute coronary syndrome. (Ann Thorac Surg 2009;87:629 –31) © 2009 by The Society of Thoracic Surgeons
G
PIIb/IIIa receptor antagonists prevent platelet aggregation and thrombus formation, improving outcomes after acute coronary syndrome [1]. However, they may lead to bleeding complications and thrombocytopenia [2], challenging the management of patients after coronary surgery.
A 63-year-old man patient presented with acute coronary syndrome (anterior ST-segment elevation depression; negative myocardial laboratory markers) after a 6-day period of unstable angina. Cardiac catheterization showed a two-vessel coronary disease involving the left main, the left anterior descending, and the left circumflex coronary arteries. The patient was scheduled for coronary artery bypass grafting and infusion with heparin (1,000 IU/h) and tirofiban (initial infusion of 0.4 mg/h for 30 minutes followed by 0.1 mg/h) was started. Initial laboratory results revealed no remarkable findings (Table 1). The baseline platelet count was 223 ⫻ 109/L. Treatment with tirofiban and heparin was continued until surgery, which occurred 8 hours later. At this time, the platelet count was 226 ⫻ 109/L. The patient underwent off-pump coronary artery bypass Accepted for publication June 10, 2008. *Both authors contributed equally to this work. Address correspondence to Dr Beiras-Fernandez, Department of Cardiac Surgery, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, 81377, Germany; e-mail: [email protected].
0003-4975/09/$36.00 doi:10.1016/j.athoracsur.2008.06.040
FEATURE ARTICLES
The Smeloff-Cutter valve was designed and has been demonstrated to have mild regurgitation [2]. This regurgitant flow prevents thrombus formation on the ball and cage of the prosthesis. Indeed, as compared with the Starr-Edwards ball-cage prosthesis (Edwards Laboratories), the Smeloff Cutter valve has a lower thromboembolism rate at 25 years (1.41% vs 2.01% per patient year) [3, 4]. Furthermore, Gometza and Duran [5] described a subset of young patients (n ⫽ 29) with an isolated Smeloff-Cutter aortic valve taking dipyridamole and aspirin, but no anticoagulants, at a thromboembolism rate of 0.9% per patient year in their series. Rao and colleagues [6] demonstrated a 2.5% per patient year thromboembolism rate in young patients taking dipyridamole and aspirin, but no anticoagulants. Several groups have published their long-term follow-up of patients with the Smeloff-Cutter aortic prosthesis. In the largest published experience of 358 patients, Starr and colleagues [7] demonstrated a 5.4%, 2.9%, and 2.6% per patient year thromboembolism rate in patients, respectively, taking no anticoagulation, antiplatelet agents, and warfarin. We believe that our patient has the oldest, functionally normal aortic mechanical valve described. Previously, a 29-year-old Harken disk mitral valve (Surgitools Inc, Woodvale, WA) has been described [8]. Although preoperative and intraoperative findings showed that in our patient the Smeloff-Cutter valve (Cutter Laboratories) was normal and functioning well, we decided to replace this 37-year-old valve because of the uncertainty of how much longer it would continue to function well.
630
CASE REPORT BEIRAS-FERNANDEZ ET AL DRUG-INDUCED THROMBOCYTOPENIA AFTER CORONARY SURGERY
Ann Thorac Surg 2009;87:629 –31
Table 1. Laboratory Values of the Patient After Tirofiban Infusion and Transfusion of Thrombocytes
A ⫽ angiography;
h ⫽ hours;
Hb ⫽ hemoglobin;
O ⫽ surgical procedure.
FEATURE ARTICLES
grafting by using the left internal thoracic artery to the left anterior descending artery and a single saphenous vein graft to the medial portion of the left circumflex artery. Anticoagulation was initially performed with 10,000 IU of unfractioned heparin and was carefully monitored with activated clotting time (⬎300 sec). Heparin was conventionally antagonized with protamine after the aortic anastomosis. However, the patient showed a severe diffuse bleeding. Intraoperative blood loss was 1,700 mL. Nine units of frozen fresh plasma, 1 unit of erythrocytes, and 1 unit of platelets were administered. The patient was transferred to the intensive care unit in stable condition with low pharmacologic support with norepinephrine (0.2 mg/h) and milrinone (0.4 mg/h). At admission, the platelet count was 77 ⫻ 109/L. The myocardial laboratory measurements were slightly increased, and the plasmatic coagulation laboratory findings were unremarkable (Table 1). Postoperative blood loss was less than 50 mL/h in the first 8 hours and less than 20 mL/h after that time. Six hours after intervention, the laboratory analyses showed a platelet count of 1 ⫻ 109/L. No clinical signs of bleeding were observed. Severe thrombocytopenia (1 ⫻ 109/L) was reconfirmed 30 minutes later, and pseudothrombocytopenia was excluded by using an alternate anticoagulant (citrate). Heparin-induced thrombocytopenia could be also excluded after negative enzyme-linked immunosorbent assay test for antibodies to platelet factor 4/heparin. The patient was transfused with 3 units of platelets with a rise in the platelet count from 1 ⫻ 109/L to 16 ⫻ 109/L after the first unit and 52 ⫻ 109/L after all of them. No thromboembolic or bleeding phenomena were observed. Six hours later (12 hours postoperatively) the platelet count was again severely reduced to 18 ⫻ 109/L, and a new transfusion of 2 thrombocyte units was necessary. The plasmatic coagulation laboratory values were not remarkable. Two hours later, the platelet count increased to 56 ⫻ 109/L and another thrombocyte unit was transfused. In the following 12 hours, the count of platelets increased slowly without transfusion and remained stable (Table 1). The patient
was discharged from the intensive care unit 4 days after surgery without thromboembolic or bleeding complications with a platelet count of 179 ⫻ 109/L.
Comment Different GPIIb/IIIa receptor inhibitors, abciximab, tirofiban, and eptifibatide, have been approved for clinical use in patients with acute coronary syndrome [3]. Abciximab has been reported to increase the incidence of thrombocytopenia in comparison with placebo, tirofiban, and eptifibatide [4]. In the RESTORE trial [5], severe thrombocytopenia (⬍ 50 ⫻ 109/L) was observed in 0.2% of the patients treated with tirofiban. Druginduced acute thrombocytopenia is defined as a decrease of the thrombocyte count to less than 20 ⫻ 109/L within 24 hours of exposure [6]. In our patient, the platelet counts were lower than 1 ⫻ 109/L at 6 hours after an exposure time of 14 hours. Differential diagnosis with other entities in patients receiving GPIIb/IIIa receptor inhibitors and heparin is mandatory. Pseudo-thrombocytopenia is defined as an artifactual miscalculation of platelets because of clumping platelets in blood samples anti-coagulated with ethylenediaminetetraacetic acid (EDTA). In our case, pseudothrombocytopenia could be excluded after repeated platelet counts in blood anti-coagulated with citrate. Heparin-induced thrombocytopenia could be excluded after a negative enzyme-linked immunosorbent assay test for antibodies to platelet factor 4/heparin. Furthermore, heparin-induced thrombocytopenia type I is associated with mild thrombocytopenia, and heparininduced thrombocytopenia type II typically occurs 4 to 10 days after starting a therapy with heparin. The profound thrombocytopenia observed in our patient was then most likely associated with tirofiban, considering the duration of the therapy (less than 24 h), the severity of the thrombocytopenia (1 ⫻ 109/L 6 hours after exposure), and the negative enzyme-linked immunosorbent assay heparin-induced thrombocytopenia test. However, the mechanism of GPIIb/IIIa recep-
tor antagonists associated with severe thrombocytopenia is not fully understood. One hypothesis suggests the induction of conformational changes in the thrombocyte receptors after therapy, which could react with pre-existing circulating antibodies [7]. Shanmugam and colleagues [8] reported that surgical revascularization could be safely performed in patients within a few hours of receiving tirofiban with little bleeding risk. However, acute profound thrombocytopenia after tirofiban can be life threatening in patients who will undergo coronary surgery, as it may increase the incidence of perioperative bleeding, thus potentially leading to reintervention. In our patient, acute thrombocytopenia presented 6 hours after offpump coronary artery bypass grafting, and increased thrombocyte substitution therapy was needed to obtain sufficient hemostasis. We believe that no data regarding acute profound thrombocytopenia after offpump coronary artery bypass grafting have been published. In our opinion, the thrombocyte count should be strictly monitored in patients presenting with an acute coronary syndrome needing coronary surgery, especially after administration of a GPIIb/IIIa receptor inhibitor. Furthermore, platelet’s transfusion should be considered if presentation of the thrombocytopenia occurs in the early postoperative period, to reduce the bleeding risk.
References 1. Boersma E, Harrington RA, Moliterno DJ, et al. Platelet glycoprotein IIb/IIIa inhibitors in acute coronary syndromes: a meta-analysis of all major randomised clinical trials. Lancet 2002;359:189 –98. 2. Demirkan B, Guray Y, Guray U, Korkmaz S. Differential diagnosis and management of acute profound thrombocytopenia by tirofiban: a case report. J Thromb Thrombolysis 2006;22:77– 8. 3. Karvouni E, Katritsis DG, Ioannidis JP. Intravenous glycoprotein IIb/IIIa receptor antagonists reduce mortality after percutaneous coronary interventions. J Am Coll Cardiol 2003; 41:26 –32. 4. Dasgupta H, Blankenship JC, Wood GC, Frey CM, Demko SL, Menapace FJ. Thrombocytopenia complicating treatment with intravenous glycoprotein IIb/IIIa receptor inhibitors: a pooled analysis. Am Heart J 2000;140:206 –1. 5. RESTORE Investigators. Effects of platelet glycoprotein IIb/ IIIa blockade with tirofiban on adverse cardiac events in patients with unstable angina or acute myocardial infarction undergoing coronary angioplasty. Randomized Efficacy Study of Tirofiban for Outcomes and REstenosis. Circulation 1997; 96:1445–53. 6. Berkowitz SD, Harrington RA, Rund MM, Tcheng JE. Acute profound thrombocytopenia after C7E3 Fab (abciximab) therapy. Circulation 1997;95:809 –13. 7. Bougie DW, Wilker PR, Wuitschick ED, et al. Acute thrombocytopenia after treatment with tirofiban or eptifibatide is associated with antibodies specific for ligand-occupied GPIIb/IIIa. Blood 2002;100:2071– 6. 8. Shanmugam G. Tirofiban and emergency coronary surgery. Eur J Cardiothorac Surg 2005;28:546 –50. © 2009 by The Society of Thoracic Surgeons Published by Elsevier Inc
CASE REPORT ATIK ET AL CATHETER ABLATION FOR POSTOPERATIVE ARRHYTHMIA
631
Recurrent Ventricular Arrhythmia After Coronary Artery Bypass Grafting Treated With Radiofrequency Catheter Ablation Fernando A. Atik, MD, Maria Fernanda M. Garcia, MD, Jose Mario Baggio, Jr, MD, Cristiano N. Faber, MD, Ricardo B. Corso, MD, Luiz Fernando Caneo, MD, and Alvaro V. Sarabanda, MD Departments of Cardiovascular Surgery, Cardiology, and Clinical Arrhythmia and Pacemaker Unit, Heart Institute of Federal District, Zerbini Foundation, Brasilia, Brazil
A 63-year-old diabetic woman was emergently submitted to coronary artery bypass grafting in the setting of acute myocardial infarction. Recurrent, drug-refractory episodes of ventricular arrhythmia occurred for 2 weeks postoperatively, despite no documentation of ongoing myocardial ischemia and optimum medical treatment. Ventricular arrhythmia was initiated by premature ventricular contractions originating from the Purkinje system within the infarct border zone. Radiofrequency catheter ablation was performed at sites where Purkinje potentials were recorded, leading to arrhythmia cessation. A week later, an implantable cardioverter defibrillator was inserted and she was discharged home a few days later. At 15-month follow-up, there were no further episodes of arrhythmia and ventricular function had improved. (Ann Thorac Surg 2009;87:631–3) © 2009 by The Society of Thoracic Surgeons
R
ecurrent, drug-refractory, new onset ventricular tachycardia (VT) and ventricular fibrillation (VF) after coronary artery bypass grafting (CABG) is uncommon, but may be associated with increased morbidity and mortality. The most likely mechanism is residual myocardial ischemia that usually relates to suboptimal anastomosis or incomplete revascularization. However, other factors may be implicated [1], including inadequate myocardial protection, myocardial reperfusion, metabolic imbalance, and anti-arrhythmic drug pro-arrhythmia. We herein report a patient who had drug-refractory, recurrent VT/VF early after CABG, and we discuss the possible mechanisms and the successful use of radiofrequency catheter ablation. A 63-year-old diabetic woman was admitted in the emergency room with a 3-hour history of sudden onset chest discomfort irradiated to the left arm and the back. On physical examination, she was found hemodynamically unstable, with early signs of pulmonary edema. Admis-
Accepted for publication June 19, 2008. Address correspondence to Dr Atik, Heart Institute of Federal District, Zerbini Foundation, Estrada Parque Contorno do Bosque s/n, 1 Andar, Sala 13, Brasília-DF, 70658-700, Brazil; e-mail: [email protected]. org.br.
0003-4975/09/$36.00 doi:10.1016/j.athoracsur.2008.06.065
FEATURE ARTICLES
Ann Thorac Surg 2009;87:631–3