Ann Thorac Surg 1996;62:280-283
© 1996 The Society of Thoracic Surgeons
Case Report
Intracoronary Thrombolysis in the Treatment of Graft Closure Immediately After CABG
Harold L. Dauerman, MD,
Donald E. Cutlip, MD,
Frank W. Sellke, MD
Cardiovascular Division, Department of Medicine, and Division of Cardiothoracic Surgery, Department of Surgery, Beth Israel Hospital and Harvard Medical School, Boston, Massachusetts
Accepted for publication January 30, 1996.
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Abstract
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A patient with a hypercoagulable state underwent coronary artery bypass grafting and was recovering uneventfully until diffuse electrocardiographic changes and cardiogenic shock developed within hours of the operation. Because of severe hemodynamic compromise on high-dose inotropic drugs and intraaortic balloon pump support, she was taken to the catheterization laboratory, where the patient was discovered to have thrombotic occlusion of all grafts, including the left internal mammary artery to the left anterior descending artery. Multiple graft percutaneous transluminal coronary angioplasty and thrombolysis with urokinase successfully opened the grafts, without bleeding complication. Anastomoses were all free of significant anatomic lesion. She has remained free of cardiac symptoms for 3.5 years after operation.
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Introduction
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It is generally thought that early thrombosis leading to graft occlusion after coronary artery bypass grafting (CABG) is due to technical factors related to the operation or to extremely poor graft run-off. However, angiographic studies examining the effects of platelet inhibitors have also shown early thrombosis to be related to graft endothelial injury, which may occur during graft procurement or due to the sudden exposure to the high-pressure pulsatile arterial system [1]. The risk of early thrombosis after cardiovascular operations is of major clinical significance in the setting of a hypercoagulable state, such as the presence of antiphospholipid antibodies [2]. Isolated venous graft failure is often not detected or of limited clinical significance, at least in the short term. Before the expanded use of percutaneous transluminal coronary angioplasty (PTCA), the treatment for clinically significant early graft closure was reoperation [3]. However, early reoperation is associated with a higher mortality and less likelihood of long-term relief of angina than the initial CABG [4]. If the patient does experience hemodynamic instability or anginal symptoms, percutaneous angioplasty of the occluded graft or native coronary circulation may offer relief without the need for immediate repeat CABG. This alternative revascularization strategy has been suggested by prior reports showing the efficacy of PTCA in patients with recurrent ischemia 2 to 90 days after CABG [5–7]. We report the use of both PTCA and intracoronary thrombolysis in a hypercoaguable patient with a complicated myocardial infarction and severe hemodynamic instability occuring immediately after CABG due to acute multiple graft thromboses.
Unstable angina developed in a 56-year-old woman after an aborted anterior myocardial infarction treated with intravenous streptokinase. Her past medical history was unremarkable except for a chronically elevated partial thromboplastin time secondary to a factor XII deficiency. She had no clinical history of coagulopathy. Physical examination was normal except for a grade 2/6 systolic murmur at the left sternal border. Laboratory examination showed prothrombin time was 9.9 seconds (control of 10.1 seconds), partial thromboplastin time greater than 150 seconds, platelet count of 156/µL, antinuclear antibody titer of 1:320, factor XII level less than 1%, and anticardiolipin (antiphospholipid) immunoglobulin G level of 21.2 g/L. The electrocardiogram showed normal sinus rhythm with 0.5-mm ST segment elevation and T-wave inversion in V1 through V3. Right and left heart catheterization revealed (1) normal left ventricular systolic function, mild biventricular diastolic dysfunction, and mild to moderate mitral regurgitation, and (2) severe native three-vessel coronary artery disease with high-grade stenoses of the mid-right coronary artery, first obtuse marginal branch, and distal left anterior descending artery.
The patient was referred for surgical revascularization. The activated clotting time was 349 seconds before cardiopulmonary bypass and 999 seconds after 340 mg of heparin was given before initiation of cardiopulmonary bypass. Separate saphenous vein bypass grafts were placed to the posterior descending artery and first obtuse marginal branch, and a left internal mammary artery graft was anastamosed to the distal left anterior descending artery without technical problem. She had 1-mm ST segment elevations anteriorly at the completion of the operation before transfer, but remained hemodynamically stable without change in pulmonary pressure or cardiac output.
Within 1 hour after arriving in the intensive care unit, the patient suffered multiple cardiac arrests with ventricular fibrillation and diffuse 5-mm ST segment elevations. An intraaortic balloon pump was placed via the femoral artery and the patient was given 5,000 units of intravenous heparin. The patient remained in cardiogenic shock (cardiac output, 2.3 L/min; central venous pressure, 21 mm Hg) on maximal inotropic support and intraaortic balloon pump augmentation. Coronary angiography showed thrombotic occlusion of the distal anastamoses of both saphenous vein bypass grafts (Fig 1
) and the left internal mammary artery graft. Discussion was made whether to return to the operating room or to attempt intracoronary thrombolysis. Because the patient was in severe hemodynamic compromise and had a thrombotic tendency, we elected to proceed with intracoronary thrombolysis. Initially a guidewire could not be passed across the distal occlusions and 50,000 to 100,000 unit injections of urokinase were given into each graft rapidly. This allowed passage of the guidewire, and the distal anastomoses were subsequently dilated with multiple 2.0-mm ACX (Advanced Cardiovascular Systems, Inc, Temecula, CA) balloon inflations. No anatomic lesion was noted in any of the bypass grafts. Additional 50,000 to 100,000 unit injections of urokinase were given into each graft to resolve residual thrombus, and Thrombolysis in Myocardial Infarction grade III flow was restored. A total of 550,000 units of urokinase was administered, and the total time until restoration of Thrombolysis in Myocardial Infarction grade III flow was 80 minutes after initial angiography. A greater dose of urokinase and prolonged infusion of urokinase were not given due to concerns about postthrombolytic bleeding. The patient did not bleed from the incisions or cutaneous puncture sites, or through the mediastinal drainage tubes.
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Fig 1. . Coronary angoiogram demonstrating thrombosed saphenous vein graft to circumflex artery (A). After the injection of 100,000 units of urokinase, the graft became patent. Percutaneous transluminal coronary angioplasty of the residual thrombus improved flow. Thrombolysis in Myocardial Infarction grade III flow was restored shortly after the injection of another 50,000 units of urokinase (B).
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The patient experienced no further cardiac events and was weaned from intraaortic balloon support at postoperative day 10. Creatine kinase level rose to a maximum of 2,592 units (14% MB) and new anterior Q waves developed. Repeat coronary angiography 3 days after the procedure showed all grafts including the left internal mammary artery to be patent without anatomic obstruction. Ejection fraction was 0.15 at that time, which improved to 25% on postoperative day 7. The patient was anticoagulated with heparin and later warfarin to prevent recurrent thromboses, but had no bleeding complication. Despite a prolonged ventilator wean and tracheostomy on postoperative day 21, the patient was discharged to home on postoperative day 32. At 3.5-year follow-up she has had no further cardiac events on warfarin anticoagulation, is in New York Heart Association class I, and is free of angina.
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Comment
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Graft occlusion within 30 days of a bypass operation occurs in 22% of patients given placebo, compared with 6% of patients given platelet inhibitors perioperatively [1]. Although technical factors have been considered to be the initiating cause of early graft closure, endothelial damage may be a major contributing factor. Platelet deposition begins as soon as the blood begins to flow through the graft, and thromboses may form frequently. Inhibitors of platelet aggregation may prevent the initiation or propagation of thrombus and thus may improve short- and long-term graft patency [1, 8, 9]. It is probable that in the present case a prothrombotic tendency due to either an antiphospholipid antibody, factor XII deficiency, or other unidentified factor contributed to the early thrombotic graft occlusions, because the operation was unremarkable technically and all grafts thrombosed soon after the operation and simultaneously. This patient had multiple risks for early graft thrombosis given her factor XII deficiency and antiphospholipid antibodies and may have benefited from aggressive preoperative antiplatelet treatment. It is uncertain if this would have prevented the occlusions in this patient, but it needs to be considered when operating on hypercoagulable patients. Severe factor XII deficiency has been reported to induce venous thromboses [10]. The risk of arterial thrombosis after cardiovascular surgery is clinically significant in the setting of antiphospholipid antibodies [11]. In a recent retrospective review of these patients undergoing cardiovascular operations, 84% suffered major postoperative complications and 63% died of complications of the operation [2]. There are currently few specific recommendations concerning the best perioperative management of these high-risk patients. We report the use of thrombolytics and thrombus angioplasty to treat the hyperacute thromboses of grafts in the first hour after a technically unremarkable bypass operation.
Intracoronary thrombolytics can be used to effectively treat graft thromboses in conjunction with PTCA [9]. There is justified hesitancy to use angioplasty in the immediate postoperative period because of concerns of disrupting fresh anastomoses. However, successful PTCA has been performed as early as 24 hours after a bypass operation [5]. There is even more caution in the use of intracoronary thrombolytics in the immediate postoperative period due to concerns of bleeding.
In the present case, anatomic lesions were not present in the grafts, suggesting that clinical improvement after a further operation would have been unlikely. Furthermore, the prothrombotic state would not have been addressed with a further operation, and repeat thrombosis would have been probable. Although we can not recommend the routine use of intracoronary thrombolysis in the immediate postoperative period, it may be a reasonable option when repeat CABG has a high risk of mortality and PTCA alone will not restore patency of the grafts.
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Footnotes
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Address reprint requests to Dr Sellke, Division of Cardiothoracic Surgery, Dana 905, Beth Israel Hospital, 330 Brookline Ave, Boston, MA 02215.
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References
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- Fuster V, Chesebro J. Role of platelets and platelet inhibitors in aortocoronary artery vein-graft disease. Circulation 1986;73:227–32.
- Ciocca RG, Choi J, Graham AM. Antiphospholipid antibodies lead to increased risk in cardiovascular surgery. Am J Surg 1995;170:198–200.
- De Feyter PJ, van Suylen R, deJaegere PPT, Topol EJ, Serruys PW. Balloon angioplasty for the treatment of lesions in saphenous vein bypass grafts. J Am Coll Cardiol 1993;21:1539–49.
- Cameron A, Kemp HG Jr, Green GE. Reoperation for coronary artery disease. Circulation 1988;78(Suppl 1):158–62.
- Schieman G, Cohen BM, Buchbinder M. Standby percutaneous transluminal coronary angioplasty for coronary artery bypass surgery. Cathet Cardiovasc Diagn 1990;21:159–61.
- Dorogy ME, Highfill WT, Davis RC. Use of angioplasty in the management of complicated perioperative infarction following bypass surgery. Cathet Cardiovasc Diagn 1993;29: 279–82.
- Kahn JK, Rutherford BD, McConahay DR, et al. Early postoperative balloon coronary angioplasty for failed coronary artery bypass grafting. Am J Cardiol 1990;66:943–6.
- Josa M, Lie JT, Bianco RL, Kaye MP. Reduction of thrombosis in canine coronary bypass vein grafts with dipyridamole and aspirin. Am J Cardiol 1981;47:1248–54.
- Van der Werf F, Vanhaecke J, de Geest H, Verstaette M, Collen D. Coronary thrombolysis with recombinant single chain urokinase-type plasminigen activator in patients with acute myocadial infarction. Circulation 1986;74:1066–70.
- Lammle B, Wiullemin WA, Huber I, et al. Thromboembolism and bleeding tendency in congential factor XII deficiency. Thromb Haemost 1991;65:117–21.
- Taylor LM, Chitwood RW, Dalman RL, Sexton G, Goodnight SH, Porter JM. Antiphospholipid antibodies in vascular surgery patients. Ann Surg 1994;220:544–51.
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Abstract
Introduction
