Asian Cardiovasc Thorac Ann 2007;15:246-248
© 2007 Asia Publishing EXchange Ltd
Lupus Anticoagulant and Off-pump Coronary Bypass: Dilemma of Anticoagulation
Madan M Maddali, MD,
Maher J Albahrani, FCCP
Department of Anesthesia, Royal Hospital, Muscat, Sultanate of Oman
For reprint information contact: Madan M Maddali, MD Tel: 968 697 133 Fax: 968 697 133 Email: madan{at}omantel.net.om, Department of Anesthesia, Royal Hospital, PB No: 1331, PC: 111, Seeb, Muscat, Sultanate of Oman.
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ABSTRACT
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Confronted with a persistently elevated activated partial thromboplastin time due to circulating lupus anticoagulant in a patient undergoing emergency off-pump coronary artery bypass surgery, the dilemma of providing adequate anticoagulation for a short cardiac surgical procedure is highlighted.
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INTRODUCTION
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Antiphospholipid antibody syndrome is characterized by the presence of antiphospholipid antibodies including lupus anticoagulant (LA) and anticardiolipin antibody in the blood, hypercoagulability, and prolonged phospholipid-dependent coagulation indices such as activated partial thromboplastin time (aPTT) and activated clotting time (ACT). Systemic lupus erythematosus, drugs, and sepsis syndrome can lead to circulating LA in the blood.1,2 Antiphospholipid syndrome may occur de novo (primary antiphospholipid syndrome), or it may be associated with systemic lupus erythematosus, rheumatic disease, or other autoimmune diseases. This report highlights the dilemma of adequate anticoagulation during cardiac surgery where ACT values may be unreliable due to circulating LA, and direct measurement of heparin concentration by heparin assay takes longer than the duration of the surgical procedure itself.
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CASE REPORT
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A 40-year-old man weighing 75 kg with unstable angina was scheduled for single-vessel off-pump coronary artery bypass (OPCAB) surgery. Angiography showed that his proximal left anterior descending artery was totally blocked at the site of a stent that had been deployed 3 months previously. His ejection fraction was 60%. Following angiography, he became hemodynamically unstable and emergency revascularization was required. He had no history of thromboembolism other than the rapid occlusion of the stent. He had no arthralgia, myopathy, livedo reticularis, cardiac valve vegetations, signs of rheumatic illness, or cognitive dysfunction. He was normotensive and non-diabetic. His preoperative hemoglobin, white blood cell and platelet counts, and renal and hepatic function were normal. Routine coagulation screening prior to cardiac catheterization showed all values within normal ranges except for aPTT (Table 1
). The aPTT was repeated immediately because of suspected sample contamination, and found to be 72.4 sec. This raised the suspicion of circulating LA, and laboratory investigations to identify this were requested.
The antiphospholipid syndrome/lupus screen showed prolongation of PTT (lupus sensitive) of 63.8 sec (normal < 48 sec), corrected PTT (lupus sensitive) of 56.1 sec (normal < 45 sec), and diluted Russell viper venom time of 32.6 sec (normal < 30 sec). The values for ß2 glycoprotein-1-dependent IgG and IgM anticardiolipin antibodies were normal. The prolonged values of aPTT and aPTT serum indicated the presence of LA. As circulating antiphospholipid antibodies may interfere with ACT values, resulting in spurious results and leading to under heparinization, we proposed that if the patient had adequate antithrombin III (AT III) values, adequate anticoagulation could be maintained with intravenous unfractionated heparin at the dose usually administered in our institute for OPCAB procedures. In addition, antiphospholipid antibody syndrome might be associated with AT III deficiency. Hence a functional AT III assay was performed and found to be normal (85 µg·dL–1, normal range: 80 to 120 µg·dL–1).
After induction of anesthesia, celite-activated clotting time (Hemochron model 401; International Technidyne Corporation, Edison, NJ, USA) and blood heparin concentrations were measured at regular intervals (Table 2). As the AT III levels were normal, we anticoagulated the patient with 100 units·kg–1 of unfractionated heparin after the left internal mammary artery was harvested and prior to division of the distal end of the internal mammary artery. Normothermia was maintained throughout the procedure. Stable hemodynamics were maintained mainly with volume supplementation. Heparin was reversed with protamine in a 1:1 ratio after completion of the coronary anastomosis. The coagulation screen at 6 and 18 hours postoperatively was normal, except for aPTT (Table 1
). The crosslinked fibrin D-dimer level was elevated postoperatively (Table 2). Cardiac enzymes, troponin T, myoglobin, and electrocardiographic recordings at regular intervals postoperatively were within normal limits. There were no signs of abnormal bleeding or thromboembolism, and the patient was discharged home on an oral anticoagulant on the 7th postoperative day.
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DISCUSSION
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The hallmark of lupus anticoagulant is prolongation of the activated partial thromboplastin time. Our patient exhibited no systemic manifestation of lupus erythematosus, rheumatic, or other autoimmune diseases and probably had a primary antiphospholipid syndrome. Circulating LA interferes with ACT values, and it is a challenge for the cardiac surgical team to monitor safe anticoagulation during surgical procedures. Management of anticoagulation during cardiopulmonary bypass for coronary bypass surgery and double-valve replacement in patients with circulating antiphospholipid antibodies has been documented.1,3,4 However, we did not come across any reference to anticoagulation for OPCAB surgery in such patients. We were faced with the problem of having to ensure adequate heparinization for a short duration of surgery when heparin assay, which has to be performed in the laboratory, takes longer than the duration of the surgical procedure.
Heparinization during OPCAB helps to maintain internal mammary artery patency after division of the distal end, and inhibits intravascular thrombin generation during coronary artery anastomosis. This also provides anticoagulation backup in case of urgent conversion to on-pump surgery. There are divergent opinions regarding the appropriate dose of heparin for OPCAB, ranging from full heparinization to more modest doses. It is generally held that an ACT > 300 sec is adequate.5 Our protocol specified 100 units·kg–1 that resulted in an ACT > 300 sec. We presumed that as regular heparin acts through AT III, the normal AT III level in our patient would ensure adequate anticoagulation. If we could not have achieved an ACT > 300 sec, we would probably have repeated the bolus of heparin. If the AT III level had been low, we would have considered ways to improve it, either by infusion of AT III concentrate or fresh frozen plasma. The other option would have been to use another thrombin inhibitor such as lepirudin, argatroban, hirulog, or desirudin, which were either not available or did not suit our immediate need.
Plasma tissue-type plasminogen activator and fibrin D-dimer levels are higher in LA-positive patients who are prone to thrombosis.6 We are unsure if the elevated postoperative fibrin D-dimer values in this case indicated a tendency for thrombosis. The postoperative cardiac enzymes and electrocardiogram showed no signs of ischemia. However, anticoagulation was initiated with heparin at 6 hours postoperatively and was overlapped with warfarin on the 3rd postoperative day. Subsequently, heparin was withdrawn on the 6th day and the patient was discharged home on warfarin.
It is important for clinicians to be aware that circulating LA may prolong aPTT. We suggest that if AT III levels are normal in such patients, the anesthesiologists should follow the usual heparinization protocols to achieve safe anticoagulation levels. However, in prolonged surgery, intra- and postoperative heparin assays may be needed to monitor anticoagulation and reversal. It may be necessary to commence anticoagulation early in the postoperative period to prevent thromboembolic episodes. Monitoring fibrin D-dimer levels may aid in the detection of subclinical thrombosis.
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REFERENCES
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- Metzdorff MT, Hanses KS, Wright GL, Fried SJ. Interference with anticoagulation monitoring by procainamide-induced lupus anticoagulant. Ann Thorac Surg 1996;61:994–5.[Abstract/Free Full Text]
- Wenzel C, Stoiser B, Locker GJ, Laczika K, Quehenberger P, Kapiotis S, et al. Frequent development of lupus anticoagulants in critically ill patients treated under intensive care conditions. Crit Care Med 2002;30:763–70.[Medline]
- Ducart AR, Collard EL, Osselaer JC, Broka SM, Eucher PM, Joucken KL. Management of anticoagulation during cardiopulmonary bypass in a patient with a circulating lupus anticoagulant. J Cardiothorac Vasc Anesth 1997;11:878–9.[Medline]
- Myers GJ, Hirsch GM. Double valve replacement in a patient with anticardiolipin antibody syndrome. Perfusion 1999;14:397–401.[Abstract/Free Full Text]
- Raja SG, Dreyfus GD. Off-pump coronary artery bypass surgery: to do or not to do? Current best available evidence. J Cardiothorac Vasc Anesth 2004;18:486–505.[Medline]
- Sakakura M, Wada H, Watanabe R, Mamamuro M, Okugawa Y, Nakasaki T, et al. Coagulation tests and anti-phospholipid antibodies in patients positive for lupus anticoagulant. Clin Appl Thromb Hemost 2000;6:144–50.[Abstract/Free Full Text]
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ABSTRACT
INTRODUCTION
