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Ann Thorac Surg 2002;74:2177-2179
© 2002 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, Harper University Hospital, Wayne State University, Detroit, Michigan, USA
b Department of Pharmacy, Harper University Hospital, Wayne State University, Detroit, Michigan, USA
c Department of Cardiology, Harper University Hospital, Wayne State University, Detroit, Michigan, USA
Accepted for publication July 10, 2002.
* Address reprint requests to Dr Baciewicz, Department of Cardiothoracic Surgery, Harper University Hospital, 3990 John R, Suite 2101, Detroit, MI 48201, USA.
e-mail: fbaciewi{at}dmc.org
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A 46-year-old man with infective endocarditis was transferred to Harper University Hospital on November 12, 2001. He was initially admitted elsewhere with fever and left leg cellulitis. His past medical history included intravenous drug use, hepatitis B and C, and deep venous thrombosis in the lower extremities, for which a Greenfield filter had been placed. A duplex study of the legs was negative for deep venous thrombosis; however, enoxaparin (1 mg/kg every 12 hours) was started on October 22, 2001. A heart murmur was auscultated, and a transthoracic echocardiogram showed mitral regurgitation with probable vegetation. Blood cultures were initially positive for Enterococcus faecalis (October 22, 2001), and he was started on ampicillin and gentamicin. His condition improved transiently, but he again developed chills and fever, and blood cultures were now positive for Enterobacter cloacae (November 11, 2001). Trimethoprim/sulfamethoxazole was added to his antibiotic regimen. His clinical condition deteriorated, and a repeat transthoracic echocardiogram (November 13, 2001) showed severe mitral regurgitation with a small mobile mass on the atrial surface of the posterior leaflet. His ejection fraction was 65%. A cardiac catheterization (November 14, 2001) showed normal coronary arteries. Moderate respiratory distress was evident, associated with pulmonary congestion caused by mitral regurgitation. He also developed progressive thrombocytopenia, 60,000/mm3 from a baseline of 250,000/mm3. Because he had received enoxaparin at the outside hospital for 2 weeks, HIT type II was suspected as the probable cause of his thrombocytopenia. A test for heparin-dependent antibodies (PF4 enzyme-linked immunosorbent assay) was sent, but the result, which was negative, became available after the operation. Because of a strong clinical suspicion of HIT type II at the time of the operation, we decided to discontinue heparin from all sources and use bivalirudin (Angiomax, The Medicines Company, Cambridge, MA) as the anticoagulant during CPB. The extracorporeal circuit consisted of a roller pump, a Capiox SX oxygenator (Terumo Cardiovascular Systems, Ann Arbor, MI), and a hard plastic reservoir. No heparin was used. The pump priming solution consisted of 2000 mL of plasmalyte and 50 mEq of bicarbonate. Blood cardioplegia was given in a retrograde and antegrade manner. A mitral valve replacement was performed (November 16, 2001) using a 27-mm Carpentier-Edwards porcine valve. The native mitral valve had a 2-cm vegetation and a 2-cm defect in the posterior leaflet. Bivalirudin was administered intravenously as a 1.25 mg/kg bolus, followed by an initial continuous infusion at 2.75 mg · kg-1 · h-1. No bivalirudin was added to the pump priming solution. The activated clotting time (ACT) was measured every 15 to 30 minutes. As shown in Figure 1, additional boluses were given as needed, and the infusion rate was adjusted to obtain an ACT of 500 to 600 seconds. The initial ACT, before administration of the drug, was 180 seconds. The last intraoperative ACT was 280 seconds, 70 minutes after discontinuation of the medication. The CPB time was 118 minutes, and the aortic cross-clamp time was 85 minutes. Two units of packed red blood cells were given after discontinuation of CPB, and two more were given postoperatively. He had an uneventful recovery. The chest tube output was 250 mL for the first 4 postoperative hours, with a total of 950 mL for the first 24 hours. These drains were removed on postoperative day 3. He completed a 6-week course of intravenous antibiotics, and was doing well in a follow-up visit 3 months after the operation.
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Alternative agents are available for anticoagulation during CPB in patients with HIT type II. They include Iloprost, a stable prostacyclin analog, which has the disadvantage of causing severe hypotension that often requires coadministration of vasopressor support [1]. Another option is the preoperative use of Ancrod, a defibrinogenating agent derived from the Malayan pit viper, which is considered a less favorable alternative because of the lack of an effective neutralizing agent and the need to decrease the patient’s plasma fibrinogen to 500 mg/L before initiating CPB, which often requires more than 12 hours [4]. Another strategy is the use of danaparoid sodium, an effective anticoagulant, but associated with larger postoperative blood loss when compared with heparin, probably as a result of its prolonged anti-Xa activity (25 hours) and the lack of a specific antidote. Also, it has a possible cross-reaction with heparin in up to 10% of patients with HIT type II [4]. Finally, we have now available the direct thrombin inhibitors, which include recombinant hirudin (lepirudin), argatroban, and bivalirudin (Angiomax) [1, 3]. These compounds do not have cross-reactivity with heparin antibodies [1, 3]. The disadvantages of their use include lack of an antidote, limited experience compared with heparin, and cost [1, 3, 4]. Among the direct thrombin inhibitors, lepirudin has been the most frequently used during cardiac procedures. Unfortunately, it lacks an easy and standardized monitoring of anticoagulant activity during CPB [4]. Its relatively long half-life (80 minutes) can increase the risk of postoperative bleeding. Argatroban (Novastan [Mitsubishi Tokyo Chemical Corp, Tokyo, Japan]) has recently been used with success during CPB in Japan [5], but it is not available for use in the United States. It has a short half-life (30 minutes) and can be effectively followed with measurement of ACT during CPB.
We decided to use bivalirudin during CPB because of its short half-life (25 minutes) and the ability to monitor its activity by measurement of ACT. The prothrombin time, activated partial thromboplastin time, thrombin time, and ACT all rise linearly with an increase in bivalirudin dose. Bivalirudin is cleared by a combination of renal elimination and intravascular proteolysis, with renal elimination thought to be the major route of clearance [3]. In patients with normal renal function, the plasma half-life is 25 minutes, whereas in hemodialysis patients it is 3.5 hours [3]. It is approved by the US Food and Drug Administration for anticoagulation during coronary angioplasty for unstable angina, with an initial intravenous bolus of 1 mg/kg, followed by an infusion of 2.5 mg · kg-1 · h-1. This results in ACT values averaging 350 seconds during the continuous infusion, with 100% of patients achieving ACT values more than 300 seconds [3]. If the continuous infusion is given for only 4 hours, coagulation function returns to baseline 1 hour after the drug is discontinued [3]. Using this regimen during coronary angioplasty for unstable angina, bivalirudin has reduced ischemic complications and bleeding when compared with unfractionated high-dose heparin infusion [2]. As seen in Figure 1,, we adjusted the dose of bivalirudin during CPB to keep the ACT between 500 and 600 seconds, using intravenous boluses in addition to the continuous infusion. The cost of bivalirudin is $325 for a 250-mg vial [3], and the total drug cost for this case was approximately $2,000. We did not encounter any clot formation in the CPB circuit during the operation, and the postoperative bleeding was acceptable as reflected by the chest tube output. We conclude that bivalirudin is a safe alternative to heparin for anticoagulation during CPB in cardiac operations.
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= bivalirudin boluses; ——— = bivalirudin infusion rate; —
— = ACT values. (CPB = cardiopulmonary bypass.)