Department of Anesthesia at UF

Bivalirudin as an Alternative Anticoagulant in Attempted Repair of an Ascending Aortic Pseudoaneurysm for a Patient with Heparin Antibody

Sinan Yavas, MD and Yong G Peng, M.D., Ph.D.
Department of Anesthesiology, University of Florida, Gainesville, Florida

Alternative anticoagulation agents are currently under investigation for patients with heparin induced thrombocytopenia (HIT) requiring open heart surgery. One such agent is bivalirudin, a semisynthetic bivalent analog of hirudin. It acts through a transient and reversible direct inhibition of thrombin. The duration of effect for bivalirudin is about two hours and it is excreted through the kidney. There is no direct antidote for bivalirudin. We report a case in which bivalirudin was used in an attempted repair of an ascending aortic pseudoaneurysm in a patient with positive heparin antibody.

The patient was a 67-year-old male, who had undergone surgical repair of a type I aortic dissection one year prior to the current admission. His postoperative course was complicated by cardicac tamponade requiring reoperation and multiple chest explorations due to the surgical complications in the ensuing months. Subsequent to his second surgery he developed HIT. Ten months after the initial surgery, the patient again presented with bleeding from his anterior chest wall. A CT scan revealed a large ascending aortic pseudoaneurysm with an aortocutaneous fistula at the mid-sternal level. The repeated test for heparin antibody was positive. He was transferred to our institution for definitive repair.

On the day of surgery, the baseline celite-activated coagulation time (ACT) was 160 s. Following uneventful anesthetic induction, a complete TEE examination revealed a left ventricular ejection fraction of 50% with moderate to severe aortic valve insufficiency. There was no evidence of wall motion abnormalities. Because of HIT, anticoagulation was established with a bolus (1 mg/kg) of bivalirudin followed an infusion of 2.5 mg/kg/hr. Prior to sternotomy, femoro-femoral cardiopulmonary bypass was established after the ACT exceeded 480 s. A complete aortic root replacement was performed under deep hypothermic circulatory arrest with technical difficulties due to adhesions. The bivalirudin infusion was reduced and eventually stopped because of a prolonging ACT. Blood-ultrafiltration was performed prior to weaning from cardiopulmonary bypass (CPB) in attempt to reduce bivalirudin concentrations. The initial separation from CPB appeared to be hemodynamically stable. However, the patient developed a severe coagulopathy that remained refractory to transfusion of massive amounts of blood products and activated factor VII. Surgical hemostasis was also incomplete with bleeding from defects at the base of the left ventricle and the ascending aorta. Although the patient’s ACT never decreased below 400 s, the surgeon decided to not go back to CPB for the further repair. The patient deteriorated despite ongoing therapy, with severe right ventricular distention from elevated pulmonary vascular resistance, and ultimately expired in the operating room.

The effectiveness of bivalirudin as a replacement for heparin in patients undergoing coronary artery bypass grafting has been well described, however minimal information is available regarding the use of bivalirudin in cases involving hypothermic circulatory arrest. Our case illustrates that alternative anticoagulants for patients with HIT may exacerbate the derangement of coagulation caused by hypothermic circulatory arrest.