Anticoagulation with Bivalirudin during Deep Hypothermic Circulatory Arrest in a Patient with Heparin-Induced Thrombocytopenia

Abstract

Heparin-induced thrombocytopenia is a well-recognized complication of anticoagulation with heparin. We present the case of a patient with recent heparin-induced thrombocy1 Unfractionated heparin (UFH) currently remains the gold standard for anticoagulation in cardiopulmonary bypass (CPB) because of its low cost, safety profile, ease of dosing, and effective reversibility with protamine. Nevertheless, it is estimated that about 17% of patients on UFH will develop an immune response through the generation of immunoglobulin-G (IgG) antibodies against the complex of heparin with platelet factor 4, which results in type II HIT in 1% to 3% of those patients. 2 The consequent immune complex induces platelet activation and consumption, causing a drastic fall in platelet count, arterial or venous thrombosis (or both), and eventual bleeding. 2,3 Patients with an established diagnosis of HIT-for whom surgery that necessitates anticoagulation is planned-should therefore be administered an alternative drug.2 As a result of both blood stasis and alterations in enzymatic activity upon extreme temperature changes, deep hypothermic circulatory arrest (DHCA) further complicates the issues of anticoagulation, and increases the need for an alternative non-heparin-based anticoagulant. An alternative drug in such an instance is the bivalent, direct thrombin inhibitor bivalirudin, which achieves anticoagulation during CPB and DHCA. 4 We report a case of type II HIT in a patient undergoing emergency surgery for an acute type A aortic dissection, requiring CPB and DHCA, in whom we successfully used bivalirudin as an anticoagulant. Case ReportAn 82-year-old man presented with chest pain and an inferior ST-elevation myocardial infarction. A computed tomographic (CT) angiogram also revealed a Stanford type A aortic dissection with a 6-cm ascending aortic aneurysm extending to the aortic arch and a large pericardial effusion with radiographic signs of tamponade. The patient also had severe aortic valve regurgitation, with a left ventricular ejection fraction of 0.62.Heparin had been initiated for atrial fibrillation at another hospital, before acute aortic dissection was diagnosed. The patient developed HIT, which was confirmed via enzyme-linked immunosorbent assay for the presence of antibodies against heparin and platelet factor 4 complex. Heparin was subsequently discontinued.The patient was taken to the operating room for repair of type A aortic dissection. Bivalirudin, a direct thrombin inhibitor, was used to achieve adequate anticoagulation

Cangrelor and Heparin for Pulmonary Thromboendarterectomy in Heparin-Induced Thrombocytopenia

“…Heparin has been considered the gold standard anticoagulant for CPB because of its short duration of action, easy reversibility, and simple point-ofcare monitoring. 1 However, in the setting of seropositive HIT, the use of heparin is contraindicated because of the high risk of intravascular thrombosis.…”