Early graft thrombosis due to antithrombin III deficiency following CABG

The serine protease inhibitor antithrombin III (AT-III), an α2-globulin synthesized in the liver and endothelial cells, is the principal in vivo inhibitor of blood coagulation inactivating mainly thrombin. AT-III deficiency presents a rare hereditary or acquired disorder that most often comes to light when a patient suffers recurrent venous thrombosis and pulmonary embolism. Triggers for the onset of the thrombosis include various mechanisms such as pregnancy, delivery, surgery, trauma, and contraceptive pill use. Decreased response to heparin may be the first sign of AT-III deficiency. Since heparin is a conditio sine qua non for cardiopulmonary bypass, rapid consumption of AT-III promoted by heparin may lead to systemic thrombosis. The effect of heparin on graft patency after CABG in patients with AT-III deficiency, particularly with respect to early graft thrombosis, has not been fully investigated. The early detection and timely treatment of this disorder may impact perioperative morbidity. We present a case of simultaneous thrombosis of three venous grafts after elective coronary artery bypass surgery in a patient with AT-III deficiency.