Platelet Protection Using the Glycoprotein IIb/IIIa Inhibitor Tirofiban in a Patient With Heparin-Induced Thrombocytopenia Undergoing Aortic Valve Replacement Requiring Cardiopulmonary Bypass

The role of platelets in the first line of defense against vasculature insult is well established. Cardiopulmonary bypass (CPB) is associated with activation of the coagulation cascade with the ultimate formation of thrombin, which activates platelets and may result in marked postoperative bleeding. Unfractionated heparin cannot be used in patients with heparin-induced thrombocytopenia (HIT) undergoing open-heart surgery requiring CPB. Alternative methods of anticoagulation are thus frequently used for patients with HIT. Studies have demonstrated that glycoprotein IIb/IIIa inhibitors protect platelets during percutaneous coronary intervention and CPB. The authors present an 84-year-old woman previously diagnosed with HIT admitted for aortic valve replacement who received the short-acting glycoprotein IIb/IIIa antagonist tirofiban as a platelet protectant. The patient was evaluated for both platelet count and function using Plateletworks (Helena Point-of-Care, Beaumont, TX, USA) periprocedurally. Anticoagulation during CPB was achieved with standard heparin dosing 300 U/kg subsequent to a bolus of tirofiban 10 mg/kg followed by an infusion of 0.15 mg/kg per minute, and discontinued 30 minutes before termination of CPB. Platelet aggregation was reduced to 12% 20 minutes after tirofiban bolus and remained low until 2 hours after aortic valve replacement, when recovery of platelet function was observed. As a result of CPB, the patient was hemodiluted. Platelets were transfused and the count increased substantially. At 2 hours and 4 hours after CPB, the platelet function approached baseline, preprocedural levels. These data suggest that this procedure is an acceptable anticoagulation strategy in patients with HIT without residual antibodies undergoing cardiac surgery requiring CPB.