Abstract 12399: Don’t Burst My Blood: Ticagrelor Induced Thrombotic Thrombocytopenic Purpura

Abstract

Background: Dual antiplatelet therapy, a fundamental component of the treatment of acute coronary syndromes (ACS), increases bleeding risk. Patients with thrombocytopenia and ACS are difficult to manage as thrombocytopenia increases the risk both of bleeding and ischemic events. Case: A 47 year old male with a medical history most significant for coronary artery disease (requiring multiple stents) and stroke who presented with chest pain and was found to have a NSTEMI. Notably, the patient stopped his ticagrelor six weeks prior to presentation. The initial CBC demonstrated clumped platelets. The patient was loaded with aspirin and ticagrelor, placed on a heparin drip and admitted. Decision Making: Exam on the morning after presentation demonstrated jaundice as well as petechiae on the patient’s extremities. He then exhibited altered mental status concerning for a seizure. Repeat labs demonstrated new severe thrombocytopenia, confirmed on a dedicated platelet count, anemia and indirect hyperbilirubinemia. A peripheral smear did not demonstrate schistocytes; however, the PLASMIC score indicated a high risk of thrombotic thrombocytopenic purpura (TTP) and he was started on plasmapheresis and steroids. His ADAMTS13 activity level returned low, confirming TTP. Common causes of TTP were excluded and Ticagrelor was deemed responsible. With continued plasmapheresis and steroids, his platelets normalized. A diagnostic left heart catheterization demonstrated patent prior stents as well as a 90% mid circumflex lesion. The patient was discharged on aspirin and rivaroxaban per the COMPASS trial, and was advised to avoid further P2Y12 inhibitors. Conclusion: This case demonstrated ticagrelor induced TTP, which has been infrequently reported in the literature. The patient was likely previously sensitized to ticagrelor and then developed TTP when he was loaded on presentation. It also demonstrates the importance of not ignoring clumped platelets and obtaining a true platelet count prior to starting triple therapy. In normal circumstances, his circumflex lesion would likely have been intervened upon; however, the patient’s intolerance of P2Y12 inhibitors limited management options during this presentation and will likely limit future interventions.