ACUTE HEPARIN-INDUCED THROMBOCYTOPENIA WITH DELAYED IN-STENT SUBACUTE THROMBOSIS OF DRUG ELUTING STENTS, INTRACARDIAC THROMBOSIS, BIVENTRICULAR HEART FAILURE, AND HYPOXIA

Abstract

TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: Heparin-induced thrombocytopenia (HIT) is a fatal complication in patients with an average exposure of one to two weeks or can be rapid (< 24hrs) on re-exposure. In susceptible patients, antibodies directed against platelet factor 4 and heparin complexes cause HIT with thrombosis (HITTS). An average incidence of HIT is 0.1%-5% in patients on heparin therapy [1] CASE PRESENTATION: A 73-year-old female with a history of coronary disease, hypertension, and hyperlipidemia came to an outside hospital with a persistent cough, dyspnea, and acute hypoxia. She was treated for acute heart failure exacerbation and non-ST segment elevation myocardial infarction (NSTEMI) based on workup. An echocardiogram (ECHO) revealed an ejection fraction (EF) of 50%. She underwent staged percutaneous coronary intervention (PCI) and placement of an everolimus-based stent in the left anterior descending artery (LAD) followed by another stent in the left circumflex artery (LCX) after three days. Following stent placements, she went into pulmonary edema and was placed on noninvasive ventilation and was transferred to our institute to further manage acute hypoxic respiratory failure. Her hypoxia worsened, requiring endotracheal intubation, vasopressor support. She was treated for heart failure exacerbation and pneumonia. A repeat ECHO revealed two right ventricular thrombi with a severe decline in biventricular EF (Figure A). Anticoagulation with heparin was started, followed by a decline in platelet count > 50% due to HIT on day two, and was switched to argatroban (Figure B). Blood work showed NSTEMI, and a coronary angiogram revealed in-stent thrombosis of both stents (Figure C). Repeat successful PCI to LAD, and LCX with thrombus aspiration was completed. The patient had a complicated clinical course and never recovered DISCUSSION: As age increases, the risk of HIT gets higher [1]. HIT increases early mortality by 50% and embolic events by 20%-50%[2,3]. An increased HIT risk in females with cardiopulmonary bypass, hemodialysis, and vascular surgery was observed [4]. Venous thrombosis may be associated with surgery and arterial thrombosis with cardiovascular disease [5]. HIT antibody rate in patients with ACS is high and can induce symptoms in the absence of thrombocytopenia [6]. The odds of early stent thrombosis are < 1%[7]. The occurrence of thrombosis during therapeutic heparin anticoagulation is a concern for HITTS regardless of platelet counts and duration of therapy. Acute NSTEMI due to in-stent and intracardiac thrombosis due to HITTS is rare CONCLUSIONS: HITTS should be suspected in coronary thrombosis of unknown origin. Immediate heparin discontinuation and alternate anticoagulation are a must in HITTS, which can present with normal platelet counts REFERENCE #1: Hogan M, Berger JS. Heparin-induced thrombocytopenia (HIT): Review of incidence, diagnosis, and management. Vasc Med. 2020;25(2):160-73 REFERENCE #2: Solanki J, Shenoy S, Downs E, Palkimas S, Goldman S, Sharma AM. Heparin-Induced Thrombocytopenia and Cardiac Surgery. Semin Thorac Cardiovasc Surg. 2019;31(3):335-44 REFERENCE #3: Warkentin TE. Think of HIT. Hematology Am Soc Hematol Educ Program. 2006;408-414. doi:10.1182/asheducation-2006.1.408 DISCLOSURES: No relevant relationships by Tarang Patel, source=Web Response No relevant relationships by SACHIN PATIL, source=Web Response No relevant relationships by Shyam Shankar, source=Web Response No relevant relationships by Tushar Tarun, source=Web Response No relevant relationships by Ritika Verma, source=Web Response