Abstract
Heparin-induced thrombocytopenia (HIT) is an immune-mediated disease with severe thromboembolic complications. HIT during percutaneous coronary intervention (PCI) can be fatal without prompt treatment. We report an unusual case of HIT observed during PCI for acute coronary syndrome (ACS). A 74-year-old female with a history of pulmonary embolism managed with unfractionated heparin (UFH) 2 years previously presented with intermittent chest pain. Coronary angiography revealed total occlusion of the mid-right coronary artery. Before and during the primary PCI, 14000 UFH units were administered. However, abundant thrombus formation in the non-culprit lesion was refractory to repeated thrombus aspiration. We suspected HIT, discontinued UFH, and administered argatroban. Despite repeated thrombus aspirations and balloon dilatation, coronary obstruction persisted; consequently, ventricular fibrillation refractory to multiple cardioversions occurred. Therefore, veno-arterial extracorporeal membrane oxygenation (VA-ECMO) was required. Platelet counts rapidly decreased to <50 % of the baseline value, and serum was highly positive for IgG-specific antiplatelet factor 4/heparin antibodies. The patient was discharged with independent gait and no major neurological disorders. This is a clinically noteworthy case of rapidly developing HIT during primary PCI for ACS, requiring VA-ECMO management, with no major neurological complications. HIT may occur immediately after re-exposure to heparin long after the first exposure. LEARNING OBJECTIVE: Without prompt treatment, heparin-induced thrombocytopenia (HIT) during percutaneous coronary intervention (PCI) can be fatal. It may lead to refractory coronary obstruction, which may need to be managed by veno-arterial extracorporeal membrane oxygenation (VA-ECMO). We present a clinically noteworthy case of rapidly developing HIT during primary PCI for acute coronary syndrome, requiring VA-ECMO management, with no major neurological complications. Physicians must be mindful that HIT may occur immediately after re-exposure to heparin long after the first exposure.