• Fizzah A Choudry, Stephen M Hamshere, Krishnaraj S Rathod, Mohammed M Akhtar, R Andrew Archbold, Oliver P Guttmann, Simon Woldman, Ajay K Jain, Charles J Knight, Andreas Baumbach, Anthony Mathur, and Daniel A Jones.
• Department of Cardiology, Barts Heart Centre, St. Bartholomew's Hospital, London, United Kingdom; Centre for Cardiovascular Medicine and Devices, William Harvey Research Institute, Queen Mary University of London, London, United Kingdom.
• J. Am. Coll. Cardiol. 2020 Sep 8; 76 (10): 1168-1176.

BackgroundCoronavirus disease-2019 (COVID-19) is thought to predispose patients to thrombotic disease. To date there are few reports of ST-segment elevation myocardial infarction (STEMI) caused by type 1 myocardial infarction in patients with COVID-19.ObjectivesThe aim of this study was to describe the demographic, angiographic, and procedural characteristics alongside clinical outcomes of consecutive cases of COVID-19-positive patients with STEMI compared with COVID-19-negative patients.MethodsThis was a single-center, observational study of 115 consecutive patients admitted with confirmed STEMI treated with primary percutaneous coronary intervention at Barts Heart Centre between March 1, 2020, and May 20, 2020.ResultsPatients with STEMI presenting with concurrent COVID-19 infection had higher levels of troponin T and lower lymphocyte count, but elevated D-dimer and C-reactive protein. There were significantly higher rates of multivessel thrombosis, stent thrombosis, higher modified thrombus grade post first device with consequently higher use of glycoprotein IIb/IIIa inhibitors and thrombus aspiration. Myocardial blush grade and left ventricular function were significantly lower in patients with COVID-19 with STEMI. Higher doses of heparin to achieve therapeutic activated clotting times were also noted. Importantly, patients with STEMI presenting with COVID-19 infection had a longer in-patient admission and higher rates of intensive care admission.ConclusionsIn patients presenting with STEMI and concurrent COVID-19 infection, there is a strong signal toward higher thrombus burden and poorer outcomes. This supports the need for establishing COVID-19 status in all STEMI cases. Further work is required to understand the mechanism of increased thrombosis and the benefit of aggressive antithrombotic therapy in selected cases.Copyright © 2020 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

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