Journal
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Volume 76, Issue 10, Pages 1168-1176Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jacc.2020.07.022
Keywords
COVID-19; primary percutaneous coronary intervention; ST-segment elevation myocardial infarction; thrombosis
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Funding
- Barts Charity
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BACKGROUND Coronavirus 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. OBJECTIVES The 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. METHODS This was a single-center, observational study of 115 consecutive patients admitted with confirmed STEMS treated with primary percutaneous coronary intervention at Barts Heart Centre between March 1, 2020, and May 20, 2020. RESULTS Patients with STEMS presenting with concurrent COVID-19 infection had higher levels of troponin T and tower 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 Ilb/Illa inhibitors and thrombus aspiration. Myocardial blush grade and left ventricular function were significantly tower in patients with COVID-19 with STEMI. Higher doses of heparin to achieve therapeutic activated dotting times were also noted. Importantly, patients with STEMS presenting with COVID-19 infection had a longer in-patient admission and higher rates of intensive care admission. CONCLUSIONS In patients presenting with STEMS 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 STEMS cases. Further work is required to understand the mechanism of increased thrombosis and the benefit of aggressive antithrombotic therapy in selected cases. (C) 2020 by the American College of Cardiology Foundation.
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