Its licence doesn't allow us to show a copy here.
Why the study?
COVID-19 is thought to predispose to thrombotic disease, but there are few reports of STEMI caused by type 1 myocardial infarction in patients with COVID-19.
Does concurrent COVID-19 infection increase thrombus burden and worsen in-hospital outcomes in patients presenting with STEMI?
Observational (n=115)
No
Does concurrent COVID-19 infection increase thrombus burden and worsen in-hospital outcomes in patients presenting with STEMI?
Answers are grounded in this paper and cite their sources.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“The authors are to be congratulated for their observations during the pandemic: they have performed a unique registry of COVID-19–positive STEMI patients with a concurrent COVID-19–negative control group and provided insight into the feasibility and challenges of primary PCI. Their detailed analysis of angiographic data supports a broader hypothesis: patients with COVID-19 infection are at a specially enhanced risk of inflammation-triggered thrombus burden.”
STEMI patients with concurrent COVID-19 infection exhibit a highly pro-thrombotic phenotype, evidenced by significantly greater multivessel thrombosis, stent thrombosis, and higher post-intervention thrombus grades, suggesting a potential need for more aggressive antithrombotic strategies.
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 STEMI treated with primary percutaneous coronary intervention at Barts Heart Centre between March 1, 2020, and May 20, 2020. Results Patients 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. Conclusions In 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.
No takes yet. Share an insight, caveat, or question.
Choudry et al. (2020) conducted an observational in ST-Segment Elevation Myocardial Infarction (STEMI) (n=115). Concurrent COVID-19 infection vs. COVID-19-negative patients was evaluated on All-cause in-hospital mortality (p=0.10).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: