Effect of aspirin on short-term outcomes in hospitalized patients with COVID-19

Vascular Medicine - Tập 26 Số 6 - Trang 626-632 - 2021
Aditya Sahai1,2, Rohan Bhandari3,1,2, Matthew Godwin3, Thomas M. McIntyre3, Mina K. Chung4,5,3, Jean‐Pierre Iskandar6, Hayaan Kamran1,2, Essa Hariri6, Anu Aggarwal3, Robert Burton6, Ankur Kalra1,2, John R. Bartholomew1,2, Keith R. McCrae4,5,7, Ayman Elbadawi8, James Bena9, Lars G. Svensson1,2, Samir Kapadia1,2, Scott J. Cameron3,1,2,7
1Section of Vascular Medicine, Department of Cardiovascular Medicine
2Section of Vascular Medicine, Department of Cardiovascular Medicine; Heart, Vascular & Thoracic Institute, Cleveland Clinic, Cleveland, OH, USA
3Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA
4Department of Cardiovascular Medicine
5Department of Cardiovascular Medicine; Heart, Vascular & Thoracic Institute, Cleveland Clinic, Cleveland, OH, USA
6Department of Internal Medicine, Cleveland Clinic, Cleveland, OH, USA
7Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA
8Division of Cardiovascular Medicine, University of Texas Medical Branch, Galveston, TX, USA
9Department of Quantitative Health Science, Cleveland Clinic, Cleveland, OH, USA

Tóm tắt

Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 is an ongoing viral pandemic marked by increased risk of thrombotic events. However, the role of platelets in the elevated observed thrombotic risk in COVID-19 and utility of antiplatelet agents in attenuating thrombosis is unknown. We aimed to determine if the antiplatelet effect of aspirin may mitigate risk of myocardial infarction, cerebrovascular accident, and venous thromboembolism in COVID-19. We evaluated 22,072 symptomatic patients tested for COVID-19. Propensity-matched analyses were performed to determine if treatment with aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) affected thrombotic outcomes in COVID-19. Neither aspirin nor NSAIDs affected mortality in COVID-19. Thus, aspirin does not appear to prevent thrombosis and death in COVID-19. The mechanisms of thrombosis in COVID-19, therefore, appear distinct and the role of platelets as direct mediators of SARS-CoV-2-mediated thrombosis warrants further investigation.

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