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Editorial
Does aspirin save lives in patients with COVID-19?
  1. Dinesh Voruganti1,
  2. Pier Paolo Bassareo2,
  3. Giuseppe Calcaterra3,
  4. J L Mehta1
  1. 1Division of Cardiology, Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
  2. 2Department of Cardiology, Mater Misericordiae University Hospital, Dublin, Ireland
  3. 3Faculty of Medicine and Surgery, University of Palermo, Palermo, Sicilia, Italy
  1. Correspondence to Dr J L Mehta, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA; arheartdoc{at}gmail.com

https://doi.org/10.1136/heartjnl-2021-320255

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    ‘An aspirin a day keeps the heart attack away’, is this also true in the prevention of thrombotic events associated with COVID-19? The rising COVID-19 pandemic has led to much work in the understanding of the pathophysiology of the disease. COVID-19 infection is thought to be an endothelial disease. Supporting this concept, it has been suggested that infection with SARS-CoV-2, the aetiological agent for COVID-19 infection, leads to a state mimicking Virchow’s triad, that is, vascular endothelial injury, blood stasis and clotting in concert with systemic inflammation resulting in systemic thrombosis.

    In keeping with this concept, moderately and critically ill patients with COVID-19 have been found to have thrombotic and thromboembolic events during the acute and convalescent state. Accordingly, there has been much interest in treating patients with COVID-19 with anticoagulants. In an analysis of several large series of critically ill patients in multiple studies (534 therapeutic anticoagulation, 564 usual care thromboprophylaxis), therapeutic anticoagulation did not improve survival or the number of days free of cardiovascular or respiratory organ support. On the other hand, among 2244 non-critically ill patients (1190 therapeutic anticoagulation, 1054 thromboembolic prophylaxis), therapeutic anticoagulation improved rates of hospital survival and reduced the use of cardiorespiratory organ support.1

    Since there is intense platelet activation secondary to endothelial injury and inflammation, there is …

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    Footnotes

    • Contributors DV wrote the initial drafts. PPB, GC and JLM edited the drafts. All authors approved the final version.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests None declared.

    • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting or dissemination plans of this research.

    • Provenance and peer review Commissioned; externally peer reviewed.

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