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Potential harmful effects of discontinuing ACE-inhibitors and ARBs in COVID-19 patients

  1. Gian Paolo Rossi  Is a corresponding author
  2. Viola Sanga  Is a corresponding author
  3. Matthias Barton  Is a corresponding author
  1. University of Padova, Italy
  2. University of Zurich, Switzerland
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Cite this article as: eLife 2020;9:e57278 doi: 10.7554/eLife.57278


The discovery that SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) RNA binds to the angiotensin converting enzyme (ACE)-2, which is highly expressed in the lower airways, explained why SARS-CoV-2 causes acute respiratory distress syndrome (ARDS) and respiratory failure. After this, news spread that ACEis and ARBs would be harmful in SARS-CoV-2-infected subjects. To the contrary, compelling evidence exists that the ACE-1/angiotensin(Ang)II/ATR-1 pathway is involved in SARS-CoV-2-induced ARDS, while the ACE-2/Ang(1-7)/ATR2/MasR pathway counteracts the harmful actions of AngII in the lung. A reduced ACE-1/ACE-2 ratio is, in fact, a feature of ARDS that can be rescued by human recombinant ACE-2 and Ang(1-7) administration, thus preventing SARS-CoV-2-induced damage to the lung. Based on the current clinical evidence treatment with ACE-inhibitors I (ACEis) or angiotensin receptor blockers (ARBs) continues to provide cardiovascular and renal protection in patients diagnosed with COVID-19. Discontinuing these medications may therefore be potentially harmful in this patient population.

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Author details

  1. Gian Paolo Rossi

    Department of Medicine-DIMED - Hypertension Unit, University of Padova, Padova, Italy
    For correspondence
    Competing interests
    No competing interests declared.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-7963-0931
  2. Viola Sanga

    Department of Medicine-DIMED - Hypertension Unit, University of Padova, Padova, Italy
    For correspondence
    Competing interests
    No competing interests declared.
  3. Matthias Barton

    University of Zurich, Zurich, Switzerland
    For correspondence
    Competing interests
    Matthias Barton, Senior Editor, eLife.


The authors declare that there was no funding for this work.

Reviewing Editor

  1. Mone Zaidi, Icahn School of Medicine at Mount Sinai, United States

Publication history

  1. Received: March 26, 2020
  2. Accepted: April 3, 2020
  3. Accepted Manuscript published: April 6, 2020 (version 1)
  4. Accepted Manuscript updated: April 8, 2020 (version 2)
  5. Accepted Manuscript updated: April 9, 2020 (version 3)
  6. Accepted Manuscript updated: April 15, 2020 (version 4)
  7. Version of Record published: May 4, 2020 (version 5)
  8. Version of Record updated: May 6, 2020 (version 6)


© 2020, Rossi et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.


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    We gratefully acknowledge support from the Andrew Sabin Family Fellowship, Center for Radiation Oncology Research, Sheikh Ahmed Center for Pancreatic Cancer Research, GE Healthcare, Philips Healthcare, and institutional funds from the University of Texas M.D. Anderson Cancer Center. We have also received Cancer Center Support Grants from the National Cancer Institute (P30CA016672 to the University of Texas M.D. Anderson Cancer Center and P30CA072720 the Rutgers Cancer Institute of New Jersey). This research has also been supported in part by grants from the National Science Foundation Grant DMS-1930583 (ZW, VC), the National Institutes of Health (NIH) 1R01CA253865 (ZW, VC), 1U01CA196403 (ZW, VC), 1U01CA213759 (ZW, VC), 1R01CA226537 (ZW, RP, WA, VC), 1R01CA222007 (ZW, VC), U54CA210181 (ZW, VC), and the University of Texas System STARS Award (VC). BC acknowledges support through the SER Cymru II Programme, funded by the European Commission through the Horizon 2020 Marie Skłodowska-Curie Actions (MSCA) COFUND scheme and the Welsh European Funding Office (WEFO) under the European Regional Development Fund (ERDF). EK has also received support from the Project Purple, NIH (U54CA210181, U01CA200468, and U01CA196403), and the Pancreatic Cancer Action Network (16-65-SING). MF was supported through NIH/NCI center grant U54CA210181, R01CA222959, DoD Breast Cancer Research Breakthrough Level IV Award W81XWH-17-1-0389, and the Ernest Cockrell Jr. Presidential Distinguished Chair at Houston Methodist Research Institute. RP and WA received serial research awards from AngelWorks, the Gillson-Longenbaugh Foundation, and the Marcus Foundation. This work was also supported in part by grants from the National Cancer Institute to SHC (R01CA109322, R01CA127483, R01CA208703, and U54CA210181 CITO pilot grant) and to PYP (R01CA140243, R01CA188610, and U54CA210181 CITO pilot grant). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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