1. Medicine
Download icon

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
Short Report
  • Cited 45
  • Views 8,582
  • Annotations
Cite this article as: eLife 2020;9:e57278 doi: 10.7554/eLife.57278

Abstract

The discovery that SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) 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.

Article and author information

Author details

  1. Gian Paolo Rossi

    Department of Medicine-DIMED - Hypertension Unit, University of Padova, Padova, Italy
    For correspondence
    gianpaolo.rossi@unipd.it
    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
    sangaviola.md@gmail.com
    Competing interests
    No competing interests declared.
  3. Matthias Barton

    University of Zurich, Zurich, Switzerland
    For correspondence
    barton@access.uzh.ch
    Competing interests
    Matthias Barton, Senior Editor, eLife.

Funding

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)

Copyright

© 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.

Metrics

  • 8,582
    Page views
  • 1,446
    Downloads
  • 45
    Citations

Article citation count generated by polling the highest count across the following sources: Crossref, PubMed Central, Scopus.

Download links

A two-part list of links to download the article, or parts of the article, in various formats.

Downloads (link to download the article as PDF)

Download citations (links to download the citations from this article in formats compatible with various reference manager tools)

Open citations (links to open the citations from this article in various online reference manager services)

  1. Further reading

Further reading

    1. Chromosomes and Gene Expression
    2. Medicine
    Karthik Amudhala Hemanthakumar et al.
    Research Article

    Aging, obesity, hypertension and physical inactivity are major risk factors for endothelial dysfunction and cardiovascular disease (CVD). We applied fluorescence-activated cell sorting (FACS), RNA sequencing and bioinformatic methods to investigate the common effects of CVD risk factors in mouse cardiac endothelial cells (ECs). Aging, obesity and pressure overload all upregulated pathways related to TGF-b signaling and mesenchymal gene expression, inflammation, vascular permeability, oxidative stress, collagen synthesis and cellular senescence, whereas exercise training attenuated most of the same pathways. We identified collagen chaperone Serpinh1 (also called as Hsp47) to be significantly increased by aging and obesity and repressed by exercise training. Mechanistic studies demonstrated that increased SERPINH1 in human ECs induced mesenchymal properties, while its silencing inhibited collagen deposition. Our data demonstrate that CVD risk factors significantly remodel the transcriptomic landscape of cardiac ECs inducing inflammatory, senescence and mesenchymal features. SERPINH1 was identified as a potential therapeutic target in ECs.

    1. Epidemiology and Global Health
    2. Medicine
    Thao Phuong Ho-Le et al.
    Research Article Updated

    This study sought to redefine the concept of fracture risk that includes refracture and mortality, and to transform the risk into "skeletal age". We analysed data obtained from 3521 women and men aged 60 years and older, whose fracture incidence, mortality, and bone mineral density (BMD) have been monitored since 1989. During the 20-year follow-up period, among 632 women and 184 men with a first incident fracture, the risk of sustaining a second fracture was higher in women (36%) than in men (22%), but mortality risk was higher in men (41%) than in women (25%). The increased risk of mortality was not only present with an initial fracture, but was accelerated with refractures. Key predictors of post-fracture mortality were male gender (hazard ratio [HR] 2.4; 95% CI, 1.79–3.21), advancing age (HR 1.67; 1.53–1.83), and lower femoral neck BMD (HR 1.16; 1.01–1.33). A 70-year-old man with a fracture is predicted to have a skeletal age of 75. These results were incorporated into a prediction model to aid patient-doctor discussion about fracture vulnerability and treatment decisions.