Journal article

Immunoinflammatory, Thrombohaemostatic, and Cardiovascular Mechanisms in COVID-19

  • Gencer, Selin Institute for Cardiovascular Prevention, Ludwig-Maximilians-Universität, Munich, Germany
  • Lacy, Michael DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany
  • Atzler, Dorothee Walther Straub Institute for Pharmacology and Toxicology, Ludwig-Maximilians-Universität, Munich, Germany
  • van der Vorst, Emiel P. C. Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands
  • Döring, Yvonne Divison of Angiology, Swiss Cardiovascular Center, Inselspital, Bern University Hospital, University of Bern, Switzerland
  • Weber, Christian Munich Cluster for Systems Neurology (SyNergy), Munich, Germany
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  • 2020-10-29
Published in:
  • Thrombosis and Haemostasis. - Georg Thieme Verlag KG. - 2020
English AbstractThe global coronavirus disease 2019 (COVID-19) pandemic has deranged the recent history of humankind, afflicting more than 27 million individuals to date. While the majority of COVID-19 patients recuperate, a considerable number of patients develop severe complications. Bilateral pneumonia constitutes the hallmark of severe COVID-19 disease but an involvement of other organ systems, namely the cardiovascular system, kidneys, liver, and central nervous system, occurs in at least half of the fatal COVID-19 cases. Besides respiratory failure requiring ventilation, patients with severe COVID-19 often display manifestations of systemic inflammation and thrombosis as well as diffuse microvascular injury observed postmortem. In this review, we survey the mechanisms that may explain how viral entry and activation of endothelial cells by severe acute respiratory syndrome coronavirus 2 can give rise to a series of events including systemic inflammation, thrombosis, and microvascular dysfunction. This pathophysiological scenario may be particularly harmful in patients with overt cardiovascular disease and may drive the fatal aspects of COVID-19. We further shed light on the role of the renin–angiotensin aldosterone system and its inhibitors in the context of COVID-19 and discuss the potential impact of antiviral and anti-inflammatory treatment options. Acknowledging the comorbidities and potential organ injuries throughout the course of severe COVID-19 is crucial in the clinical management of patients affecting treatment approaches and recovery rate.
Language
  • English
Open access status
bronze
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Persistent URL
https://folia.unifr.ch/global/documents/234698
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