Thromb Haemost
DOI: 10.1055/s-0040-1718735
Review Article

Immunoinflammatory, Thrombohaemostatic, and Cardiovascular Mechanisms in COVID-19

Selin Gencer*
1  Institute for Cardiovascular Prevention, Ludwig-Maximilians-Universität, Munich, Germany
,
Michael Lacy*
1  Institute for Cardiovascular Prevention, Ludwig-Maximilians-Universität, Munich, Germany
2  DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany
,
Dorothee Atzler
1  Institute for Cardiovascular Prevention, Ludwig-Maximilians-Universität, Munich, Germany
2  DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany
3  Walther Straub Institute for Pharmacology and Toxicology, Ludwig-Maximilians-Universität, Munich, Germany
,
Emiel P. C. van der Vorst
1  Institute for Cardiovascular Prevention, Ludwig-Maximilians-Universität, Munich, Germany
2  DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany
4  Interdisciplinary Center for Clinical Research (IZKF), Institute for Molecular Cardiovascular Research (IMCAR), RWTH Aachen University, Aachen, Germany
5  Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands
,
Yvonne Döring
1  Institute for Cardiovascular Prevention, Ludwig-Maximilians-Universität, Munich, Germany
2  DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany
6  Divison of Angiology, Swiss Cardiovascular Center, Inselspital, Bern University Hospital, University of Bern, Switzerland
,
Christian Weber**
1  Institute for Cardiovascular Prevention, Ludwig-Maximilians-Universität, Munich, Germany
2  DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany
7  Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Centre, Maastricht, The Netherlands
8  Munich Cluster for Systems Neurology (SyNergy), Munich, Germany
› Author Affiliations
Funding This study was supported by Deutsche Forschungsgemeinschaft (SFB1123).

Abstract

The 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.

* These authors contributed equally to this manuscript and share first authorship.


** The review process for this paper was fully handled by Gregory Y. H. Lip, Editor-in-Chief.




Publication History

Received: 03 July 2020

Accepted: 14 September 2020

Publication Date:
29 October 2020 (online)

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