Immunoinflammatory, Thrombohaemostatic, and Cardiovascular Mechanisms in COVID-19.
Thromb Haemost
; 120(12): 1629-1641, 2020 Dec.
Article
in English
| MEDLINE | ID: covidwho-894451
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.
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Renin-Angiotensin System
/
Cardiovascular Diseases
/
SARS-CoV-2
/
COVID-19
/
Inflammation
Type of study:
Observational study
/
Prognostic study
Limits:
Humans
Language:
English
Journal:
Thromb Haemost
Year:
2020
Document Type:
Article
Affiliation country:
S-0040-1718735
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