Immunoinflammatory, Thrombohaemostatic, and Cardiovascular Mechanisms in COVID-19
| Autor: | Christian Weber, Selin Gencer, Emiel P. C. van der Vorst, Yvonne Döring, Michael Lacy, Dorothee Atzler |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty BLOCKADE Central nervous system INHIBITION MYOCARDITIS ACE2 Context (language use) KAPPA-B CORONAVIRUS Disease 030204 cardiovascular system & hematology Systemic inflammation SARS-COV-2 RECEPTOR ACE2 ANGIOTENSIN-ALDOSTERONE SYSTEM Renin-Angiotensin System 03 medical and health sciences 0302 clinical medicine RAAS cardiovascular disease medicine Humans Intensive care medicine Pandemics Inflammation Hemostasis NITRIC-OXIDE business.industry SARS-CoV-2 Microcirculation Immunity COVID-19 Thrombosis Hematology medicine.disease Theme Issue Article Pathophysiology 3. Good health ADIPOSE-TISSUE 030104 developmental biology medicine.anatomical_structure ATHEROSCLEROSIS Respiratory failure Cardiovascular Diseases medicine.symptom business |
| Zdroj: | Thrombosis and Haemostasis |
| ISSN: | 2567-689X 0340-6245 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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