Endothel, vaskuläre Funktion und COVID-19

Sabrina Kopp; Thomas Münzel; Philip Wenzel

doi:10.1055/a-1319-0964

Aktuelle Kardiologie, Table of Contents

Aktuelle Kardiologie 2021; 10(01): 32-38
DOI: 10.1055/a-1319-0964

Kurzübersicht

Endothel, vaskuläre Funktion und COVID-19

Endothelium, Vascular Function and COVID-19

Sabrina Kopp

¹Zentrum für Kardiologie, Kardiologie I, Universitätsmedizin der Johannes Gutenberg-Universität Mainz, Deutschland

,

Thomas Münzel

¹Zentrum für Kardiologie, Kardiologie I, Universitätsmedizin der Johannes Gutenberg-Universität Mainz, Deutschland

,

Philip Wenzel

¹Zentrum für Kardiologie, Kardiologie I, Universitätsmedizin der Johannes Gutenberg-Universität Mainz, Deutschland

²Deutsches Zentrum für Herz-Kreislauf-Forschung e. V., Standort RheinMain, Deutschland

³Centrum für Thrombose und Hämostase, Universitätsmedizin der Johannes Gutenberg-Universität Mainz, Deutschland

› Author Affiliations

Abstract

Zusammenfassung

Seit Beginn der COVID-19-Pandemie konnten zahlreiche Erkenntnisse über den 3-phasigen Verlauf einer SARS-CoV-2-Infektion, den Infektionsweg und die Bedeutung einer vaskulären Dysfunktion gewonnen werden. Im Rahmen der Infektion kann es zu einer hyperinflammatorischen Phase mit sekundären Organschäden bis hin zum Tod kommen. Diese schweren Krankheitsverläufe gehen mit einer unkontrollierten Freisetzung von Entzündungsmediatoren und Zytokinen einher. Auf zellulärer Ebene bedingt der membrangebundene ACE-2-Rezeptor die Invasion des Virus und stimuliert über einen 2. Mechanismus die Metalloprotease ADAM17 sowie die Freisetzung von Zytokinen. Vasokonstriktive Veränderungen sowie die systemischen Inflammationsreaktionen führen zu hypoxischen Organschäden und thrombotischen Komplikationen. Die mikrovaskuläre Dysfunktion, Mikroangiopathien – insbesondere der kleinen Lungengefäße – sowie eine Endotheliitis können Erklärungsansätze für die ausgeprägte systemische, mikrovaskuläre Störung bei schweren Infektionen mit SARS-CoV-2 liefern.

Abstract

The global involvement of coronavirus disease 19 (COVID-19) provokes multiple findings about the clinical course in three phases, the infection pathway and the vascular function. Severe course of SARS-CoV-2-infection is defined as massive inflammatory reaction with elevated pro-inflammatory cytokines resulting in acute respiratory stress syndrome and the involvement of secondary organ damages with even life-threatening cardiovascular and pulmonary complications. Mechanistically, SARS-CoV-2 invades human cells with binding at angiotensin converting enzyme 2 and following another secondary pathway with ADAM17-mediated systemic release of cytokines and pro-inflammatory markers. Systemic inflammation and vasoconstriction lead to hypoxia and pro-thrombotic complications. Microvascular dysfunction, microangiopathy of small lung vessels and endotheliitis may provide new approaches for systemic inflammation due to SARS-CoV-2 infection.

Schlüsselwörter

Endothel - vaskuläre Funktion - SARS-CoV-2 - ACE-2

Key words

endothelium - vascular function - SARS-CoV-2 - ACE 2

Full Text

References

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