Focus on clinical practice: angiotensin-converting enzyme 2 and corona virus disease 2019: pathophysiology and clinical implications

• Published in: Journal of cardiovascular medicine (Hagerstown, Md.) Vol. 21; no. 9; p. 630
• Main Authors: Barillà, Francesco, Bassareo, Pier Paolo, Calcaterra, Giuseppe, Romeo, Francesco, Mehta, Jawahar L
• Format: Journal Article
• Language: English
• Published: United States 01.09.2020
• Subjects: Angiotensin Receptor Antagonists - pharmacology; Angiotensin-Converting Enzyme 2; Angiotensin-Converting Enzyme Inhibitors - pharmacology; Betacoronavirus - physiology; Cardiovascular Diseases - complications; Cardiovascular Diseases - drug therapy; Cardiovascular Diseases - metabolism; Coronavirus Infections - metabolism; Coronavirus Infections - virology; COVID-19; Humans; Pandemics; Peptidyl-Dipeptidase A - metabolism; Pneumonia, Viral - metabolism; Pneumonia, Viral - virology; Renin-Angiotensin System - drug effects; Renin-Angiotensin System - physiology; SARS-CoV-2; Spike Glycoprotein, Coronavirus - metabolism; Virus Internalization
• ISSN: 1558-2035
• DOI: 10.2459/JCM.0000000000001071

: ACE2 receptor has a broad expression pattern in the cellular membrane and provides a protective action against the development of cardiovascular diseases. Recently, this enzyme has become of extreme interest during the pandemic infection of COVID-19 (coronavirus disease 2019). This virus invades alveolar epithelium and cardiomyocytes using ACE2 as a transmembrane receptor. ACE2 is a counter-regulatory peptide that degrades Ang II into Ang 1-7, thereby attenuating the biological effects of the AT1 receptor. The binding between the spike protein of COVID-19 and the enzyme is crucial for the virus to enter the target cells, but whether an increase in ACE2 activity could facilitate the infection is not yet demonstrated. However, this aspect has raised many concerns about the use of ACE inhibitors or ARBs in infected patients or patients at risk of infection. It appears that cellular infection leads to a reduction in ACE2 expression and an increase in the activity of the Ang II--AT1 axis, which leads to the release of pro-inflammatory cytokines, ARDS, myocarditis, and hypercoagulability with the possibility of exacerbation of acute coronary syndrome, induction of pulmonary embolism, or appearance of disseminated intravascular coagulation. Therefore, ACE inhibitors or angiotensin receptor blocker drugs should be continued in infected patients, as their discontinuation can increase Ang II activity and induce injury to the lungs or cardiovascular system.