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Faced with the emergence of a new disease, and particularly of a disease of pandemic proportions, understanding the pathophysiological basis of the disease is fundamental and is the very essence of research. But the danger, particularly in an urgent situation, is to take therapeutic measures or to take public health measures, based solely on basic research data. The debate on the interaction between renin-angiotensin-system (RAS) blockers and COVID-19 is an excellent illustration of this risk.
ACE inhibitors and angiotensin receptor blockers (ARB) play a central role in the management of cardiovascular disease, including hypertension, diabetes, coronary artery disease and heart failure and are used in a considerable number of patients. Myocardial injury is common in patients with COVID-19 disease, particularly those with diabetes or hypertension, and may contribute to increased risk in these patients.1
As RAS inhibitors are commonly prescribed in patients with cardiovascular conditions, who are precisely at increased risk of complications in the case of SARS-COV-2 infection, it has been suggested that those medications could have a deleterious role in this context. Among the mechanisms most frequently put forward is the link between the ACE2 receptors and host cell infection.2
ACE2 is present in the organism as membrane-bond and in a soluble form. It is a membrane glycoprotein found in the heart, vascular endothelium, kidney and also in lung parenchyma, bronchus and small intestine. Experimental studies suggest that RAS blockers can upregulate ACE2 expression.2 3 It has been shown that membrane-bound ACE2 mediates SARS-COV-2 infection via spike (S) protein binding, facilitating viral entry into host cells, which, however, requires the preliminary action of another enzyme, transmembrane protease serine S2 …
Editor's note The linked article to which this Editorial refers can be found in Volume 106, Issue 19 of Heart.
Contributors The authors contributed equally in drafting this editorial.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests TS reports grants from AstraZeneca, Bayer, Daichi-Sankyo, GSK, MSD, Novartis and personnel fees from AstraZeneca, BMS, Novartis and Sanofi. ND has received grants, personal fees and non-financial support from Amgen, AstraZeneca, Bayer, BMS, Sanofi, personal fees from Boehringer Ingelheim, Intercept, MSD, Novo Nordisk, Pfizer, Servier and UCB, all outside the submitted work.
Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Patient consent for publication Not required.
Provenance and peer review Commissioned; internally peer reviewed.
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