Coronavirus Disease 2019 (COVID‐19): Do Angiotensin‐Converti
Get authentic, real-time news that helps you fight COVID-19 better.
Install PlexusMD App for doctors. It's free.
Most patients with cardiovascular comorbidities qualify for angiotensin‐converting enzyme inhibitor (ACEI) or angiotensin II receptor blocker (ARB) therapy. Of note, Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2 uses the receptor angiotensin‐converting enzyme (ACE) 2 for entry into target cells. Ferrario et al reported that both ACEI and ARB could significantly increase mRNA expression of cardiac ACE2. On the basis of these thoughts, we recently generated the hypothesis that these drugs might play a role in the severe course of COVID‐19 cases. More importantly, no clinical‐epidemiological data have been put forward and it is unknown whether the hypothesized mechanism plays a pivotal role in COVID‐19.

The lay press picked up the theory, causing concern and even anxiety among patients and their healthcare providers. Because of the lack of current evidence of a potential negative impact of these medications on COVID‐19, we currently support the position statement of the European and American Societies of Cardiology, who express that ACEIs and ARBs are safe and should be continued and prescribed according to established guidelines.

According to the latest analysis of the National Health and Nutrition Examination Survey ACEIs/ARBs are the most prevalent antihypertensive medication among all drug classes.14 Unfortunately, the European Centre for Disease Prevention and Control does not record any previous drugs in its data collection on COVID‐19 patients.15 Until now, no data are available about the association between previous drug intake and severity of COVID‐19 pulmonary outcome. This brings up 4 key questions:

1. Are these cardiovascular comorbidities simply confounders (as they occur frequently with higher age and have been shown to predispose to worse outcome with influenza type A H1N1 infection)?

2. Is there is a link between the comorbidities and SARS‐CoV‐2 (ie, are patients with heart failure at a higher risk of pulmonary outcome)?

3. Does the comorbidities‐associated intake of some drug classes improve or worsen infectivity or the course of COVID‐19?

4. If renin‐angiotensin system blockade emerges in one way or another as a possible mediator, are there difference between ACEIs and ARBs?

Regardless of these deliberations, we would like to emphasize that many older patients are on renin‐angiotensin system blockade because of latent or manifest left ventricular dysfunction and that discontinuation of these drugs may exacerbate frank heart failure. There is little doubt that heart failure is prone to have an unfavorable effect on pulmonary outcome in the course of COVID‐19.

1 share