One thing that is interesting about the COVID-19 is that similar to SARS, there is higher mortality in patients with cardiovascular disease. There also seem to be significant cardiac injuries (e.g. myocarditis) that are occurring with severe infection.
It’s known that SARS-COV-2 uses ACE2 (in part) for entry to into target cells. It’s also known that systemic ACE / ARB use increases the expression of ACE2 in cardiac cells. I can’t find reference to it’s effect in alveolar tissue, but ACE2 is expressed there, and thought to be involved in the pathogenesis of ARDS (effectively the presentation of severe COVID-19).
Could those on ACE / ARB be at risk for a more severe course due to up regulation of ACE2 at the cell surface, independent of other cardiac risk factors?
If so, perhaps widespread substitution of these agents for another might reduce the risk.
(I can’t find a reference to see how long it takes to return to previous expression levels after drug withdrawal)
The most natural group to look at here would be patients with isolated hypertension, many of which may be on an ACE, but also other agents with reasonable equipoise. Other patient groups on ACE I are also of interest.
COVID-19 and the cardiovascular system Nature Reviews Cardiology
Hoffmann M, Kleine-Weber H, Krüger N, Müller M, Drosten C, Pöhlmann S. The novel coronavirus 2019 (2019-nCoV) uses the SARS-coronavirus receptor ACE2 and the cellular protease TMPRSS2 for entry into target cells. bioRxiv 2020:2020.01.31.929042.