Introduction
The COVID-19 pandemic has caused worldwide social, economic and
political disruption. Its pathogenesis is largely due to extensive
disruption of innate and adaptive immunity, altered interferon
responses, and coagulation abnormalities that lead to microvascular
immunothrombosis. Many of these changes are caused by endothelial
dysfunction.1
Antiviral treatments for COVID-19 have been only marginally effective.
Antibody treatments (convalescent plasma and monoclonal antibody
preparations) for severe disease have also been disappointing. Some
investigators have suggested repurposing drugs that are already licensed
for use against other diseases.2 Some of these drugs
target the host response to infection, not the virus itself. One of
these drugs is dexamethasone, which improves survival in COVID-19
patients who require oxygen treatment but not in those who do not
require oxygen.3
Cardiovascular drugs have also attracted interest because many of them
(including statins) affect endothelial dysfunction.4Experts recommend continuing statin treatment in COVID-19 patients who
are already being treated.5 This recommendation is
based largely on numerous observational studies that suggest continuing
treatment is safe. Nonetheless, most of these studies are based on
outpatient-documented treatment. Because they do not consider the
effects of statin withdrawal after hospital admission, their estimates
of statin effectiveness are likely to be imprecise. It is unclear
whether investigators recognize that statin withdrawal could be a
problem.