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.