In this interesting correspondence just published in the Lancet, Varga et al. demonstrate endothelial cell involvement across vascular beds of different organs in a series of patients with COVID-19 finding evidence of direct viral infection of the endothelial cell and diffuse endothelial inflammation. Indeed, although the virus uses ACE2 receptors expressed by pneumocytes in the epithelial alveolar lining to infect the host, causing lung injury, the ACE2 receptor is also widely expressed on endothelial cells in other organs. Widespread endothelial dysfunction can occur either through direct viral infection of the endothelium or an immune-mediated response. These very interesting findings suggest that SARS-CoV-2 infection facilitates the induction of endotheliitis in several organs as a direct consequence of viral involvement and the host inflammatory response providing a rationale for therapies to stabilise the endothelium (anti-inflammatory anti-cytokine drugs, ACE inhibitors, statins), whilst tackling viral replication. This strategy could be particularly relevant for vulnerable patients with pre-existing endothelial dysfunction, which is associated with male sex, smoking, hypertension, diabetes, obesity, and established cardiovascular disease, all of which are associated with adverse outcomes in COVID-19.
by Marialuisa Zedde and Francesco Cavallieri