Introduction
It has been widely reported that the Severe Acute Respiratory Syndrome
Coronavirus 2 (SARS-CoV-2) attaches human cells by using the Angiotensin
Converting Enzyme 2 (ACE2) receptor (1), which is expressed in several
organs, including the endothelial cells (2). Whether vascular impairment
described during coronavirus disease 2019 (COVID-19) infection is
primarily due to the direct involvement of the endothelial cells by the
virus or secondarily to the inflammatory host response is currently
unknown, but there is evidence that SARS-CoV-2 can directly infect human
blood vessel. (3)
Recently, Varga et colleagues, described autopsy findings from three
patients who died from COVID-19, showing direct viral infection of the
endothelium systemic and endotheliitis with proliferation of lymphocytes
and macrophages, and loss of integrity of the endothelial monolayer (4).
These patients, however, were affected by concomitant cardiovascular
disease such as hypertension, diabetes, obesity, and coronary artery
disease, underlying a potential pre-existing endothelial dysfunction.