Endothelial dysfunction in COVID-19 patients assessed with Endo-PAT2000

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, but 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. We therefore aimed to demonstrate in vivo the presence of endothelial dysfunction in six COVID-19 patients without cardiovascular risk factors or pre-existing cardiac condition, using the Endo-PAT 2000, a device able to measure endothelial vasodilation function in a rapid and non-invasive way. Four patients were positive for endothelial dysfunction, with RHI values between 1.13-1.56 (average value 1.32, normal values >1.67); in one of the two negative patients the reported RHI value was slightly above the cutoff (1.72). Our findings confirm that COVID-19 patients are at higher risk of developing endothelial dysfunction. In addition, our results demonstrate that endothelial impairment may occur even in the absence of cardiovascular risk factors.

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 and 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.