Discussion
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.
Endothelial dysfunction may play a pivotal role in the pathophysiology
of the infection process and may identify a subset of patient at a
higher risk of worse outcome. In a small series of patients who died
from COVID-19, severe endothelial injury associated with intracellular
virus detection, disruption of endothelial cell membranes, widespread
pulmonary vascular thrombosis and occlusion of alveolar capillaries with
significant new vessel growth, was observed (6). Early recognition of
endothelial impairment at an early stage of the disease, before the
development of the mentioned histological complications, appears
critical. Whether the evidence of endothelial dysfunction, through
noninvasive approaches, can predict worse clinical outcomes or higher
risk of thromboembolic events needs to be proven by recruiting a larger
number of affected patients. Nevertheless, our results contribute to the
knowledge of the pathophysiological mechanisms related to COVID-19
infection.