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.