Assessment of Endothelial Vasodilator Function in COVID-19 Patients

Coronavirus disease 2019 (COVID-19), secondary to infection by severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) has caused a global pandemic with significant adverse effects on the health, social and economic systems in different countries of the world.

The entry receptor utilized by SARS-CoV-2 is Angiotensin-Converting Enzyme 2 (ACE-2), localized at the membrane of epithelial and endothelial cells and muscle cells of blood vessels. Hypothetically, this interaction of SARS-CoV-2 with essential elements of the blood vessels may conduct to endothelial dysfunction. In fact, it has been demonstrated several degrees of endothelial compromise in the kidney, small bowel and lungs from histological analysis in fatidic cases.

The pathophysiological mechanisms by which vascular endothelial dysfunction can complicate the evolutionary course of viral infections are of two types:

1. On the one hand, acute endothelial dysfunction can produce ischemic events as a consequence of thrombotic or vasomotor processes. Some of these events are acute coronary syndromes, pulmonary thromboembolism and peripheral angiopathy, all of which have been reported in COVID-19 patients.
2. On the other hand, vascular endothelial dysfunction can trigger or amplify systemic inflammatory reactions leading to multi-organ failure. Vascular hyperpermeability generated by vascular endothelial dysfunction is key in the processes of infiltration of immune cells and in the amplification of the inflammatory response that occurs in the context of the cytokine storm associated with the viral infection. This process contributes to release large amounts of IL 6, IL-1B and TNF alpha by vascular endothelial cells, thus the expression of vascular adhesion molecules.

In this study, the investigators sought to evaluate the status of vascular endothelial function in COVID-19 patients from a non-invasive approach.