key: cord-0688273-sxj1vxpe
authors: De Lorenzo, Andrea; Escobar, Silas; Tibiriçá, Eduardo
title: Systemic endothelial dysfunction: a common pathway for COVID-19, cardiovascular and metabolic diseases
date: 2020-05-18
journal: Nutr Metab Cardiovasc Dis
DOI: 10.1016/j.numecd.2020.05.007
sha: ff7a8b356e59b3a077acc9db178fc59f89353aae
doc_id: 688273
cord_uid: sxj1vxpe

Some of the mechanisms and conditions underlying endothelial dysfunction.A-human skin capillaries, visualized with high-resolution intravital color microscopy in the finger of a patient with obesity, metabolic syndrome and coronary artery disease.B- healthy control. The reduced number of capillaries can be noticed in A compared to B. [Figure: see text]

Amidst the pandemic that has mesmerized the entire world, as it has not spared anyone according to any specific characteristic, some conditions have in fact emerged as risk factors for a complicated evolution of COVID-19. Cardiovascular and metabolic diseases, including hypertension and diabetes, have been associated with more severe presentations and/or adverse prognosis [1] .

As Li et al point out in their recent paper [2] , there is a complex network of predisposing factors in patients with cardiovascular disease. However, an important player in the scenario of cardiovascular and metabolic disease was overlooked.

Endothelial dysfunction -the impairment of the ability of the endothelium to maintain vascular homeostasis -is the final common pathway for diabetes/insulin resistance, hypertension, and dyslipidemia. The inflammatory state, increased oxidative stress, altered nitric oxide bioavailability, and insulin resistance, are key factors of endothelial dysfunction [3, 4] . Additionally, as SARS-CoV-2 infects the host cells by means of the transmembrane angiotensin-converting enzyme (ACE)-II receptor, which is expressed in endothelial cells, there is substrate for a direct pathogenic effect of the virus [5] .

Other noxious influences over the endothelium include the effects of proinflammatory cytokines ("cytokine storm"), resulting in vascular endothelial cell apoptosis and leading to lung microvascular dysfunction, vascular leakage, alveolar edema and ultimately hypoxia. Moreover, proinflammatory cytokines increase the expression of adhesion molecules, resulting in endothelial activation, procoagulant and proadhesive changes, worsening microvascular flow and, consequently, tissue perfusion. Pulmonary endothelial activation has been recently demonstrated, in an autopsy study of 10 patients with COVID-19. Histological findings were exsudative/proliferative diffuse alveolar damage, but endothelial tumefaction in pulmonar capillaries and fibrinous thrombi in small pulmonary arterioles were also found [6] . Funding: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study

A close-up on COVID-19 and cardiovascular diseases, Nutrition, Metabolism and Cardiovascular Diseases

Impaired microvascular function in obesity: implications for obesity-associated microangiopathy, hypertension, and insulin resistance

Mechanisms of endothelial dysfunction in obesity-associated hypertension

Pathological evidence of pulmonary thrombotic phenomena in severe COVID-19