Endothelial dysfunction in COVID-19: Current findings and therapeutic implications

• Published in: Atherosclerosis 2020-12, Vol.314, p.58-62
• Main Authors: Nägele, Matthias P., Haubner, Bernhard, Tanner, Felix C., Ruschitzka, Frank, Flammer, Andreas J.
• Format: Article
• Language: English
• Subjects: Angiotensin Receptor Antagonists - therapeutic use; Angiotensin-Converting Enzyme Inhibitors - therapeutic use; Animals; Blood Coagulation; Cardiovascular Diseases - drug therapy; Cardiovascular Diseases - epidemiology; Cardiovascular Diseases - physiopathology; Cardiovascular Diseases - virology; Coronavirus; COVID-19; COVID-19 - drug therapy; COVID-19 - epidemiology; COVID-19 - physiopathology; COVID-19 - virology; Endothelial dysfunction; Endothelium, Vascular - drug effects; Endothelium, Vascular - physiopathology; Endothelium, Vascular - virology; Host-Pathogen Interactions; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use; Prognosis; Renin angiotensin system; Review; Risk Factors; SARS-CoV-2 - pathogenicity; SARS-CoV2; Statin
• ISSN: 0021-9150; 1879-1484
• DOI: 10.1016/j.atherosclerosis.2020.10.014

Coronavirus disease 2019 (COVID-19) increases the risk of several non-pulmonary complications such as acute myocardial injury, renal failure or thromboembolic events. A possible unifying explanation for these phenomena may be the presence of profound endothelial dysfunction and injury. This review provides an overview on the association of endothelial dysfunction with COVID-19 and its therapeutic implications. Endothelial dysfunction is a common feature of the key comorbidities that increase risk for severe COVID-19 such as hypertension, obesity, diabetes mellitus, coronary artery disease or heart failure. Preliminary studies indicate that vascular endothelial cells can be infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and evidence of widespread endothelial injury and inflammation is found in advanced cases of COVID-19. Prior evidence has established the crucial role of endothelial cells in maintaining and regulating vascular homeostasis and blood coagulation. Aggravation of endothelial dysfunction in COVID-19 may therefore impair organ perfusion and cause a procoagulatory state resulting in both macro- and microvascular thrombotic events. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) and statins are known to improve endothelial dysfunction. Data from smaller observational studies and other viral infections suggests a possible beneficial effect in COVID-19. Other treatments that are currently under investigation for COVID-19 may also act by improving endothelial dysfunction in patients. Focusing therapies on preventing and improving endothelial dysfunction could improve outcomes in COVID-19. Several clinical trials are currently underway to explore this concept. [Display omitted] •New evidence implicates endothelial dysfunction in the pathophysiology of COVID-19.•It may explain complications such as multi-organ damage or thrombotic events.•Targeted interventions such as RAS inhibitors or statins may improve outcomes.•Studies on interventions that affect endothelial dysfunction are underway in COVID-19.