By Katherine Kozlowski, medical writer and contributor to Vein News
COVID-19 is an endothelial disease
Libby et al (2020) investigated COVID-19 as an endothelial disease because SARS-Cov-2 (the agent causing COVID-19) often manifests in the later stages as endothelial dysfunction.
The vascular endothelium is a layer of cells lining the cardiovascular system and is present throughout the body in organs and vascular tissue. This endothelium functions to control hemostasis (limiting blood loss), fibrinolysis (the breakdown of blood clots), vasomotion (normal changes in arteriolar diameter), inflammation, oxidative stress, vascular permeability, and structural support.
While many of these functions of the vascular endothelium function as defense and control homeostasis (balance within the body), overactivation of defense mechanisms can damage a person’s body.
Cytokines are biological chemicals released from vascular endothelial cells to allow communication among them and signal the immune system to start working. The later stages of COVID-19 often involve a “cytokine storm”, which is an accelerated and exaggerated release of cytokines throughout the body, eventually leading to an over-reaction of the immune response. This excessive immune response can be damaging to a patient, interfering with normal cell function in the body.
Treatments targeting COVID-19 as an endothelial disease that are under evaluation include anticoagulation and antiplatelet therapies, anti-inflammatory therapies, and targeted cytokine inhibition.
Considering the widespread effects of SARS-Cov-2 on the lungs, heart, brain, kidney, and vasculature, Libby et al suggests that COVID-19 be considered an “endothelial disease” to unify the pathophysiological image of the disease as well as provide a structured foundation for treatment methods, as evidence for effective treatment is still limited at this time.
Libby, P and Lüscher T. COVID-19 is, in the end, an endothelial disease. European Heart J 2020; 41(32): 3038-3044.