COVID-19 Demonstrates That Inflammation Is a Hyperviscous State

Abstract

Many of the complications of severe coronavirus disease-2019 (COVID-19) are caused by blood hyperviscosity driven by marked hyperfibrinogenemia. This results in a distinctive hyperviscosity syndrome which affects areas of high and low shear. A change in blood viscosity causes a threefold inverse change in blood flow, which increases the risk of thrombosis in both arteries and veins despite prophylactic anticoagulation. Increased blood viscosity decreases perfusion of all tissues, including the lungs, heart, and brain. Decreased perfusion of the lungs causes global ventilation-perfusion mismatch which results in silent hypoxemia and decreased efficacy of positive pressure ventilation in treating pulmonary failure in COVID-19. Increased blood viscosity causes a mismatch in oxygen supply and demand in the heart, resulting in myocarditis and ventricular diastolic dysfunction. Decreased perfusion of the brain causes demyelination because of a sublethal cell injury to oligodendrocytes. Hyperviscosity can cause stasis in capillaries, which can cause endothelial necrosis. This can lead to the rarefaction of capillary beds, which is noted in "long-COVID." The genome of the virus which causes COVID-19, severe acute respiratory syndrome coronavirus 2, contains an extraordinarily high number of the oligonucleotide virulence factor 5'-purine-uridine-uridinepurine-uridine-3', which binds to toll-like receptor 8, hyperactivating innate immunity. This can lead to a marked elevation in fibrinogen levels and an increased prevalence of neutrophil extracellular traps in pulmonary failure, as seen in COVID-19 patients.

Case report: unprecedented case of infantile cerebral infarction following COVID-19 and favorable outcome

“…This heightened blood viscosity can exacerbate the reduction in tissue oxygenation and nutrition, thereby perpetuating a detrimental cycle ( 29 ). A significant correlation between elevated whole blood viscosity and increased mortality rates was determined in patients with COVID-19 ( 30 ).Alterations in blood viscosity can profoundly impact blood flow dynamics, potentially tripling the risk of thrombus formation in both arteries and veins ( 31 ). Although the infant in this case exhibited respiratory symptoms due to COVID-19, there was no involvement of the lungs or signs of hypoxemia.…”

New Onset Anemia, Worsened Plasma Creatinine Concentration, and Hyperviscosity in a Patient With a Monoclonal IgM Paraprotein

“…Sluggish blood flow, which pathologist Rudolph Virchow identified as a cause of thrombosis, is simply a manifestation of increased blood viscosity [ 1 ]. The role of acute hyperviscosity in thrombosis became clear in severe COVID-19 [ 19 ]. An increased incidence of thrombosis in relatively young patients in intensive units on prophylactic anticoagulation was noted early in the pandemic.…”

A Brief Overview of Neutrophils in Neurological Diseases

“…Once inside the brain, it can constrict the capillaries and reduce the blood flow via binding ACE2 on the pericytes [77]. SARS-CoV-2 also increases the viscosity of the blood, which causes the reduced blood flow in the cerebral capillaries [78]. As seen in other dementia or stroke models, this reduction in the blood flow might be one of the mechanisms behind cognitive impairment in the long COVID-19.…”