The Detrimental Role of Elevated Blood Viscosity in Patients With COVID-19

Abstract

Inflammation causes hyperviscosity.  This phenomenon is fully expressed in coronavirus 2019.  The cardiac complications of coronavirus 2019 are most commonly caused by hyperviscosity, not viral invasion of endothelial cells or cardiomyocytes.  This hyperviscosity is caused by high concentrations of acute phase reactants, especially fibrinogen, and immunoglobins.   These increase erythrocyte aggregation which causes sludging of blood in areas of low shear in the coronary circulation, veins and microvasculature.  This can lead to thrombosis.  Coronary thrombosis occurs in association with several infectious diseases and even immunization.  In the early twentieth century, Osler noted right ventricular dilation, a common complication of coronavirus 2019, in response to hyperviscosity caused by infection.  Perfusion is inversely proportional to blood viscosity.  Diastolic dysfunction, another common complication of coronavirus 2019, is a consequence of this hypoperfusion.  Therapeutic plasmapheresis is the therapy of choice for reducing blood viscosity and restoring normal perfusion.  All tissues are underperfused when blood viscosity is elevated.  This reduces delivery of metabolic substrates needed to maintain cellular function.  Post-covid syndrome may be the result of torpid recovery after prolonged hypoperfusion.  D-ribose is a versatile metabolic substrate which may hasten improvement of post-inflammatory illness.