![]() ![]() Males, smokers, those over age 65, and those with chronic obstructive pulmonary disease, hyperlipidemia, and diabetes have an increased risk of thrombotic complications of COVID-19. The influx of fibrinolytic activity and dilution of activated coagulation factors is also reduced.4 Shear-mediated endothelial production of antiplatelet molecules such as nitric oxide and prostacyclin is decreased in these areas. ![]() Sluggish blood flow is simply a manifestation of increased blood viscosity. ![]() Areas of low shear occur naturally in veins and in areas of changing arterial geometry, such as branches, curves, and dilatations, making these vascular regions prone to thrombosis.4 Blood viscosity is a more sensitive marker than plasma viscosity for the risk of thrombosis because it reflects changes caused by hemoconcentration and intrinsic erythrocyte abnormalities.Īs noted by the famous pathologist Rudolph Virchow in the 19th century, areas of sluggish blood flow are prone to thrombosis. This increases blood viscosity exponentially at low shear (slow flow). All patients with plasma viscosity > 3.5 cP had thrombosis.2 For comparison, normal whole blood viscosity at a high shear rate (100/s) is 3.26 ± 0.43 cP.3 Thus, blood viscosity has the potential to be extraordinarily high in COVID-19 patients.įibrinogen and other acute-phase reactants act like glue and foster erythrocyte aggregation. A recent report of 15 critically ill COVID-19 patients showed all had elevated plasma viscosity, ranging from 1.9 to 4.2 centipoise (cP) (normal range: 1.4-1.8 cP). As noted recently in BMJ, fibrinogen concentrations can be extraordinarily high in severe COVID-19, reaching 10-14 g/L.1 This is reflected in the markedly increased plasma viscosity of COVID-19 patients. The high incidence of thrombosis in COVID-19 patients is caused by elevated blood viscosity due to hyperfibrinogenemia. ![]()
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