Blood hyperviscosity in acute and recent COVID-19 infection

Abstract

BACKGROUND: Elevated estimated blood viscosity (EBV), derived from hematocrit and globulins, is associated with thrombotic complications, organ failure, and higher mortality in COVID-19 patients. Although informative, EBV does not account for cellular interactions or fibrinogen. OBJECTIVE: Investigate whether patients with acute and recent COVID-19 have altered WBV profiles. METHODS: Cross-sectional study of 58 patients: 15 in the intensive care unit with acute COVID-19, 32 convalescent (9 < 8weeks [W] from acute infection, 23 > 8 W), and 11 controls without COVID-19. WBV was measured at high (300 s–1) and low (5 s–1) shear rates (HSR, LSR) using a scanning capillary viscometer. RESULTS Acute and convalescent patients < 8 W had mean WBV at LSR (16.0 centipoise [cP] and 15.1 cP) and HSR (5.1 cP and 4.7 cP). Mean WBV of convalescent > 8 W and control patients were 12.3 cP and 13.0 cP at LSR, and 4.1 cP and 4.2 cP at HSR. Acute and < 8 W patients had significantly higher WBV at both HSR and LSR compared to patients > 8 W (all p≤0.01). No significant differences in WBV were observed between acute and < 8 W patients, or between patients > 8 W and controls. CONCLUSIONS: Hyperviscosity provides a possible explanation for thrombotic risk in acute and convalescent (< 8 W) patients. These findings have important implications for thromboprophylaxis.

COVID-19 hemodynamic and thrombotic effect on the eye microcirculation after hospitalization: A quantitative case-control study

“…The cause of the disease is an RNA beta coronavirus (SARS-COV2) which infects endothelial cells after binding to the angiotensin converting enzyme 2 (ACE2) receptor and entering the cell interior with the help of the transmembrane protease serine type 2 (TMPRSS2). Then a cascade of events may follow, depending on the subject, including endothelial cell activation and dysfunction [13,14,35], diffuse alveolar damage, increased blood viscosity [36,37], hypercoagulation, thrombotic microangiopathy, acute respiratory distress syndrome (ARDS), local and systemic hypoxia, and death.…”

PurUUpurU: An Oligonucleotide Virulence Factor in RNA Viruses

“…By increasing plasma concentrations of large proteins such as fibrinogen and decreasing the albumin concentrations, the acute phase reaction increases blood viscosity [ 5 ]. Driven by the high copy number of purUUpurU in the genome of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [ 1 ], blood viscosity in COVID-19 was increased by 17.6% in a study of 15 patients hospitalized in an intensive care unit [ 14 ]. An increase in blood viscosity causes a threefold inverse change in tissue perfusion [ 15 ].…”

Coagulation and hemorheology profile of patient with stroke and COVID-19: A case series during second wave pandemic

“…This is presumably because the stroke has a major role in increasing blood viscosity. With good management of stroke, patient improvement will lead to more significant changes in blood viscosity [12]. Because the physician has a strong understanding of the impact of coagulation and hemorheology factors on the prognosis of COVID-19 patients with stroke, it seems that coagulation and hemorheology factors have been evaluated in order to provide early therapy.…”