Impact of COVID‐19 on red blood cell rheology

Coronavirus disease 2019 (COVID-19) is an infectious caused by severe acute respiratory coronavirus 2 (SARS-CoV-2). Among hospitalized patients, many have developed typical manifestations of sepsis-like cold extremities, weak peripheral pulses or metabolic acidosis, indicating microcirculation dysfunction.1 Microvascular dysfunction has been reported in sepsis2, 3 and could be partly red blood cell (RBC) rheological alterations such as decreased RBC deformability (RBCD),4 increased aggregation5 abnormal morphology/physiology.6 Whether COVID-19 patients also impaired rheology unknown. The aim this preliminary study was to compare the haemorheological profile (RBCD, aggregation, viscosity) between sepsis healthy controls. Seven (COVID) Edouard-Herriot Hospital (Hospices Civils de Lyon, France) were included. diagnosis made specific real-time polymerase chain reaction (RT-PCR; n = 5) and/or chest computerized tomography (n 7). admitted for non-COVID-related (SEPSIS) seven controls (CONTROL) SEPSIS identified quick Sequential Organ Failure Assessment (quickSOFA) score according Sepsis-3 definition.7 Clinical reports reviewed a physician collect general clinical characteristics (Table I). approved local ethics committee (No. 20-108) Hospices Lyon biological resource centre (CRB HCL, BB-0033-00046). Haematological parameters determined using haematology analyser (XN-9000; Sysmex Corporation, Kobe, Japan) COVID patients. aggregation measured ektacytometry, Myrenne aggregometer cone/plate viscometer respectively, previously described.8 Hemox-Analyzer (TCS, Medical Products Division, Southampton, PA, USA) used plot oxygen haemoglobin dissociation curves determine P50 values (the tension at which 50% Hb saturated with oxygen), adjustment pH 7.4 temperature 37°C.9 Gender distribution not different three groups age group significantly higher than CONTROL (P < 0.05). No other differences detected. In group, none smokers, but every patient had co-morbidities obesity, high pressure, diabetes, syndrome, cardiac, hepatic renal failure. globally marked lung alterations, evidenced extent parenchymal lesions (>50% 43% cases; data shown) transfer intensive care unit (ICU) them (none group). any died during study. White counts C-reactive protein lower common did differ these two groups. There no RBCD compared low shear stresses (i.e., from 0.53 Pa; P addition, stresses, ranging 1.69 30 Pa reduced Maximum both Blood viscosity difference fibrinogen levels shown Despite available concentrations above normal range (reference our laboratory: 2–4 g/l). stasis groups, while rate group. Our results showed that rate, individuals, individuals only. comparison static condition, increases chance RBCs make contact aggregate, would better reflect in-vivo conditions. It possible observed relative g/l reference value laboratory, contributing factor aggregation,10 further work needed test contribution aggregability cellular factors). Clot stability affected properties.11 Indeed, enhanced affect clot structure increase their resistance. lack smears present allow us clearly differentiate agglutination, may pathophysiology. decrease Pa. Changes membrane lipids composition fragmentation explain reduction patients.12 maximum suggesting internal loss surface/volume ratio, elasticity, contrast patients.13 properties, possibly because haematocrit tended contrasts recent where calculated gas analyzer.14 suggest SARS-CoV-2 does affinity directly, due hypoxia/metabolic adaptations.14 conclusion, shows properties are This risks thromboembolic events, well microvascular flow. Nevertheless, sample size limited studies needed. authors thank Biological Resource Centre Lyon. Céline Renoux, Romain Fort, Elie Nader, Philippe Joly, Emeric Stauffer, Mélanie Robert, Agnès Cibie, Alexandra Gauthier Connes designed research Renoux Sandrine Girard included Camille Boisson, Nader Joly performed research. analysed data. wrote paper. All revised paper critically final version. declare conflicts interest.