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• W3205670216 abstract "TOPIC: Critical Care TYPE: Original Investigations PURPOSE: Infection with SARS-CoV-2 causes diffuse endothelialitis leading to multi organ system failure and an increased risk of thromboembolism. The mechanism for these observations remains uncertain, and the phenomenon seems more pronounced in patients with COVID-19 than in patients with other severe infectious illnesses. Previous work has revealed alterations in red blood cell aggregation in septic patients from causes other than COVID-19, but if this occurs in COVID-19 and how it may influence the endothelium is unknown The purpose of our study is to examine how plasma constituents from patients with COVID-19, particularly fibrinogen, when coupled with red blood cells from a healthy volunteer may disrupt the endothelial glycocalyx (an important regulator of endothelial cell health) in a system designed to mimic the microvasculature. METHODS: Plasma was obtained from 11 hospitalized patients with COVID-19 with known elevated fibrinogen levels and 4 healthy volunteers. Each sample was recombined with red blood cells obtained from a healthy volunteer to yield a hematocrit of 25%. Microfluidics devices with serial branches of channel widths measuring 120µm, 90µm, 60µm, 40µm and 30µm were cultured with human umbilical vein endothelial cells under steady shear rates, an experimental condition well characterized and published by our lab. These cultured devices were stained with wheat germ agglutinin to visualize the endothelial glycocalyx. Fluorescent images were obtained prior to and after perfusion of the reconstituted plasma samples at a steady flow rate for 30 minutes. Change in glycocalyx presence was measured and evaluated for each channel size in the device and results were compared between the healthy volunteer and COVID-19 groups. RESULTS: From the largest to the smallest width channel there was a significant decrease in the proportion of residual glycocalyx via repeated measure ANOVA analysis in the COVID-19 group (p=0.00422) that was not present in the healthy volunteer group (p=0.380). When comparing the residual glycocalyx between the healthy volunteers and the COVID-19 group in each channel size by two-tailed t-test, only the smallest channel in the device demonstrated a significant decrease (0.46±0.09 vs 0.66±0.16, p=0.02). The average concentration of fibrinogen in the COVID-19 group was greater than 770 mg/dL and additional experiments from our lab which have been previously presented have shown that these high fibrinogen levels lead to increase red cell aggregation at channel sizes equivalent to those in this study independent of the presence of endothelial cells. CONCLUSIONS: From the results of these studies, we conclude that red cell aggregation is an essential component of the microvascular pathophysiology in COVID-19 particularly at the smallest venule and near capillary vessel size. While there may be additional effect from the upregulated inflammatory pathways in COVID-19, the 30 minute perfusion time in these studies make an enzymatic or subcellular pathway less likely. These findings present a novel mechanism that would benefit from further prognostic and even therapeutic investigation. CLINICAL IMPLICATIONS: Understanding the unique pathophysiology of COVID-19 associated microvascular dysfunction is essential to how we assess adjunctive therapies in the future and our findings promotes the significance of the fibrinogen regulatory pathways in SARS-CoV-2 infection. DISCLOSURES: No relevant relationships by Kirby Fibben, source=Web Response No relevant relationships by Elizabeth Iffrig, source=Web Response No relevant relationships by Wilbur Lam, source=Web Response No relevant relationships by Cheryl Maier, source=Web Response No relevant relationships by Guido Silvestri, source=Web Response" @default.
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• W3205670216 date "2021-10-01" @default.
• W3205670216 modified "2023-10-13" @default.
• W3205670216 title "FIBRINOGEN-RBC INTERACTIONS PLAY A KEY ROLE IN COVID-19-ASSOCIATED ENDOTHELIAL DYSFUNCTION" @default.
• W3205670216 doi "https://doi.org/10.1016/j.chest.2021.07.987" @default.
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