• Sara Tehrani and Patrik Gille-Johnson.
• Karolinska Institutet, Department of Clinical Sciences, Danderyd University Hospital, Division of Internal Medicine and Infectious Diseases, Stockholm, Sweden.
• Shock. 2021 Dec 1; 56 (6): 964968964-968.

BackgroundEndothelial and microvascular dysfunction may be a key pathogenic feature of severe COVID-19. The aim of this study was to investigate endothelial-dependent and endothelial-independent skin microvascular reactivity in patients with critical COVID-19.MethodsTwelve patients with COVID-19 treated with non-invasive or invasive mechanical ventilation were included in the study. We investigated skin microvascular reactivity on 2 separate days during hospitalization (study day 1 and 2) and at least 3 months after disease onset (study day 3). Twelve controls with no confirmed or suspected COVID-19 infection during 2020 were also examined. Skin perfusion was investigated through Laser Speckle Contrast Imaging before and after iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP) to determine the endothelial-dependent and the endothelial-independent vasodilation, respectively.ResultsCompared to controls, patients with critical COVID-19 had higher basal skin perfusion and reduced responses to endothelial-dependent (ACh, P = 0.002) and endothelial-independent (SNP, P = 0.01) vasodilator drugs on study day 1. In addition, the ACh/SNP ratio was significantly reduced in patients (0.50 ± 0.36 vs. 0.91 ± 0.49 in controls, P = 0.02). Three months after disease onset, surviving patients tended to have reduced ACh-mediated vasodilation compared to controls (P = 0.08).ConclusionsThis small-sized pilot study demonstrates that critical COVID-19 infection is associated with microvascular impairment and, in particular, a markedly reduced endothelial function. Our results also suggest that microvascular function may not be fully recovered 3 months after disease onset.Copyright © 2021 by the Shock Society.

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