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Tehrani S, Gille-Johnson P
Shock - (-) - [2021-05-04; online 2021-05-04]
Endothelial 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. Twelve patients with COVID-19 treated with non-invasive or invasive mechanical ventilation were included in the study. We investigated skin microvascular reactivity on two separate days during hospitalization (study day 1 and 2) and at least three 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 (LSCI) before and after iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP) to determine the endothelial-dependent and the endothelial-independent vasodilation, respectively. Compared 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 versus 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). This 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 three months after disease onset.
PubMed 33958544
DOI 10.1097/SHK.0000000000001803
Crossref 10.1097/SHK.0000000000001803
pii: 00024382-900000000-97251