Abstract
BackgroundCOVID-19 is primarily a respiratory disease; however, there is also evidence that it causes endothelial damage in the microvasculature of several organs. The aim of the present study is to characterize in vivo the microvascular reactivity in peripheral skeletal muscle of severe COVID-19 patients.MethodsThis is a prospective observational study carried out in Spain, Mexico and Brazil. Healthy subjects and severe COVID-19 patients admitted to the intermediate respiratory (IRCU) and intensive care units (ICU) due to hypoxemia were studied. Local tissue/blood oxygen saturation (StO2) and local hemoglobin concentration (THC) were non-invasively measured on the forearm by near-infrared spectroscopy (NIRS). A vascular occlusion test (VOT), a three-minute induced ischemia, was performed in order to obtain dynamic StO2 parameters: deoxygenation rate (DeO2), reoxygenation rate (ReO2), and hyperemic response (HAUC). In COVID-19 patients, the severity of ARDS was evaluated by the ratio between peripheral arterial oxygen saturation (SpO2) and the fraction of inspired oxygen (FiO2) (SF ratio).ResultsHealthy controls (32) and COVID-19 patients (73) were studied. Baseline StO2 and THC did not differ between the two groups. Dynamic VOT-derived parameters were significantly impaired in COVID-19 patients showing lower metabolic rate (DeO2) and diminished endothelial reactivity. At enrollment, most COVID-19 patients were receiving invasive mechanical ventilation (MV) (53%) or high-flow nasal cannula support (32%). Patients on MV were also receiving sedative agents (100%) and vasopressors (29%). Baseline StO2 and DeO2 negatively correlated with SF ratio, while ReO2 showed a positive correlation with SF ratio. There were significant differences in baseline StO2 and ReO2 among the different ARDS groups according to SF ratio, but not among different respiratory support therapies.ConclusionPatients with severe COVID-19 show systemic microcirculatory alterations suggestive of endothelial dysfunction, and these alterations are associated with the severity of ARDS. Further evaluation is needed to determine whether these observations have prognostic implications. These results represent interim findings of the ongoing HEMOCOVID-19 trial.Trial registration ClinicalTrials.gov NCT04689477. Retrospectively registered 30 December 2020.
Highlights
COVID-19 is primarily a respiratory disease; there is evidence that it causes endothelial damage in the microvasculature of several organs
COVID-19 typically begins as an infection of the upper airway, it can progress to severe respiratory disease, including acute respiratory distress syndrome (ARDS)
The main result of our study is that severe COVID-19 patients admitted in the intensive care units (ICU) showed altered microcirculatory status in the peripheral muscle, and the degree of such alterations correlated with the severity of the respiratory disease
Summary
COVID-19 is primarily a respiratory disease; there is evidence that it causes endothelial damage in the microvasculature of several organs. Since its first identification in December 2019, over 190 million people have been diagnosed of severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) infection worldwide, and Coronavirus disease 2019 (COVID-19) has been responsible for over 4 million deaths [1]. 80% of those infected with COVID-19 will develop only mild symptoms, critically ill patients, presenting with acute respiratory hypoxemic failure, account for up to 15% of cases [2, 3]. COVID-19 typically begins as an infection of the upper airway, it can progress to severe respiratory disease, including acute respiratory distress syndrome (ARDS). Monitoring endothelial function emerges as a potential biomarker of COVID-19 severity for prognostic purposes or monitoring the effect of new treatment options [8, 9]
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