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Endothelial Dysfunction in Covid-19

Endothelial Dysfunction and Oxidative Stress in ICU and Non-ICU Covid-19 Patients With Hypoxemic Respiratory Failure

Status
UNKNOWN
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT04830683
Acronym
ENDOCOVID
Enrollment
85
Registered
2021-04-05
Start date
2020-04-27
Completion date
2021-04-01
Last updated
2021-04-09

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Covid19, Hypoxemic Respiratory Failure

Keywords

Endothelial Dysfunction, Covid19

Brief summary

SARS-CoV-2 targets endothelial cells via the angiotensin-converting enzyme 2 receptor. The specific impact of the resulting endothelial injury is currently unknown but may contribute to the pro-coagulant state classically described during Covid-19 disease and commonly associated with an exacerbated activation of the renin-angiotensin-aldosterone system.

Detailed description

We prospectively compared clinical and biological parameters in ICU- and non-ICU-admitted Covid-19 patients, ICU-admitted patients with septic shock unrelated to Covid-19 and matched control subjects. Primary hemostasis and coagulation parameters and endothelial biomarkers are measured. Activation of the renin-angiotensin-aldosterone system is monitored through measurements of plasma renin, angiotensin II, aldosterone, and serum soluble angiotensin-converting enzyme 2. Vascular oxidative status is assessed by measuring plasma lipids peroxides. Neutrophilic polymorphonuclear activation is assessed by measuring plasma levels of Triggering receptor expressed on myeloid cells-1. Vascular nitric oxide bioavailability is measured by quantification of the concentration of heme-nitrosylated hemoglobin (HbNO) in venous erythrocytes using Electron Paramagnetic Resonance spectroscopy. Structural abnormalities of vascular endothelial cells were analyzed by Transmission Electron- and Scanning Electron Microscopy.

Interventions

None listed

Sponsors

Cliniques universitaires Saint-Luc- Université Catholique de Louvain
Lead SponsorOTHER

Study design

Observational model
COHORT
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
18 Years to 75 Years

Inclusion criteria

* positive result on a reverse-transcriptase-polymerase chain reaction testing performed on nasopharyngeal swab at hospital admission

Exclusion criteria

* ICU admission more than five days after admission on a general ward, * concomitant bacterial infection * older than 75 years * cirrhosis

Design outcomes

Primary

MeasureTime frameDescription
Vascular oxidative stress in Covid-19 versus septic shock and control patientsICU or general ward hospital admissionHbNO (nmol/L) and NOX levels (μM/L), oxidative stress with plasma lipids peroxides (mmol/L) levels and soluble TREM-1 measurements. Blood HbNO levels directly correlate with endothelial function and inversely with major cardiovascular risk factors. The nitrite/nitrate levels (NOx) are the the stable end products of NO metabolism that also suggest NO production. Plasma lipids peroxides reflets the surrounding endovascular oxidative stress. sTREM-1 participates in the sepsis-induced ROS production through activation of NADPH oxidase (NOX)-2 during the respiratory burst of activated polymorphonuclear.

Secondary

MeasureTime frameDescription
Vascular Renin-angiotensin-aldosterone system measurements in Covid-19 versus septic shock and control patientsICU or general ward hospital admissionRenin (pg/mL), Agiotensin II (fmol/mL), Aldosterone (pg/mL) measurements. The RAAS system is a classical activator of vascular NOX2 and ROS production.

Countries

Belgium

Contacts

Primary ContactVIRGINIE MONTIEL, MD, PhD
virginie.montiel@uclouvain.be0032496503912

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026