Endothelial Function and COVID-19

NCT ID: NCT04525443

Last Updated: 2021-02-26

Basic Information

• Recruitment Status: COMPLETED
• Total Enrollment: 110 participants
• Study Classification: OBSERVATIONAL
• Study Start Date: 2020-06-03
• Study Completion Date: 2021-02-11

Brief Summary

The present study aims to investigate the endothelial vasodilator function in patients with COVID-19

Detailed Description

Coronavirus disease 2019 (COVID-19), secondary to infection by severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) has caused a global pandemic with significant adverse effects on the health, social and economic systems in different countries of the world.

The entry receptor utilized by SARS-CoV-2 is Angiotensin-Converting Enzyme 2 (ACE-2), localized at the membrane of epithelial and endothelial cells and muscle cells of blood vessels. Hypothetically, this interaction of SARS-CoV-2 with essential elements of the blood vessels may conduct to endothelial dysfunction. In fact, it has been demonstrated several degrees of endothelial compromise in the kidney, small bowel and lungs from histological analysis in fatidic cases.

The pathophysiological mechanisms by which vascular endothelial dysfunction can complicate the evolutionary course of viral infections are of two types:

1. On the one hand, acute endothelial dysfunction can produce ischemic events as a consequence of thrombotic or vasomotor processes. Some of these events are acute coronary syndromes, pulmonary thromboembolism and peripheral angiopathy, all of which have been reported in COVID-19 patients.

2. On the other hand, vascular endothelial dysfunction can trigger or amplify systemic inflammatory reactions leading to multi-organ failure. Vascular hyperpermeability generated by vascular endothelial dysfunction is key in the processes of infiltration of immune cells and in the amplification of the inflammatory response that occurs in the context of the cytokine storm associated with the viral infection. This process contributes to release large amounts of IL 6, IL-1B and TNF alpha by vascular endothelial cells, thus the expression of vascular adhesion molecules.

In this study, the investigators sought to evaluate the status of vascular endothelial function in COVID-19 patients from a non-invasive approach.

The evaluation of systemic vascular endothelial function will be performed non-invasively using peripheral arterial tonometry with EndoPat system (Itamar). It is a technique that determines the endothelial-dependent changes in arterial tone of the vascular network of the index finger of both hands. Using bio-sensors placed on the pad of the index finger of both hands, an assessment of arterial tone is carried out at three stages: 1) at baseline; 2) during an ischemia caused by the inflation of a pressure cuff in one of the arms to occlude the brachial artery for 5 minutes; 3) and in a situation of reactive hyperemia during the recovery of arterial irrigation after deflating the pressure cuff. The arterial tone signals detected by plethysmography at the three described times are converted into digital signals for each arm explored, and the EndoPat software automatically determines the hyperemic vascular response.

To avoid biases in the analysis of systemic vascular endothelial function in COVID-19 patients, the research team led by Dr. Amir Lerman from the Mayo Clinic, Rochester, USA will blindly carry out the analysis of the EndoPat results. For this, the EndoPat study reports will be sent in an analyzable format for each patient included in the study, completely anonymized and at blind fashion with respect to the group that patient belongs, the moment in which EndoPat assessment was made (days from the onset of symptoms in the case of the study group), blinded for the results of blood tests related to inflammation, and for the clinical evolution of the patient.

Conditions

COVID-19

Study Design

• Observational Model Type: CASE_CONTROL
• Study Time Perspective: PROSPECTIVE

Study Groups

Patients with active SARS-CoV-2 infection.

Patients admitted for COVID-19 at Hospital Clínico San Carlos with positive SARS-CoV-2 polymerase chain reaction (PCR).

No interventions assigned to this group

Patients with past, not active, SARS-CoV-2 infection.

Patients with past infection (not active), demonstrated by serology and PCR.

No interventions assigned to this group

People without concurrent or past SARS-CoV-2 infection

Health personnel from the Cardiology Service of Hospital Clínico San Carlos who demonstrate by serology that they have not had SARS-CoV-2 infection.

No interventions assigned to this group

Eligibility Criteria

Inclusion Criteria

• Study group No. 1: age ≥ 18 years; COVID-19 confirmed with positive PCR. Availability of informed consent.
• Study group No. 2: age ≥ 18 years; Past SARS-CoV-2 infection demonstrated by PCR and serology.
• Control group: age ≥ 18 years; absence of concurrent or previous SARS-CoV2 infection demonstrated by serology, and absence of acute or chronic diseases related to endothelial dysfunction, mainly acute or chronic infectious or inflammatory processes and known peripheral vascular disease.

Exclusion Criteria

• Impossibility of performing the endothelial function test.
• Recent puncture of the radial artery (<15 days).
• Hemodynamic instability.
• Unavailability of signed informed consent.

• Eligible Sex: ALL
• Accepts Healthy Volunteers: Yes

Sponsors

Mayo Clinic

OTHER

Sponsor Role: collaborator

Hospital San Carlos, Madrid

OTHER

Sponsor Role: lead

Responsible Party

Hernan D. Mejia-Renteria

Principal Investigator

Responsibility Role: PRINCIPAL_INVESTIGATOR

Locations

Mayo Clinic

Rochester, Minnesota, United States

Hospital Clínico San Carlos

Madrid, , Spain

Countries

United States; Spain

Other Identifiers

20/451

Identifier Type: -

Identifier Source: org_study_id