The Role of Adaptive Immunity in COVID-19 Associated Myocardial Injury

Withdrawn

• Conditions: Cardiovascular Disease Acute; COVID; Cardiomyopathies

• Registration Number: NCT04340921
• Lead Sponsor: Barts & The London NHS Trust

Brief Summary

COVID-19 is associated with complications including ARDS and myocardial injury, which informs prognosis and patient outcome. The laboratory plans to perform immunophenotyping of peripheral T-cells in patients with COVID-19 and complications (ARDS, ITU admission, myocardial injury) and map this against clinical patient outcomes. The aim is to determine if there is a specific T-cell immunophenotype associated with COVID-19 and/or complications, which can be used to inform prognosis and potential therapies.

Detailed Description

Infection with the novel coronavirus COVID-19 is designated a pandemic by the World Health Organisation (WHO).COVID-19 infection can result in severe lung inflammation which, when present, dominates the clinical course for most patients. However, other organs may also be involved and the cardiovascular (CV) system appears to have complex interactions with COVID-19. Published reports suggest evidence of heart muscle damage in 20-40% of hospitalised cases presenting as cardiac chest pain, heart failure, abnormal heart rhythms and cardiac death.

Many affected were previously well, but approximately half of those admitted to hospital COVID-19 have other medical problems, increasing in those requiring ITU admission or those that died. Patients with pre-existing CV conditions have some of the worst outcomes. Although pre-existing disorders reduce an individual's capacity to withstand severe illness, it is also likely that CV diseases may increase the risk of developing complicated COVID-19 disease. Our hypothesis is that immunological abnormalities acquired as a consequence of pre-existing disorders is responsible for this.

A question central to potential therapeutic options is the extent to which COVID-19 related myocardial injury results from viral replication (cytopathic), is immune mediated or is due to other mechanisms. Given that rapid onset cardiac injury can occur at 7-14 days after onset of COVID symptoms we propose to evaluate the contribution of adaptive T-cell mediated immunity in patients with and without myocardial injury. If successful, we may be able to identify treatments that suppress discrete components of the immune system to prevent myocardial damage without depressing protective immune function.

Study Timeline

• Study First Submitted: 2020-04-03
• Study First Submitted QC: 2020-04-07
• Study First Posted: 2020-04-10
• Study Start: 2020-05-14
• Status Verified: 2023-04
• Primary Completion: 2023-04-14
• Study Completion: 2023-04-14
• Last Update Submitted: 2023-04-19
• Last Update Posted: 2023-04-21

Recruitment & Eligibility

• Status: WITHDRAWN
• Sex: All
• Target Recruitment: Not specified

Inclusion Criteria

Not provided

Exclusion Criteria

Not provided

Study & Design

• Study Type: OBSERVATIONAL
• Study Design: Not specified

Primary Outcome Measures

Name	Time	Method
T-cell immunophenotype	12 months from enrollment	T-cell immunophenotype

Secondary Outcome Measures

Name	Time	Method
ITU admission	12 months from enrolment	Admission to the intensive care
Mortality	12 months from enrolment	death, survival to discharge
Myocardial injury	12 months from enrolment	Defined by troponin rise to \>99th centile

Trial Locations

Locations (1)

Barts Health Nhs Trust; 🇬🇧 London, United Kingdom