Multi-modality Imaging & Immunophenotyping of COVID-19 Related Myocardial Injury
Overview
- Phase
- Not Applicable
- Intervention
- Not specified
- Conditions
- COVID19
- Sponsor
- University of Cambridge
- Enrollment
- 21
- Locations
- 1
- Primary Endpoint
- Diagnosis
- Status
- Completed
- Last Updated
- last year
Overview
Brief Summary
Cardiovascular involvement in coronavirus disease-2019 (COVID-19) encompasses a wide range of vascular and myocardial pathologies, including both acute and long-term sequelae. The MIIC-MI study aims to investigate mechanisms of cardiac injury in COVID-19 using multi-modality imaging and immunophenotyping to better understand the link with adverse patient outcomes.
Detailed Description
Cardiovascular involvement in coronavirus disease-2019 (COVID-19) encompasses a wide range of vascular and myocardial pathologies, including both acute and long-term sequelae. Cardiac Troponin elevation, a marker of acute myocardial injury, has been identified in up to 28% of hospitalized patients with coronavirus disease 2019 (COVID-19) and is associated with an increased mortality risk. However, the predominant aetiology of myocardial injury relating to COVID-19 remains unclear. The Troponin leak could either signify direct cardiac involvement in COVID-19 or serve as a non-specific marker of a severe systemic insult. There have been numerous reports of acute myocarditis in patients with COVID-19. Other contributory mechanisms of cardiac Troponin elevation in patients with COVID-19 that are also driven by a proinflammatory state include acute myocardial infarction due to atherosclerotic plaque rupture (type 1) or demand ischemia (type 2), endothelial and microvascular dysfunction, immune-mediated activation of coagulation and fibrinolytic systems, and stress cardiomyopathy. Longer-term effects of COVID-19 on the cardiovascular system are also unknown. Many individuals with post-acute sequalae of SARS-CoV-2 infection (or 'long COVID') have unexplained cardiac symptoms. Patients may also present with new-onset heart failure after COVID-19, which is not attributed to another cause. We aim to identify patterns of myocardial injury in COVID-19 using non-invasive multi-modality cardiac imaging, paired with cytokine/chemokine testing, immunophenotyping of peripheral blood cells and coagulation profiles. A better understanding of the mechanisms underlying the excess mortality risk attributable to myocardial injury in COVID-19 is needed and may help to improve patient care.
Investigators
Jason Tarkin
Wellcome Clinical Research Career Development Fellow
University of Cambridge
Eligibility Criteria
Inclusion Criteria
- •Patients \>18 years old
- •Confirmed COVID-19 infection AND Troponin I elevation \>99th percentile of upper reference limit OR new-onset heart failure OR unexplained cardiac symptoms
- •Able to give written, informed consent
Exclusion Criteria
- •Women of child-bearing potential not using adequate contraception
- •Contra-indication to MRI scanning
- •Contrast allergy or contrast-nephropathy
- •Chronic kidney disease (eGFR \<30 mL/min/1.73 m2)
- •Previous myocardial infarction
- •Uncontrolled atrial fibrillation
- •Uncontrolled chronic inflammatory disease
- •Severe lymphopenia (\<0.2 x109/L)
- •Treatment with immunomodulatory therapies within the last month (excluding inhaled or topical steroid therapy)
- •Any medical condition, in the opinion of the investigator, that prevents the participant from lying flat during scanning, or from participating in the study
Outcomes
Primary Outcomes
Diagnosis
Time Frame: Baseline
Number of participants with a diagnosis of COVID-19 related myocarditis, Type 1 or 2 myocardial infarction and/or other mechanism of cardiac injury confirmed by multi-modality imaging.
Secondary Outcomes
- Coagulation markers(Baseline)
- Immune markers(Baseline)