Myocardial Fibrosis, Myocardial Infarction
Conditions
Brief summary
The investigators here propose to investigate the timing and pattern of myocardial fibrosis activity following acute myocardial infarction using hybrid 68Ga-FAPI positron emission tomography and cardiovascular magnetic resonance. The investigators hypothesise that peak fibrosis activity will occur within 2-4 weeks of acute myocardial infarction and will predict subsequent scar formation and cardiac remodelling. Simultaneously, matrix remodelling and fibrosis activity in aortic and coronary atheroma will be assessed enabling the exploration of the presence of unstable atheroma.
Detailed description
Fibrosis is a fundamental process underlying almost all cardiomyopathic conditions. Established fibrosis can be detected by existing imaging techniques including cardiovascular magnetic resonance. However, these techniques are not specific for fibrosis and do not directly measure fibrosis activity or matrix remodelling. This limits the ability to detect early disease and differentiate active from end-stage phenotypes. Fibroblast activation protein is a key factor in fibrogenesis that is expressed in the myocardium following myocardial infarction and in thin-capped fibroatheroma. Radiolabelled fibroblast activation protein inhibitor (68Ga-FAPI) measures in vivo fibrosis activity and matrix remodelling, as supported by preliminary pilot studies. The timing and pattern of myocardial fibrosis activity following acute myocardial infarction will be investigated using hybrid 68Ga-FAPI positron emission tomography. The investigators hypothesise that peak fibrosis activity will occur within 2-4 weeks of acute myocardial infarction and will predict subsequent scar formation and cardiac remodelling. Simultaneously, matrix remodelling and fibrosis activity in aortic and coronary atheroma will also be assessed allowing exploration of the presence of unstable atheroma. This project will enhance understanding of fibrosis activity and matrix remodelling in myocardial infarction and unstable atherosclerotic plaque with potential future application to a broad range of cardiovascular diseases.
Interventions
RADIATION68Gallium FAPI PET/MR scan
68Gallium FAPI PET/MR scan
Sponsors
University of Edinburgh
Study design
Observational model
COHORT
Time perspective
PROSPECTIVE
Eligibility
Sex/Gender
ALL
Age
50 Years to No maximum
Healthy volunteers
Yes
Inclusion criteria
* specific to cohort; * aged 50 years or older
Exclusion criteria
* Claustrophobia * Inability to undergo MRI * eGFR \<30ml/min/1.73\^m2
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Time of maximal fibrosis activity following myocardial infarction | 12 weeks | SUVmax and TBR of 68Ga-FAPI uptake within the infarct, border zone, and remote myocardium |
| Whether fibrosis activity predicts myocardial scar volume and ventricular remodelling | 12 months | As measured by CMR 12 months following acute MI |
| Fibrosis activity and myocardial remodelling within atherosclerotic plaque in patients with myocardial infarct | 12 weeks | SUVmax and TBR of 68Ga-FAPI uptake within areas of atherosclerotic plaque in the aorta and/or carotid arteries |
Countries
United Kingdom
Outcome results
None listed