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| ID | Type | Description | Link |
|---|---|---|---|
| E202251 | Other Identifier | University of Edinburgh |
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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.
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.
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| Label | Type | Description | Intervention Names |
|---|---|---|---|
| Healthy volunteers | Age- and sex- matched to participants, those aged 50 or over without known heart disease. n=20 |
| |
| Acute myocardial infarction - multi-timepoint imaging | Those aged 50 or over with recent myocardial infarction who will be imaged using PET/MR at 1,2,4, and 12 weeks post-MI. n=20 |
| |
| Acute or chronic myocardial infarction - single timepoint imaging | Those aged 50 or over with recent (n=20) or prior established (>24 months, n=20) myocardial infarction who will be imaged at a single timepoint (1,2,4, or 12 weeks post-MI for acute, at the time of enrolement to the study for chronic). |
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| Name | Type | Description | Arm Group Labels | Other Names |
|---|---|---|---|---|
| 68Gallium FAPI PET/MR scan | Radiation | 68Gallium FAPI PET/MR scan |
|
| Measure | Description | Time Frame |
|---|---|---|
| Time of maximal fibrosis activity following myocardial infarction | SUVmax and TBR of 68Ga-FAPI uptake within the infarct, border zone, and remote myocardium | 12 weeks |
| Whether fibrosis activity predicts myocardial scar volume and ventricular remodelling | As measured by CMR 12 months following acute MI | 12 months |
| Fibrosis activity and myocardial remodelling within atherosclerotic plaque in patients with myocardial infarct | SUVmax and TBR of 68Ga-FAPI uptake within areas of atherosclerotic plaque in the aorta and/or carotid arteries | 12 weeks |
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Inclusion Criteria:
Exclusion Criteria:
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Healthy volunteer participants (cohort 1, n=20): those without significant or serious comordibity or known cardiac disease
Participants with acute myocardial infarction (cohorts 2 and 3, n=40): ST-elevation myocardial infarction within 3 weeks of enrollment
Participants with chronic myocardial infarction (n=20): ST-elevation myocardial infarction 24 months or more prior to enrollment
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| Facility | Status | City | State | ZIP | Country | Contacts |
|---|---|---|---|---|---|---|
| Royal Infirmary of Edinburgh | Edinburgh | City Of Edinburgh | EH16 4SA | United Kingdom |
| PubMed Identifier | Type | Citation | Retractions |
|---|---|---|---|
| 39772364 | Derived | Barton AK, Craig NJ, Loganath K, Joshi S, Tsampasian V, Mahendran M, Lenell J, Tzolos E, Singh T, Whittington B, Nash J, Williams MC, van Beek EJR, MacAskill MG, Berkeley B, Vezaides S, Brittan M, Baker AH, Sellers S, Fletcher A, Clark T, Waight C, Slart RHJA, Berman D, Dey D, Slomka P, Newby DE, Dweck MR. Myocardial Fibroblast Activation After Acute Myocardial Infarction: A Positron Emission Tomography and Magnetic Resonance Study. J Am Coll Cardiol. 2025 Feb 18;85(6):578-591. doi: 10.1016/j.jacc.2024.10.103. Epub 2025 Jan 8. |
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| ID | Term |
|---|---|
| D009203 | Myocardial Infarction |
| ID | Term |
|---|---|
| D017202 | Myocardial Ischemia |
| D006331 | Heart Diseases |
| D002318 | Cardiovascular Diseases |
| D014652 | Vascular Diseases |
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Blood draw for all participants with recent or prior established myocardial infarction at each attendance for PET/MR scanning
| D007238 |
| Infarction |
| D007511 | Ischemia |
| D010335 | Pathologic Processes |
| D013568 | Pathological Conditions, Signs and Symptoms |
| D009336 | Necrosis |