Vascular Inflammation Imaging Using Somatostatin Receptor Positron Emission Tomography (VISION)
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|ClinicalTrials.gov Identifier: NCT02021188|
Recruitment Status : Completed
First Posted : December 27, 2013
Last Update Posted : August 24, 2016
|Condition or disease|
|Atherosclerosis Stroke Transient Ischemic Attack Chronic Stable Angina Acute Coronary Syndrome|
Clinical events in atherosclerosis are largely driven by inflammation. Molecular imaging of atherosclerosis can potentially identify high-risk lesions, help guide treatment and illuminate the underlying biology of the disease. 18F-fluorodeoxyglucose (18F-FDG) PET is the gold-standard nuclear molecular imaging technique with well-established roles in atherosclerosis imaging. However, the arterial 18F-FDG signal is non-specific, although it is related to increased macrophage activity with contributions from hypoxia and angiogenesis. Coronary artery imaging with 18F-FDG is particularly difficult, mainly due to high background myocardial cell 18F-FDG uptake, which obscures interpretation of the coronary signal. Efforts to suppress myocardial 18F-FDG uptake with dietary manipulation are challenging for patients and have limited efficacy.
PET tracers currently used in cancer imaging, such as 68Ga-DOTATATE, are potentially more specific for inflammation and also lack myocardial muscle uptake. 68Ga-DOTATATE might therefore be better suited than 18F-FDG for imaging inflammation, particularly within the coronary arteries. The VISION study is a prospective, observational study designed to investigate the biology of plaque inflammation in atherosclerosis, using PET imaging with the somatostatin receptor ligand 68Ga-DOTATATE. 50 subjects with atherosclerosis will undergo sequential PET/CT imaging with 68Ga-DOTATATE and 18F-FDG, along with contrast angiography of the carotid and coronary arteries. Autoradiography and immunohistochemistry of excised carotid plaques will be used to validate the imaging data. If successful, 68Ga-DOTATATE imaging will offer a cheaper, more specific non-invasive measure of inflammation than 18F- FDG, particularly in the coronary arteries. This opens up the possibility of better risk stratification for patients with atherosclerosis and could provide a non-invasive platform to test the effects of novel anti-atherosclerosis drugs.
|Study Type :||Observational|
|Actual Enrollment :||42 participants|
|Official Title:||The Vascular Inflammation Imaging Using Somatostatin Receptor Positron Emission Tomography Study|
|Study Start Date :||August 2014|
|Actual Primary Completion Date :||August 2016|
|Actual Study Completion Date :||August 2016|
Carotid artery disease
Participants with symptomatic or asymptomatic carotid artery plaques
Coronary artery disease
Participants with stable coronary artery disease or recent acute coronary syndrome
- Correlation of 68Ga-DOTATATE PET signal to carotid plaque inflammation [ Time Frame: Baseline ]This primary outcome measure is correlation between carotid artery 68Ga-DOTATATE PET signal (TBR) and the underlying degree of carotid inflammation, measured by CD68 immunohistochemistry, in patients undergoing carotid endarterectomy.
- Comparison of 68Ga-DOTATATE signal between symptomatic and asymptomatic carotid plaques [ Time Frame: Baseline (<1 month from event) ]
- Correlation of carotid artery and coronary artery 68Ga-DOTATATE uptake [ Time Frame: Baseline ]
- Correlation of Framingham Cardiovascular Risk Scores to arterial 68Ga-DOTATATE uptake [ Time Frame: Baseline ]
- Correlation between carotid artery 68Ga-DOTATATE autoradiographic signal and degree of carotid inflammation, measured by CD68 immunohistochemistry [ Time Frame: Baseline ]
- Comparison of myocardial 68Ga-DOTATATE and 18F-FDG uptake [ Time Frame: Baseline (2 scans within 1 week) ]
Biospecimen Retention: Samples With DNA
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT02021188
|Cambridge University Hospitals NHS Foundation Trust|
|Cambridge, Cambridgeshire, United Kingdom, CB2 0QQ|
|Principal Investigator:||James HF Rudd, PhD, FRCP||University of Cambridge|