Molecular Imaging of Coronary Plaque Vulnerability Using 18F-Fluorocholine PET-MRI in Patients with Coronary Artery
Jochem A J van der Pol1,2, Braim Rahel3, Yvonne J M van Cauteren4
1Department of Radiology & Nuclear Medicine, Maastricht University Medical Center, 6229 HX Maastricht, The Netherlands.
Abstract:
Background/Objectives: 18F-fluorocholine is a positron emission tomography (PET) tracer earlier found to be a marker of macrophage content in carotid plaques. We aimed to assess the feasibility of 18F-choline PET-MRI to non-invasively localize vulnerable coronary plaques, using optical coherence tomography (OCT) as a reference standard. Methods: Patients with recent myocardial infarction who were scheduled for a secondary angiography of a non-culprit vessel underwent 18F-fluorocholine coronary PET-MRI. Subsequently, OCT was performed during the secondary angiography. Maximum target-to-background (TBRmax) values of 18F-fluorocholine uptake were determined in two vessel sections that contained either vulnerable or stable plaques as defined by OCT. The OCT-based definition of a vulnerable plaque was a fibrous cap thickness < 70 µm. To enhance the detectability of coronary plaques using PET, three different motion-correction strategies were used: multigate respiratory gating motion correction (MRG-MOCO), extended MR-based motion correction (eMR-MOCO), and extended MR-based motion correction with ECG gating (eMR-MOCO-ECG). Results: Fifteen patients were included in this study. One patient needed to be excluded due to extravasation of the tracer. In another patient, no region with only a stable plaque could be identified. TBRmax values were as follows for three different reconstructions in vulnerable versus stable plaques: MRG-MOCO: mean TBRmax 1.45 vs. 1.35, p = 0.52 (n = 13); eMR-MOCO: mean TBRmax 1.47 vs. 1.27, p = 0.26 (n = 11); eMR-MOCO-ECG: mean TBRmax 1.49 vs. 1.26, p = 0.21 (n = 11). Conclusions: 18F-fluorocholine uptake in vulnerable atherosclerotic plaques in coronary arteries was not significantly different from uptake in stable plaques, even though advanced motion-correction methods were applied. That may be caused by multiple factors, such as small coronary plaque size, tracer biology, or remaining cardiac motion.
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