Myocardial infarction and stroke are the most prevalent global causes of death. Each year 15 million people worldwide die due to myocardial infarction or stroke. Rupture of a vulnerable atherosclerotic plaque is the main underlying cause of stroke and myocardial infarction. Key features of a vulnerable plaque are inflammation, a large lipid-rich necrotic core (LRNC) with a thin or ruptured overlying fibrous cap, and intraplaque hemorrhage (IPH). Noninvasive imaging of these features could have a role in risk stratification of myocardial infarction and stroke and can potentially be utilized for treatment guidance and monitoring. The recent development of hybrid PET/MRI combining the superior soft tissue contrast of MRI with the opportunity to visualize specific plaque features using various radioactive tracers, paves the way for comprehensive plaque imaging. In this review, the use of hybrid PET/MRI for atherosclerotic plaque imaging in carotid and coronary arteries is discussed. The pros and cons of different hybrid PET/MRI systems are reviewed. The challenges in the development of PET/MRI and potential solutions are described. An overview of PET and MRI acquisition techniques for imaging of atherosclerosis including motion correction is provided, followed by a summary of vessel wall imaging PET/MRI studies in patients with carotid and coronary artery disease. Finally, the future of imaging of atherosclerosis with PET/ MRI is discussed.

BACKGROUND AND PURPOSE: Intraplaque hemorrhage contributes to lipid core enlargement and plaque progression, leading to plaque destabilization and stroke. The mechanisms that contribute to the development of intraplaque hemorrhage are not completely understood. A higher incidence of intraplaque hemorrhage and thin/ruptured fibrous cap (upstream of the maximum stenosis in patients with severe [$70%] carotid stenosis) has been reported. We aimed to noninvasively study the distribution of intraplaque hemorrhage and a thin/ruptured fibrous cap in patients with mild-to-moderate carotid stenosis.MATERIALS AND METHODS: Eighty-eight symptomatic patients with stroke (,70% carotid stenosis included in the Plaque at Risk study) demonstrated intraplaque hemorrhage on MR imaging in the carotid artery plaque ipsilateral to the side of TIA/stroke. The intraplaque hemorrhage area percentage was calculated. A thin/ruptured fibrous cap was scored by comparing pre-and postcontrast black-blood TSE images. Differences in mean intraplaque hemorrhage percentages between the proximal and distal regions were compared using a paired-samples t test. The McNemar test was used to reveal differences in proportions of a thin/ruptured fibrous cap. RESULTS:We found significantly larger areas of intraplaque hemorrhage in the proximal part of the plaque at 2, 4, and 6 mm from the maximal luminal narrowing, respectively: 14.4% versus 9.6% (P ¼ .04), 14.7% versus 5.4% (P , .001), and 11.1% versus 2.2% (P ¼ .001). Additionally, we found an increased proximal prevalence of a thin/ruptured fibrous cap on MR imaging at 2, 4, 6, and 8 mm from the MR imaging section with the maximal luminal narrowing, respectively: 33.7% versus 18.1%, P ¼ .007; 36.1% versus 7.2%, P , .001; 33.7% versus 2.4%, P ¼ .001; and 30.1% versus 3.6%, P ¼ .022. CONCLUSIONS:We demonstrated that intraplaque hemorrhage and a thin/ruptured fibrous cap are more prevalent on the proximal side of the plaque compared with the distal side in patients with mild-to-moderate carotid stenosis. ABBREVIATIONS: FC ¼ fibrous cap; IPH ¼ intraplaque hemorrhage; QIR TSE ¼ quadruple inversion recovery turbo spin-echo; TRFC ¼ thin/ruptured fibrous cap R upture of a vulnerable atherosclerotic plaque is an important underlying cause of myocardial infarction and stroke. 1 Noninvasive visualization of plaque vulnerability has demonstrated that intraplaque hemorrhage (IPH) contributes to enlargement of the lipid core and plaque progression, leading to plaque destabilization. 2,3 Indeed, we and others have demonstrated that IPH on MR imaging is a strong predictor of future cerebrovascular events. [4][5][6] This finding has led to the recognition of IPH as a key marker and pathologic factor contributing to plaque vulnerability.

Carotid radiofrequency coils inside a PET/MRI system can result in PET quantification errors. We compared the performance of a dedicated PET/MRI carotid coil against a coil for MRI-only use. An 18F-fluorodeoxyglucose (18F-FDG) phantom was scanned without and with an MRI-only coil and with the PET/MRI coil. The decay-corrected normalized activity was compared for the different coil configurations. Eighteen patients were scanned with the three coil configurations. The maximal standardized uptake values (SUVmax) and signal-to-noise ratios (SNR) were calculated. Repeated measures ANOVA was performed to assess the differences in SUVmax and SNR between the coil configurations. In the phantom study, the PET/MRI coil demonstrated a slight decrease (<5%), while the MRI-only coil showed a substantial decrease (up to 10%) in normalized activity at the position of coil elements compared to no dedicated coil configuration. In the patient study, the SUVmax values for both no surface coil (3.59 ± 0.15) and PET/MRI coil (3.54 ± 0.15) were significantly higher (p = 0.03 and p = 0.04, respectively) as compared to the MRI-only coil (3.28 ± 0.16). No significant difference was observed between PET/MRI and no surface coil (p = 1.0). The SNR values for both PET/MRI (7.31 ± 0.44) and MRI-only (7.62 ± 0.42) configurations demonstrated significantly higher (p < 0.001) SNR values as compared to the no surface coil (3.78 ± 0.22), while no significant difference was observed in SNR between the PET/MRI and MRI-only coil (p = 1.0). This study demonstrated that the PET/MRI coil can be used for PET imaging without requiring attenuation correction while acquiring high-resolution MR images.