Findings from in vitro studies demonstrated the ability of MRI to identify various plaque components [65, 66] and T2-weighted sequences have shown promise for the differentiation of plaque components [65, 67]. Serfaty et al.  used T2-weighted MR imaging to measure fibrous cap thickness and lipid core volume. Unfortunately, their ex vivo study was limited by overestimation of the lipid core. Shinnar et al.  suggested the use of two echo times to differentiate the lipid core from fibrocellular areas that contain lipid. However, one limitation of T2-weighted MR imaging is an inherently low SNR. In vivo application of these techniques is supported by the strong agreement demonstrated between in vivo and ex vivo measurements of vessel wall thickness and T2 relaxation of plaque components [69, 70]. Wasserman et al.  used gadolinium (Gd) in combination with Tl-weighted MRI to describe plaque morphology and demonstrated not only that delayed hyperenhancement preferentially occurs in fibrocellular tissue, but also that SNR is substantially enhanced compared to T2-weighted imaging. Similar results were reported by Yuan et al.  who showed that the strongest MRI signal enhancement was observed in fibrocellular tissue and that only modest contrast agent uptake occurred in the lipid core of the carotid vessel wall. A study by Jaffer et al. , which included participants who were free of clinically apparent coronary disease, revealed evidence of aortic atherosclerosis in 38% of the women and 41% of the men. Atherosclerotic prevalence was more apparent in the abdominal than in the thoracic aorta. These data demonstrate the ability of MR vessel wall imaging to detect subclinical atherosclerotic disease, and to better risk stratify patients with asymptomatic heart disease. However, it should be noted that all these studies were performed under ex vivo conditions, in animal models, or in the carotids or aorta as a surrogate for in vivo human coronary arteries, and that a clear correlation between carotid/aortic plaque and coronary events has not been established [73, 74]. Together with the current understanding that luminal disease underestimates plaque burden and that the majority of acute coronary syndromes occur at sites without previously flow-limiting stenoses (<50%) [60,75], this demonstrates a clear need for an imaging method that allows direct and non-invasive access to the coronary or bypass graft vessel wall. However, coronary vessel lumen, and, especially wall imaging, are among the most challenging tasks for cardiovascular MRI. There are specific technical difficulties that have hampered the transfer of carotid or aortic plaque imaging approaches to the coronary vessel wall. These include the small dimensions (0.5-2mm) of the coronary vessel wall, a very complex geometry, cardiac and respiratory motion, and the proximity of the coronary artery walls to epicardial fat and coronary blood. As discussed above, recent advances in MRI hardware and new imaging software have made it possible to visualize the native coronary artery vessel wall in selected cases [58, 59, 76]. However, limited spatial resolution still hampers further progress and limits the accuracy and sensitivity of quantitative measurements . A major step forward is expected with the availability of higher spatial resolution on 3T MRI systems and by simultaneously taking advantage of vessel wall hyperenhancement after contrast injection.
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