MRI of Aortic Atherosclerosis

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Imaging the aorta with MRI may have clinical usefulness (Fig. 2). Assessing and monitoring plaque burden in the aorta will allow for monitoring response to anti-atherosclerosis therapy. Aortic atherosclerosis has been previously show to be associated with a higher risk of ischemic stroke or cerebrovascular infarction (71-73). Additionally, plaque burden in the aorta may serve as a surrogate marker of systemic plaque burden. Furthermore, by imaging the aorta we may also gain screening information regarding aneurysms. The main difficulties in imaging the aorta lie in the thoracic aorta where respiratory motion and blood flow are nuisances and where it becomes a challenge to obtain submillimeter resolution for adequate sensitivity.

There has been an array of studies looking at atherosclerosis in the aorta. One such study looked at asymptomatic patients from the Framingham Heart Study. In that study, it was shown by MRI that the atherosclerotic plaque prevalence and burden increased significantly with age (74). Interestingly, they also found that in their study group there was greater burden of disease in the abdominal aorta than in the thoracic aorta (74). In a similar analysis, it was found that asymptomatic aortic atherosclerosis detected by MRI was strongly associated with the Framingham Heart Study coronary risk score and other long-term coronary risk factors (75). Taniguchi et al. recently used MRI to study the relationship between aortic atherosclerosis and risk factors for coronary artery disease (CAD) (76). They found that thoracic atherosclerosis was closely linked to traditional risk factors for CAD such as high cholesterol, age, and smoking (76).

Fayad et al. looked at atheromatous plaque in the thoracic aorta (Fig. 2). In that study, they used T1, T2 and proton-density weighted scans to evaluate plaque composition (77). Imaging was performed using rapid high-resolution fast-spin-echo sequence. Blood and blood flow artifacts were suppressed using velocity-selective flow suppression prepulses. In the same study, they compared MRI with transesophageal ultra-sonography/echocardiography (TEE) in the assessment of atherosclerosis. The results of the study showed that, based on cross-sectional imaging, MRI and TEE correlated strongly in terms of mean maximum plaque thickness and plaque composition (77).

Mri Atherosclerosis
Figure 2 MRI of aortic atherosclerosis. Axial and sagittal slices through the aorta showing a large atherosclerotic lesion (arrows point to the wall of the aorta; arrowheads point to the atherosclerotic plaque).

In another study, Summers et al. used MRI to demonstrate that, when compared to a control group of patients, the wall thickness of the ascending aorta is increased in patients with homozygous mutations leading to familial hypercholesterolemia (78). In this study, the plaque components could not be analyzed accurately because only Tl-weighted spin-echo images were acquired for the study.

In imaging atherosclerosis another application of MRI is the evaluation of regression subsequent to therapeutic interventions such as pharmacotherapy. Corti and Fayad et al. demonstrated that MRI could be used to evaluate the efficacy of cholesterol-lowering therapy using 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) in asymptomatic untreated patients with aortic and carotid atherosclerosis as well as elevated levels of low-density lipoprotein (LDL) (79). MRI was used to detect and assess aortic and carotid atherosclerosis in patients at different intervals following commencement of cholesterol-lowering therapy with simvastatin (HMG-CoA reductase inhibitor) (79,80). The results showed that MRI could be used to visualize and assess regression of atherosclerotic lesions following pharmacologic intervention (79). At 12 months, it was shown that there was a significant decrease in vessel wall area without a change in the vessel lumen area. These findings were in agreement with previous experimental animal research (81-83). Interestingly, there was a dramatic early decrease in LDL levels following initiation of treatment with simv-astatin. However, despite this finding a minimum of 12 months of therapy was needed in order to observe changes in vessel walls. Even at six months, no significant changes were observed. Recently, there have been a couple of MRI studies that have compared the effect of high and low doses of statins on atherosclerosis regression (84,85). Both of these studies used MRI to demonstrate that atherosclerosis regression was probably related more to the reduction in LDL rather than the dosage of the statin used (84,85).

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