A new MRI method is proposed for separately quantifying the two principal forms of tissue storage (nonheme) iron: ferritin iron, a dispersed, soluble fraction that can be rapidly mobilized, and hemosiderin iron, an aggregated, insoluble fraction that serves as a long-term reserve. The method utilizes multiple spin echo sequences, exploiting the fact that aggregated iron can induce nonmonoexponential signal decay for multiple spin echo sequences. The method is validated in vitro for agarose phantoms, simulating dispersed iron with manganese chloride, and aggregated iron with iron oxide microspheres. To demonstrate feasibility for human studies, preliminary in vivo data from two healthy controls and six patients with transfusional iron overload are presented. For both phantoms and human subjects, conventional R 2 and R 2 * relaxation rates are also measured in order to contrast the proposed method with established MRI iron quantification techniques. Quantification of dispersed (ferritin-like) iron may provide a new means of monitoring the risk of iron-induced toxicity in patients with iron overload and, together with quantification of aggregated (hemosiderin-like) iron, improve the accuracy of estimates for total storage iron.

Purpose:To investigate the feasibility of measuring myocardial T2 at 3 Tesla for assessment of tissue iron in thalassemia major and other iron overloaded patients. Materials and Methods:A single-breathhold electrocardiogram-triggered black-blood multi-echo spin-echo (MESE) sequence with a turbo factor of 2 was implemented at 3 Tesla (T). Myocardial and liver T2 values were measured with three repeated breathholds in 8 normal subjects and 24 patients. Their values, together with the T2* values measured using a breathhold multi-echo gradient-echo sequence, were compared with those at 1.5T in the same patients.Results: At 3T, myocardial T2 was found to be 39.6 Ϯ 7.4 ms in normal subjects. In patients, it ranged from 12.9 to 50.1 ms. T2 and T2* were observed to correlate in heart ( ϭ 0.93, Ͻ 0.0001) and liver (P ϭ 0.95, P Ͻ 0.0001). Myocardial T2 and T2* at 3T were also highly correlated with the 1.5T measurements. Preliminary results indicated that myocardial T2 quantitation was relatively insensitive to B1 variation, and reproducible with 3.2% intra-exam and 3.8% inter-exam variations. Conclusion:Myocardial T2 quantitation is feasible at 3T. Given the substantially decreased T2* and increased B0 inhomogeneity, the rapid myocardial T2 measurement protocol demonstrated here may present a robust alternative to study cardiac iron overload at 3T.

Myocardial Elastography (ME), a radio-frequency (RF) based speckle tracking technique, was employed in order to image the entire two-dimensional (2D) transmural deformation field in full view, and validated against tagged Magnetic Resonance Imaging (tMRI) in normal as well as reperfused (i.e., treated myocardial infarction (MI)) human left ventricles. RF ultrasound and tMRI frames were acquired at the papillary muscle level in 2D short-axis (SA) views at nominal frame rates of 136 (fps; real time) and 33 fps (electrocardiogram (ECG)-gated), respectively. In ultrasound, in-plane, 2D (lateral and axial) incremental displacements were iteratively estimated using one-dimensional (1D) cross-correlation and recorrelation techniques in a 2D search with a 1D matching kernel. In tMRI, cardiac motion was estimated by a template-matching algorithm on a 2D grid-shaped mesh. In both ME and tMRI, cumulative 2D displacements were estimated and then used to estimate 2D Lagrangian finite systolic strains, from which polar (i.e., radial and circumferential) strains, namely angle-independent measures, were further obtained through coordinate transformation. Principal strains, which are angle-independent and less centroid-dependent than polar strains, were also computed and imaged based on the 2D finite strains with a previously established strategy. Both qualitatively and quantitatively, angle-independent ME is shown to be capable of 1) estimating myocardial deformation in good agreement with tMRI estimates in a clinical setting and of 2) differentiating abnormal from normal myocardium in a full left-ventricular view. Finally, the principal strains are suggested to be an alternative diagnostic tool of detecting cardiac disease with the characteristics of their reduced centroid dependence.

Visualization of the major intracranial arteries was comparable with 3.0- and 7.0-T scanners; the 7.0-T scanner was superior for visualizing smaller vessels. Results indicated that ToF-MRA is an easily performed imaging technique that can be included as part of a standard magnetic resonance imaging examination and should be included in the imaging protocol of dogs suspected of having cerebrovascular disease.

With transfusional iron overload, almost all the excess iron is sequestered intracellularly as rapidly mobilizable, dispersed, soluble, ferritin iron, and as aggregated, insoluble hemosiderin iron for longterm storage. Established magnetic resonance imaging (MRI) indicators of tissue iron (R2, R2*) are principally influenced by hemosiderin iron and change slowly, even with intensive iron chelation. Intracellular ferritin iron is evidently in equilibrium with the low-molecular-weight cytosolic iron pool that can change rapidly with iron chelation. We have developed a new magnetic resonance imaging (MRI) method to separately measure ferritin and hemosiderin iron, based on the nonmonoexponential signal decay induced by aggregated iron in multiple-spin-echo sequences. We have initially validated the method in agarose phantoms and in human liver explants and shown the feasibility of its application in patients with thalassemia major. Measurement of tissue ferritin iron is a promising new means to rapidly evaluate the effectiveness of iron-chelating regimens.