Actively-shielded ultrahigh field MRI/NMR superconducting magnet design

Active shielding technology has been widely applied to the superconducting magnetic resonance imaging (MRI) and nuclear magnetic resonance (NMR) magnets design, revealing excellent performance on the stray field control. For such a highly homogeneous field superconducting magnet design, an appropriate optimization strategy is essential to guarantee the magnetic field homogeneity in the central region and the expected 5 Gauss line range, especially for the ultrahigh field superconducting magnet. Based on the compensating field optimization method, an actively-shielded whole-body 14T MRI magnet and an actively-shielded 1.3GHz NMR magnet were presented, and detailed analyses were conducted to evaluate the feasibility of the designs. The developed magnet design method, coil pattern, wire arrangement, and stress/strain adjustment will be used to guide the corresponding project implementation.

Interelement Decoupling Strategies at UHF MRI

Moving to the ultrahigh field magnetic resonance imaging (UHF MRI) brought many benefits such as potentially higher signal-to-noise ratio, contrast-to-noise ratio, and improved spectral resolution. The UHF MRI regime also introduced some challenges which could prevent full exploitation of mentioned advantages. A higher static magnetic field means increase in Larmor frequency, which further implies the shorter wavelength in a tissue. The shorter wavelength causes interferences of the RF signal and inhomogeneous excitation, which can be partially resolved by the introduction of the multichannel coil arrays. The biggest problem in UHF multichannel densely populated arrays is the existence of the interelement coupling, which should be minimized as much as possible. This article presents the nonconventional, recently developed decoupling techniques used in UHF MRI.

Ultrahigh-field cardiovascular magnetic resonance T1 and T2 mapping for the assessment of anthracycline-induced cardiotoxicity in rat models: validation against histopathologic changes

Background Chemotherapy-induced cardiotoxicity is a well-recognized adverse effect of chemotherapy. Quantitative T1-mapping cardiovascular magnetic resonance (CMR) is useful for detecting subclinical myocardial changes in anthracycline-induced cardiotoxicity. The aim of the present study was to histopathologically validate the T1 and T2 mapping parameters for the evaluation of diffuse myocardial changes in rat models of cardiotoxicity. Methods Rat models of cardiotoxicity were generated by injecting rats with doxorubicin (1 mg/kg, twice a week). CMR was performed with a 9.4 T ultrahigh-field scanner using cine, pre-T1, post-T1 and T2 mapping sequences to evaluate the left ventricular ejection fraction (LVEF), native T1, T2, and extracellular volume fraction (ECV). Histopathological examinations were performed and the association of histopathological changes with CMR parameters was assessed. Results Five control rats and 36 doxorubicin-treated rats were included and classified into treatment periods. In the doxorubicin-treated rats, the LVEF significantly decreased after 12 weeks of treatment (control vs. 12-week treated: 73 ± 4% vs. 59 ± 9%, P = 0.01). Increased native T1 and ECV were observed after 6 weeks of treatment (control vs. 6-week treated: 1148 ± 58 ms, 14.3 ± 1% vs. 1320 ± 56 ms, 20.3 ± 3%; P = 0.005, < 0.05, respectively). T2 values also increased by six weeks of treatment (control vs. 6-week treated: 16.3 ± 2 ms vs. 10.3 ± 1 ms, P < 0.05). The main histopathological features were myocardial injury, interstitial fibrosis, inflammation, and edema. The mean vacuolar change (%), fibrosis (%), and inflammation score were significantly higher in 6-week treated rats than in the controls (P = 0.03, 0.03, 0.02, respectively). In the univariable analysis, vacuolar change showed the highest correlation with native T1 value (R = 0.60, P < 0.001), and fibrosis showed the highest correlation with ECV value (R = 0.78, P < 0.001). In the multiple linear regression analysis model, vacuolar change was a significant factor for change in native T1 (P = 0.01), and vacuolar change and fibrosis were significant factors for change in ECV (P = 0.006, P < 0.001, respectively) by adding other histopathological parameters (i.e., inflammation and edema scores) Conclusions Quantitative T1 and T2 mapping CMR is a useful non-invasive tool reflecting subclinical histopathological changes in anthracycline-induced cardiotoxicity.