Objective: Quantitative Magnetic Resonance Imaging (MRI) holds great promise for the early detection of cartilage deterioration. Here, a Magnetic Resonance Fingerprinting (MRF) framework is proposed for comprehensive and rapid quantification of T ₁, T ₂ ^∗, and T _RAFF2 with whole-knee coverage. Methods: A MRF framework was developed to achieve quantification of Relaxation Along a Fictitious Field in the 2nd rotating frame of reference (T _RAFF2) along with T ₁ and T ₂ ^∗. The proposed sequence acquires 65 measurements of 25 high-resolution slices, interleaved with 7 inversion pulses and 40 RAFF2 trains, for whole-knee quantification in a total acquisition time of 3:25 min. Comparison with reference T ₁, T ₂ ^∗, and T _RAFF2 methods was performed in phantom and in seven healthy subjects at 3 T. Repeatability (test-retest) with and without repositioning was also assessed. Results: Phantom measurements resulted in good agreement between MRF and the reference with mean biases of -54, 2, and 5 ms for T ₁, T ₂ ^∗, and T _RAFF2, respectively. Complete characterization of the whole-knee cartilage was achieved for all subjects, and, for the femoral and tibial compartments, a good agreement between MRF and reference measurements was obtained. Across all subjects, the proposed MRF method yielded acceptable repeatability without repositioning (R ²≥ 0.94) and with repositioning (R ²≥ 0.57) for T ₁, T ₂ ^∗, and T _RAFF2. Significance: The short scan time combined with the whole-knee coverage makes the proposed MRF framework a promising candidate for the early assessment of cartilage degeneration with quantitative MRI, but further research may be warranted to improve repeatability after repositioning and assess clinical value in patients.

Magnetic Resonance Imaging (MRI) is the clinical gold standard for the assessment of myocardial viability but requires injection of exogenous gadolinium-based contrast agents. Recently, T1ρ-mapping has been proposed as a fully non-invasive alternative for imaging myocardial fibrosis without the need for contrast agent injection. However, its applicability at high fields is hindered by susceptibility to MRI system imperfections, such as inhomogeneities in the B0 and B1+ fields. In this work we propose a single breath-hold ECG-triggered single-shot bSSFP sequence to enable T1ρ-mapping in vivo at 3T. Adiabatic T1ρ preparations are evaluated to reduce B0 and B1+ sensitivity in comparison with conventional spin-lock (SL) modules. Numerical Bloch simulations were performed to identify optimal parameters for the adiabatic pulses. Experiments yield T1ρ values in the myocardium equal to 48.13±54.08 ms for the best adiabatic preparation and 16.01±20.75 ms for the reference non-adiabatic SL, with 26.91% against 89.74% relative difference in T1ρ values across two shimming conditions. Both phantom and in vivo measurements show increased myocardium/blood contrast and improved resilience against system imperfections compared to non-adiabatic T1ρ preparations, enabling the use at 3T. Clinical relevance- Adiabatically-prepared T1ρ-mapping sequences form a promising candidate for non-contrast evaluation of ischemic and non-ischemic cardiomyopathies at 3T.

Quantitative Magnetic Resonance Imaging (MRI) can enable early diagnosis of knee cartilage damage if imaging is performed during the application of load. Mechanical loading via ropes, pulleys and suspended weights can be obstructive and require adaptations to the patient table. In this paper, a new lightweight MRI-compatible elastic loading mechanism is introduced. The new device showed sufficient linearity (|α/β| = 0.42 ± 0.25), reproducibility (CoV = 5 ± 2%), and stability (CoV = 0.5 ± 0.1%). In vivo and ex vivo scans confirmed the ability of the device to exert sufficient force to study the knee cartilage under loading conditions, inducing up to a 29% decrease in T2 of the central medial cartilage. With this device mechanical loading can become more accessible for researchers and clinicians, thus facilitating the translational use of MRI biomarkers for the detection of cartilage deterioration.