Background: Cardiovascular magnetic resonance (CMR) T1ρ mapping can be used to detect ischemic or nonischemic cardiomyopathy without the need of exogenous contrast agents. Current 2D myocardial T1ρ mapping requires multiple breath-holds and provides limited coverage. Respiratory gating by diaphragmatic navigation has recently been exploited to enable free-breathing 3D T1ρ mapping, which, however, has low acquisition efficiency and may result in unpredictable and long scan times. This study aims to develop a fast respiratory motioncompensated 3D whole-heart myocardial T1ρ mapping technique with high spatial resolution and predictable scan time. Methods: The proposed electrocardiogram (ECG)-triggered T1ρ mapping sequence is performed under freebreathing using an undersampled variable-density 3D Cartesian sampling with spiral-like order. Preparation pulses with different T1ρ spin-lock times are employed to acquire multiple T1ρ-weighted images. A saturation prepulse is played at the start of each heartbeat to reset the magnetization before T1ρ preparation. Image navigators are employed to enable beat-to-beat 2D translational respiratory motion correction of the heart for each T1ρ-weighted dataset, after which, 3D translational registration is performed to align all T1ρ-weighted volumes. Undersampled reconstruction is performed using a multi-contrast 3D patch-based low-rank algorithm. The accuracy of the proposed technique was tested in phantoms and in vivo in 11 healthy subjects in comparison with 2D T1ρ mapping. The feasibility of the proposed technique was further investigated in 3 patients with suspected cardiovascular disease. Breath-hold late-gadolinium enhanced (LGE) images were acquired in patients as reference for scar detection. Results: Phantoms results revealed that the proposed technique provided accurate T1ρ values over a wide range of simulated heart rates in comparison to a 2D T1ρ mapping reference. Homogeneous 3D T1ρ maps were obtained for healthy subjects, with septal T1ρ of 58.0 ± 4.1 ms which was comparable to 2D breath-hold measurements (57.6 ± 4.7 ms, P = 0.83). Myocardial scar was detected in 1 of the 3 patients, and increased T1ρ values (87.4 ± 5.7 ms) were observed in the infarcted region. Conclusions: An accelerated free-breathing 3D whole-heart T1ρ mapping technique was developed with high respiratory scan efficiency and near-isotropic spatial resolution (1.7 × 1.7 × 2 mm 3) in a clinically feasible scan time of~6 mins. Preliminary patient results suggest that the proposed technique may find applications in non-contrast myocardial tissue characterization.

Background The immune system orchestrates the repair of infarcted myocardium. Imaging of the cellular inflammatory response by 18F-FDG PET/MRI in the heart has been demonstrated in preclinical and clinical studies. However, the clinical relevance of post-MI 18F-FDG uptake in the heart has not been elucidated. The objective of this study was to explore the value of 18F-FDG-PET/MRI in patients after AMI as a biosignal for left ventricular functional outcome. Methods and Results We prospectively enrolled 49 patients with STEMI and performed 18F-FDG-PET/MRI 5 days after PCI and follow-up cardiac MRI after 6–9 months. In a subset of patients, 99mTc-sestamibi-SPECT was performed with tracer injection prior to revascularization. Cellular innate immune response was analyzed at multiple time points. Segmental comparison of 18F-FDG-uptake and LGE showed substantial overlap (κ=0.66), while quantitative analysis demonstrated that 18F-FDG extent exceeded LGE extent (33.2±16.2 %LV vs. 20.4±10.6 %LV, p<0.0001) and corresponded to the area-at-risk (r=0.87, p<0.0001). The peripheral blood count of CD14high/CD16+ monocytes correlated with the infarction size and 18F-FDG signal extent (r=0.53, p<0.002 and r=0.42, p<0.02, respectively). 18F-FDG uptake in the infarcted myocardium was highest in areas with transmural scar and the SUVmean was associated with left ventricular functional outcome independent of infarct size (ΔEF: p<0.04, ΔEDV: p<0.02, ΔESV: p<0.005). Conclusions In the current study, the intensity of 18F-FDG uptake in the myocardium after AMI correlated inversely with functional outcome at 6 months. Thus, 18F-FDG uptake in infarcted myocardium may represent a novel biosignal of myocardial injury.