Purpose To develop a heart-rate independent breath-held joint T1-T2 mapping sequence for accurate simultaneous estimation of co-registered myocardial T1 and T2 maps. Methods A novel preparation scheme combining both a saturation pulse and T2-preparation in a single R-R interval is introduced. The time between these two pulses, as well as the duration of the T2-preparation is varied in each heartbeat, acquiring images with different T1 and T2 weightings, and no magnetization dependence on previous images. Inherently co-registered T1 and T2 maps are calculated from these images. Phantom imaging is performed to compare the proposed maps to spin echo references. In vivo imaging is performed in ten subjects, comparing the accuracy and precision of the proposed technique to existing myocardial T1 and T2 mapping sequences of the same duration. Results Phantom experiments show that the proposed technique provides accurate quantification of T1 and T2 values over a wide-range (T1: 260ms to 1460ms, T2: 40ms to 200ms). In vivo imaging shows that the proposed sequence quantifies T1 and T2 values similar to a saturation-based T1 mapping and a conventional breath-hold T2 mapping sequence, respectively. Conclusion The proposed sequence allows joint estimation of accurate and co-registered quantitative myocardial T1 and T2 maps in a single breath-hold.

Objective: We sought to investigate the association of the EAT with CMR parameters of ventricular remodelling and left ventricular (LV) dysfunction in patients with non-ischemic dilated cardiomyopathy (DCM). Design and Methods: One hundred and fifty subjects (112 consecutive patients with DCM and 48 healthy controls) underwent CMR examination. Function, volumes, dimensions, the LV remodelling index (LVRI), the presence of late gadolinium enhancement (LGE) and the amount of EAT were assessed. Results: Compared to healthy controls, patients with DCM revealed a significantly reduced indexed EAT mass (31.7 6 5.6 g/m 2 vs 24.0 6 7.5 g/m 2 , p<0.0001). There was no difference in the EAT mass between DCM patients with moderate and severe LV dysfunction (23.5 6 9.8 g/m 2 vs 24.2 6 6.6 g/m 2 , P ¼ 0.7). Linear regression analysis in DCM patients showed that with increasing LV end-diastolic mass index (LV-EDMI) (r ¼ 0.417, P < 0.0001), increasing LV end-diastolic volume index (r ¼ 0.251, P ¼ 0.01) and increasing LV end-diastolic diameter (r ¼ 0.220, P ¼ 0.02), there was also a significantly increased amount of EAT mass. However, there was no correlation between the EAT and the LV ejection fraction (r ¼ 0.0085, P ¼ 0.37), right ventricular ejection fraction (r ¼ 0.049, P ¼ 0.6), LVRI (r ¼ 0.116, P ¼ 0.2) and the extent of LGE % (r ¼ 0.189, P ¼ 0.1). Among the healthy controls, the amount of EAT only correlated with increasing age (r ¼ 0.461, P ¼ 0.001), BMI (r ¼ 0.426, P ¼ 0.003) and LV-EDMI (r ¼ 0.346, P ¼ 0.02). Conclusion: In patients with DCM the amount of EAT is decreased compared to healthy controls irrespective of LV function impairment. However, an increase in LV mass and volumes is associated with a significantly increase in EAT in patients with DCM.