Simultaneous Assessment of Left Atrial Fibrosis and Epicardial Adipose Tissue Using 3D Late Gadolinium Enhanced Dixon MRI.

BACKGROUND: Epicardial adipose tissue (EAT) may induce left atrium (LA) wall inflammation and promote LA fibrosis. Therefore, simultaneous assessment of these two important atrial fibrillation (AF) risk factors would be desirable. PURPOSE: To perform a comprehensive evaluation of 3D Dixon water-fat separated late gadolinium enhancement (LGE-Dixon) MRI by analysis of repeatability and systematic comparison with reference methods for assessment of fibrosis and fat. STUDY TYPE: Prospective. POPULATION: Twenty-eight, 10, and 7 patients, respectively, with clinical indications for cardiac MRI. FIELD STRENGTH/SEQUENCE: A 1.5-T scanner, inversion recovery multiecho spoiled gradient echo. ASSESSMENT: Twenty-eight patients (age 58 ± 19 years, 15 males) were scanned using LGE-Dixon. A 5-point Likert-type scale was used to grade the image quality. Another 10 patients (age 46 ± 19 years, 9 males) were scanned using LGE-Dixon and 3D proton density Dixon (PD-Dixon). Finally, seven patients (age 62 ± 14 years, 4 males) were scanned using LGE-Dixon and conventional LGE. The scan time, intraobserver and interobserver variability, and levels of agreement were assessed. STATISTICAL TESTS: Student's t-test, one-way ANOVA, and Mann-Whitney U-test were used; P < 0.05 was considered significant, intraclass correlation coefficient (ICC). RESULTS: The scan time (minutes:seconds) for LGE-Dixon (n = 28) was 5:01 ± 1:40. ICC values for intraobserver and interobserver measurements of LA wall fibrosis percentage were 0.98 (95% CI, 0.97-0.99) and 0.97 (95% CI, 0.94-0.99) while of EAT were 0.92 (95% CI, 0.82-0.97) and 0.90 (95% CI, 0.80-0.95). The agreement for LA fibrosis percentage between the LGE-Dixon and the conventional LGE was 0.92 (95% CI, 0.66-0.99) and for EAT volume between the LGE-Dixon and the PD-Dixon was 0.93 (95% CI, 0.72-0.98). CONCLUSION: LA fibrosis and EAT can be assessed simultaneously using LGE-Dixon. This method allows a high level of intraobserver and interobserver repeatability as well as agreement with reference methods and can be performed in a clinically feasible scan time. EVIDENCE LEVEL: 2 TECHNICAL EFFICACY STAGE: 3.

Faster 3D saturation-recovery based myocardial T1 mapping using a reduced number of saturation points and denoising.

PURPOSE: To accelerate the acquisition of free-breathing 3D saturation-recovery-based (SASHA) myocardial T1 mapping by acquiring fewer saturation points in combination with a post-processing 3D denoising technique to maintain high accuracy and precision. METHODS: 3D SASHA T1 mapping acquires nine T1-weighted images along the saturation recovery curve, resulting in long acquisition times. In this work, we propose to accelerate conventional cardiac T1 mapping by reducing the number of saturation points. High T1 accuracy and low standard deviation (as a surrogate for precision) is maintained by applying a 3D denoising technique to the T1-weighted images prior to pixel-wise T1 fitting. The proposed approach was evaluated on a T1 phantom and 20 healthy subjects, by varying the number of T1-weighted images acquired between three and nine, both prospectively and retrospectively. Following the results from the healthy subjects, three patients with suspected cardiovascular disease were acquired using five T1-weighted images. T1 accuracy and precision was determined for all the acquisitions before and after denoising. RESULTS: In the T1 phantom, no statistical difference was found in terms of accuracy and precision for the different number of T1-weighted images before or after denoising (P = 0.99 and P = 0.99 for accuracy, P = 0.64 and P = 0.42 for precision, respectively). In vivo, both prospectively and retrospectively, the precision improved considerably with the number of T1-weighted images employed before denoising (P<0.05) but was independent on the number of T1-weighted images after denoising. CONCLUSION: We demonstrate the feasibility of accelerating 3D SASHA T1 mapping by reducing the number of acquired T1-weighted images in combination with an efficient 3D denoising, without affecting accuracy and precision of T1 values.

Simultaneous Assessment of Cardiac Inflammation and Extracellular Matrix Remodeling after Myocardial Infarction.

Background: Optimal healing of the myocardium following myocardial infarction (MI) requires a suitable degree of inflammation and its timely resolution, together with a well-orchestrated deposition and degradation of extracellular matrix (ECM) proteins. Methods and Results: MI and SHAM-operated animals were imaged at 3,7,14 and 21 days with 3T magnetic resonance imaging (MRI) using a 19F/1H surface coil. Mice were injected with 19F-perfluorocarbon (PFC) nanoparticles to study inflammatory cell recruitment, and with a gadolinium-based elastin-binding contrast agent (Gd-ESMA) to evaluate elastin content. 19F MRI signal co-localized with infarction areas, as confirmed by late-gadolinium enhancement, and was highest 7days post-MI, correlating with macrophage content (MAC-3 immunohistochemistry) (ρ=0.89,P<0.0001). 19F quantification with in vivo (MRI) and ex vivo nuclear magnetic resonance (NMR) spectroscopy correlated linearly (ρ=0.58,P=0.020). T1 mapping after Gd-ESMA injection showed increased relaxation rate (R1) in the infarcted regions and was significantly higher at 21days compared with 7days post-MI (R1[s-1]:21days=2.8 [IQR,2.69-3.30] vs 7days=2.3 [IQR,2.12-2.5], P<0.05), which agreed with an increased tropoelastin content (ρ=0.89, P<0.0001). The predictive value of each contrast agent for beneficial remodeling was evaluated in a longitudinal proof-of-principle study. Neither R1 nor 19F at day 7 were significant predictors for beneficial remodeling (P=0.68;P=0.062). However, the combination of both measurements (R1<2.34Hz and 0.55≤19F≤1.85) resulted in an odds ratio of 30.0 (CI95%:1.41-638.15;P=0.029) for favorable post-MI remodeling. Conclusions: Multinuclear 1H/19F MRI allows the simultaneous assessment of inflammation and elastin remodeling in a murine MI model. The interplay of these biological processes affects cardiac outcome and may have potential for improved diagnosis and personalized treatment.