QF1-007 - Regional B1 Inhomogeneity Results in Falsely Attenuated Creatine CEST-MRI Contrast in the Healthy Heart at 3T

Background: Chemical exchange saturation transfer (CEST) MRI is an emerging molecular imaging method for non-invasive assessment of cardiomyocyte metabolites including creatine. Cardiac CEST-MRI has identified reduced creatine in the setting of obesity or myocardial infarction [1,2]. While B₀ compensation is routinely performed, the effects of B₁ inhomogeneity are generally ignored. The labeling efficiency, and thus generated contrasts, for creatine, amide proton transfer (APT) and magnetization transfer (MT) are a function of saturation power. We assessed whether B₁ inhomogeneity across the heart of healthy individuals leads to variability in measured creatine CEST and MT contrasts including values that are consistent with infarcted myocardium at 3T.

Methods: 6 healthy volunteers with no history of cardiovascular disease, diabetes, or smoking, aged 20–31 years old were recruited. Participants were imaged on a 3T Siemens Trio scanner. First, B₀ and B₁ field maps of one short axis slice were acquired. Then, cardiac CEST was performed (saturation offsets from -10ppm to +10ppm) using a 1311ms train of gaussian saturation pulses (pulse duration=36ms, duty cycle=0.63, and peak B₁=1.2µT), followed by a segmented echo planar imaging gradient echo readout (FOV=300x253mm, spatial resolution=1.56x1.56mm, slice thickness=8mm, TR=4.7ms, TE=2.59ms, and FA=25°) timed to end-diastole. The left ventricle was segmented using the American Heart Association classification to generate regional Z-spectra as shown in Figure 1 that were fit with a multi-pool Lorentzian method [3] to quantify creatine and APT contrasts, nuclear Overhauser effect, MT and direct saturation of water.

Results: Average individual spatial variability in saturation B₁ was 23±6%, resulting in significant regional Z-spectral differences (Fig. 1). B₁ variation was minimal in septal segments and both substantial and non-uniform in the free-wall (Fig 2). Subsequently, creatine contrast was significantly reduced, and MT elevated along the lateral wall (Fig 2). MT contrast and water direct saturation (DS) were significantly correlated with the deviation from prescribed B₁ (Fig 3).

Conclusion: Generation of creatine CEST contrast requires that the correct peak B₁ saturation power be spatially consistent across the heart. Spatial B₁ inhomogeneity generates inconsistent creatine CEST labeling and further complicates the detection of creatine via increased MT, direct saturation, and spillover from APT labeling. The impact at 3T is sufficient to result in abrogated creatine CEST contrast consistent with infarcted tissue in the hearts of healthy individuals. These results imply that cardiac CEST-MRI requires both more advanced design of saturation pulses to maximize spatial uniformity, and analysis methods that account for B₁ inhomogeneity in quantification of underlying metabolite contrasts.