Conventionally, evaluation of myocardial T1-times is limited to a single snapshot of the cardiac cycle, leaving much of the dependence between functional and tissue characterization unstudied. Here, we propose an ECG-triggered steady-state Look-Locker technique that allows for functional, cardiac phase-resolved native T1-mapping. Integratedly acquired phase-resolved B1+-maps are used for T1-time correction. High accuracy and good consistency of the T1-times across cardiac phases is shown in phantom scans. In-vivo T1-times show slight underestimation and similar precision compared to saturation-recovery T1-mapping. High visual image quality at all cardiac phases is obtained at temporal resolutions up to 40ms in a single breath-hold.
Sequence: In the proposed Look-Locker CINE (LLCine) sequence, T1-quantification is based on magnetization readout during the approach to pulsed steady-state. Initially, magnetization is driven to steady-state using FLASH excitations, and an inversion pulse is applied (Fig. 1). Then imaging pulses are played continuously, while the pulsed inversion-recovery curve is sampled with segmented k-space sampling for each cardiac phase. After reaching steady-state again, magnetization is re-inverted, and the next k-space segment is acquired. This recovery to pulsed steady-state spans several heartbeats. Hence, multiple time points on the inversion-recovery curve are sampled, allowing for spatially- and temporally-resolved quantification of T1-time throughout cardiac cycle. Dummy pulses without signal acquisition fill the end of cardiac cycles after acquiring the last cardiac phase, to maintain pulsed steady-state, and minimize effects of R-R interval variability. Reconstruction: Apparent relaxation during continuous FLASH excitations is described6 by T1*
$$M_z(t)=M_0\left(1–B\cdot e^{-\frac{t}{T_1^*}}\right)$$ $$B=1-\cos(\alpha_{inv})$$ $$\frac{1}{T_1^*} = \frac{1}{T_1} - \frac{\log( \cos( \alpha ) ) }{T_R}$$
Hence, actual T1 can be derived from this sequence, given TR and excitation flip angle (FA). Efficiency of the rectangular inversion pulse (B in Eq. 2 above) can be used to estimate B1+-inhomogeneities and calculate the actual FA as:
$$\frac{\alpha}{\alpha^{nom}}\approx\frac{\alpha_{inv}}{\alpha_{inv}^{nom}}$$ $$T_1=\left(\frac{1}{T_1}-\frac{\log(\cos(\frac{\arccos(1-B)}{\alpha_{inv}^{nom}}\cdot\alpha_{nom}))}{T_R}\right)^{-1}$$
Numerical Simulations: The conditioning of extracting T1 from T1* depends on TR and FA. Numerical simulations were performed to minimize T1-error sensitivity by optimizing these two parameters. Bloch-simulations for the proposed sequence were performed for TR=3.5,4, …15.0ms and FA=1°,2°,...20°. T1-times were then calculated from 1000 noisy simulations, and evaluated for accuracy and precision at all parameter values. Imaging: All imaging was performed at 3T (Siemens Magnetom Prisma) and the following imaging parameters were used in the remainder of the study: TR/TE/FA=5/2.5ms/3°, FOV=300x300mm2, resolution=1.9x1.9mm2, slice thickness=10mm, temporal resolution=40-60ms, breath-hold duration=19-23s. SAPPHIRE T1-mapping7 was performed for comparison. Phantom imaging was performed to test T1-mapping accuracy, and consistency of the T1 estimate across the cardiac phases. In-vivo imaging of a mid-ventricular short-axis slice was performed on 10 healthy subjects (4male, 32±15y/o). T1-times were evaluated using septal ROIs drawn for each cardiac phase. In-vivo precision was defined as T1-time variation within the ROIs.
Numerical simulations indicate diminished precision and accuracy for short TR and high FA, both causing rapid apparent relaxation. T1-precision is also compromised with low FA due to insufficient signal. Optimal T1-sensitivity, at breath-hold scan-times was achieved at TR/FA=5ms/3°.
In phantom experiments (Fig. 2), LLCine is in good agreement with SAPPHIRE T1-mapping (NRMSE=3.1%) and highly consistent across phases (Coefficient-of-Variation (CoV)=2.1±0.9%). In-vivo T1-maps display a high level of homogeneity in the myocardium and good delineation towards the blood pool at all phases (Fig. 3). In-vivo T1-times after B1+-correction fall into the expected range at 3T, while uncorrected T1-maps exhibit underestimation (Fig. 4). Minor variations of the in-vivo T1-times are observed throughout the cardiac cycle (CoV=1.9%). In-vivo precision is comparable to SAPPHIRE T1-mapping, with slightly higher variability at late diastolic phases. B1+-maps generated by the proposed approach are visually homogeneous and largely T1-insensitive, with increased variability towards the end of cardiac cycle.
This study demonstrates the feasibility of cardiac phase-resolved T1-mapping at temporal resolutions as fine as 40ms in a single breath-hold. The integrated phase-resolved B1+-maps were leveraged to correct for flip-angle deviations, in order to maximize accuracy.
The sequence parameters were numerically optimized for the expected T1 range at 3T. Hence, if tissue with T1-times other than native myocardium, e.g. post-contrast, is to be evaluated, a dedicated parameter optimization should be performed to allow for adequate recovery durations and accuracy.
In the proposed sequence, sample-points on the inversion-recovery curve are dependent on cardiac phase. Later cardiac phases lack acquisition of short inversion times, hence increased in-vivo variability was observed. However, since myocardium remains largely stationary during diastolic quiescence, temporal acquisition/reconstruction window can be increased in later phases, for improving SNR to mitigate this effect.
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