Saturation recovery allows T1 mapping in the human heart at 7T with a commercial MRI scanner
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KeywordsSaturation Recovery Wide Clinical Application Oxford Biomedical Research Saturation Delay Saturation Recovery Method
Myocardial T1 mapping at 1.5T and 3T distinguishes powerfully between normal and diseased tissue with focal and diffuse pathology. We recently reported the first human myocardial T1s at 7T using the ShMOLLI+IE inversion recovery sequence. Yet even using a unique 7T scanner with 16kW RF output, perfect magnetization inversion was impossible. We now introduce a saturation recovery method to enable myocardial T1 mapping with standard commercial 7T MRI scanners.
The saturation recovery single-shot acquisition (SASHA, Chow, 2013) sequence was modified for 7T by using: an optimised train of 4xHS8 pulses to saturate and 10 FLASH readouts with saturation delays (TS): non-saturated, 100, 200, 300, 400, 500, 600, 650ms, 1hb + 100ms and 1hb + 700ms in a 12 heartbeat breath-hold. Data were acquired with a Siemens 7T MRI scanner (with 8kW RF), an 8-element cardiac coil and ECG gating. Signals were fitted pixelwise to "s(TS) = A - B exp(-TS / T1)".
10 healthy subjects (males, 22-45yrs, 70-84kg) were recruited according to ethics regulations. For each subject, coil tuning, B0- shims, B1-shims and the central frequency were optimised over the left ventricle. Then 7T SASHA native (i.e. non-contrast) T1 mapping was performed in SA and HLA views.
In three subjects, post-contrast T1 maps were acquired ~5min after 2 peripheral bolus injections of Dotarem with a power injector (Accutron MR, MEDTRON).
In-vivo, the native 7T SASHA T1s in the interventricular septum were 1939±73ms. Native T1s in the LV blood pool showed strong artefacts, likely due to blood flow. The post-contrast T1s were 999, 1107 and 1674ms in myocardium and 472, 567 and 966ms in blood for Dotarem doses of 2x 50, 50 & 25 and 2x 13.5 µmol/kg in the three subjects respectively. Post-contrast T1 maps were acquired too soon after bolus infusion to permit calculation of extra-cellular volumes.
These myocardial T1s agree with our ShMOLLI+IE finding of a myocardial T1 = 1925 ± 48 ms. However, with ShMOLLI+IE we had to use a 4-parameter model-based fitting procedure to correct for imperfect inversion, read-out induced saturation and spin history effects. In contrast, with 7T SASHA, it is now possible to achieve comparable T1s using a simple 3-parameter fit (on the scanner). Note that these considerations at 7T are different to the well-known differences between MOLLI and SASHA T1s at 1.5 and 3T caused by imperfect inversion, T2 relaxation, and magnetization transfer.
Saturation recovery allows T1 mapping in the human heart using a commercial 7T MRI scanner. T1s from 7T SASHA with 3-parameter fitting and ShMOLLI+IE with 4-parameter fitting are comparable in normal volunteers at 7T. Our findings hold promise for wider clinical applications of T1 mapping at ultra-high fields.
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