Longitudinal relaxation time editing for acetylcarnitine detection with 1H-MRS
Lucas Lindeboom1,2, Yvonne M.H. Bruls1,2, Petronella A. van Ewijk1, Matthijs K.C. Hesselink2, Joachim E. Wildberger1, Patrick Schrauwen2, and Vera B. Schrauwen-Hinderling1,2

1Radiology, Maastricht University Medical Center, Maastricht, Netherlands, 2Human Biology and Human Movement Sciences, Maastricht University Medical Center, Maastricht, Netherlands


The use of a long TE enables detection of acetylcarnitine with 1H-MRS. However, in (very) obese subjects, suppression of overlapping lipid resonances becomes problematic, even with long TE. We here show short T1 metabolites, such as lipids, can additionally be suppressed with a new T1 editing approach.


Recent research suggests that acetylcarnitine formation is essential in maintaining glucose homeostasis and metabolic flexibility (1). We have previously shown that acetylcarnitine can be measured in skeletal muscle in vivo with 1H-MRS using long TE and that obese and T2DM patients are charaterzied by low acetylcarnitine concentrations (2). These subjects are however also characterized by high myocellular lipid signals, which challenges uncontaminated acetylcarnitine detection. We here investigated whether the relative short T1 of the overlapping lipid resonances (3) offers a way to suppress residual lipid signals in subjects with high myocellular lipid signals. We developed an approach that alternates standard signal acquisition with an inversion recovery sequence with an intermediate TI. Subtraction of both signals will result in destruction of short T1 signals, while metabolites with a long T1 will be retained. We explored the use of this approach for the detection of acetylcarnitine in skeletal muscle in vivo.


The T1 editing approach is visualized in figure 1. In a first experiment, a conventional inversion recovery sequence, all spins are inverted by an adiabatic hyperbolic secant pulse with a bandwidth of 5000 Hz, and allowed to relax back to equilibrium during TI. In the following experiment, the frequency of the inversion pulse is set far off resonance, essentially reducing this second experiment to a normal PRESS (4) localization experiment. As the phase of the receiver is switched between the two acquisitions, short T1 metabolite signals will be cancelled. Signal yield for metabolites with a relative long T1 will be higher. The performance of this approach was tested in 4 obese subjects (male subjects, age 67 ± 3 years and BMI 30 ± 1 kg/m2), with high myocellular lipid and low acetylcarnitine signals. Experiments were approved by the institutional medical ethics committee and written informed consent was obtained from the subjects prior to these experiments. All experiments were performed on a 3T clinical MR system (Achieva 3T-X, Philips Healthcare, Best, The Netherlands) using a two-element flexible surface receive coil. Subjects were positioned supine and feet first in the magnet bore. The coil was placed over the vastus lateralis muscle. A voxel of 40 mm x 20 mm x 60 mm was positioned in the vastus lateralis muscle, based on anatomical MR images. All spectra were acquired with a TR of 6000 ms. Spectral bandwidth was 2 kHz, number of acquired data points 2048, number of averages (NSA) 20 and a 4 step phase cycling was applied. A short TE (40 ms) PRESS spectrum was acquired and compared with acquisition with the T1 editing approach with a TI of 900 ms and identical TE. Subsequently, also a long TE (350 ms) PRESS spectrum was compared with the T1 edited acquisitions with both intermediate and long TE (150 ms and 350 ms respectively).


The spectra collected from one of the obese subjects are shown in figure 2. In all four subjects, the acetylcarnitine peak was not detectable in the short TE spectra. With long TE, residual lipid signals were hindering accurate quantification of the acetylcarnitine peak. The T1 editing approach clearly reduces lipid signals, both with short and long TE. However, when the T1 editing approach was used with a TE of 40 or 150 ms, residual lipid signals were still visible. Combination of the T1 editing approach with a TE 350 ms resulted in enhanced suppression of lipid signals, resulting in a well-resolved acetylcarnitine peak in all subjects. Acetylcarnitine signal intensity is reduced by approximately 40% when using a TI of 900 ms.


Longitudinal relaxation time editing in addition to the long TE protocol is a feasible strategy to improve detection of the acetylcarnitine peak in subjects with high lipid signals in skeletal muscle, although signal intensity is reduced by approximately 40 % when compared to the long TE protocol alone. The application of the T1 editing approach in other tissues, and in identifying metabolites that have been uncovered to date, requires future evaluation.


No acknowledgement found.


1. Muoio et al. Cell Metab. 2012; 2. Lindeboom et al. JCI 2014; 3. Wang et al. JMRI 2009; 4. Bottomley et al. Ann NY Acad Sci 1987.


Figure 1. Schematic representation of the T1 editing approach.

Figure 2. Evaluation of the performance of the T1 editing approach with short TE (panel A) and long TE (panel B). Combination of T1 editing and a TE of 350 ms, leads to an uncontaminated acetylcarnitine peak, even in subjects with (very) high myocellular lipid signals.

Proc. Intl. Soc. Mag. Reson. Med. 24 (2016)