PURPOSE: Even at 7T, cardiac 31 P MRSI is fundamentally limited by low SNR, leading to long scan times and poor temporal and spatial resolutions. Compartment-based reconstruction algorithms such as magnetic resonance spectroscopy with linear algebraic modelling (SLAM) and spectral localization by imaging (SLIM) may improve SNR or reduce scan time without changes to acquisition. Here we compare the repeatability and SNR performance of these compartment-based methods, applied to three different acquisition schemes at 7T. METHODS: 12 healthy volunteers were scanned twice. Each scan session consisted of a 6.5 minute 3D acquisition-weighted (AW) cardiac 31 P phase-encode based MRSI acquisition and two 6.5 minute truncated k-space acquisitions with increased averaging (4 × 4 × 4 central k-space phase encodes and fSLAM optimized k-space phase encodes). Spectra were reconstructed using: (i) AW Fourier-reconstruction; (ii) AW SLAM; (iii) AW SLIM; (iv) 4 × 4 × 4 SLAM; (v) 4 × 4 × 4 SLIM; and (vi) fSLAM optimized SLAM (fSLAM) acquisition-reconstruction combinations. The PCr/ATP ratio, the PCr SNR, and spatial response functions were computed, in addition to coefficients of reproducibility and variability. RESULTS: Using the compartment-based reconstruction algorithms with the AW 31 P acquisition resulted in a significant increase in SNR compared to previously published Fourier-based MRSI reconstruction methods, while maintaining the measured phosphocreatine-to-adenosine triphosphate ratio and improving inter-scan reproducibility. The alternative acquisition strategies with truncated k-space performed no better than the common AW approach. CONCLUSION: Compartment-based spectroscopy approaches provide an attractive reconstruction method for cardiac 31 P spectroscopy at 7T, improving reproducibility and SNR without the need for a dedicated k-space sampling strategy.This work was supported by the Engineering and Physical Sciences Research Council
(EPSRC) and Medical Research Council (MRC) (EP/L016052/1). All authors
acknowledge the support of the British Heart Foundation (BHF) (FS/19/18/34252), the
Oxford BHF Centre for Research Excellence (RE/13/1/30181) and the UK National
Institute for Health Research (NIHR). JYCL acknowledges funding from the NIHR
Oxford Biomedical Research Centre and support from the Fulford Junior Research
Fellowship at Somerville College. JJM acknowledges support from a Novo Nordisk
Postdoctoral Fellowship scheme run in conjunction with the University of Oxford, and
also by St Hugh’s and Wadham college and a Starter Grant from the Novo Foundation,
(NNF21OC0068683). PAB was supported by a Newton Abraham Visiting Professorship
from Lincoln College. LV and CTR are supported by Sir Henry Dale Fellowships from the
Wellcome Trust and the Royal Society [Grant numbers 221805/Z/20/Z (LV) and
098436/Z/12/B (CTR)]. For the purpose of open access, the author has applied a CC BY
public copyright licence to any Author Accepted Manuscript version arising from this
submission. LV acknowledges the Slovak Grant Agencies VEGA (2/0004/23) and APVV
(19-0032). CTR acknowledges the NIHR Cambridge Biomedical Research Centre
(BRC-1215-20014). The views expressed are those of the authors and not necessarily
those of the NIHR or the DHSC
