Purpose Recently, we introduced a quantum coherence based method (ge‐HSQC) for indirect 13C‐MRS in the liver to track 13C‐labeled lipids into the hepatic lipid pool in vivo. This approach is more robust in case of respiratory motion, however, inherently leads to a signal loss of 50% when compared with a conventional J‐difference editing technique (JDE). Here, we intend to improve the robustness of a regular JDE (STEAM‐ACED) with the use of a BIlinear Rotation Decoupling (BIRD) filter to achieve 100% higher signal gain when compared with ge‐HSQC. Methods To determine the efficiency of the BIRD filter 1H‐[13C] lipid spectra were acquired on 3T from a peanut oil phantom, with three different MR sequences: ge‐HSQC, STEAM‐ACED, and the BIRD filter together with STEAM‐ACED (BIRD‐STEAM‐ACED). Finally, our proposed method is tested in vivo in five healthy volunteers with varying liver fat content. In these subjects we quantified the 1H‐[13C]‐signal from the hepatic lipid pool and determined 13C enrichment, which is expected to be 1.1% according to the natural abundance of 13C. Results The application of the proposed BIRD filter reduces the subtraction artifact of 1H‐[12C] lipid signal efficiently in JDE experiments, which leads to a signal gain of 100% of 1H‐[13C]‐lipid signals when compared with the ge‐HSQC. Phase distortions in vivo were minimal with the use of BIRD compared with STEAM‐ACED, which enabled us to robustly quantify the 13C‐enrichment in all five subjects. Conclusion The BIRD‐STEAM‐ACED sequence is an efficient and promising tool for 13C‐tracking experiments in the human liver in vivo.

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Cardiac energy status, measured as phosphocreatine (PCr)/adenosine triphosphate (ATP) ratio with 31P-Magnetic Resonance Spectroscopy (31P-MRS) in vivo, is a prognostic factor in heart failure and is lowered in cardiometabolic disease. It has been suggested that, as oxidative phosphorylation is the major contributor to ATP synthesis, PCr/ATP ratio might be a reflection of cardiac mitochondrial function. The objective of the study was to investigate whether PCr/ATP ratios can be used as in vivo marker for cardiac mitochondrial function. We enrolled thirty-eight patients scheduled for open-heart surgery in this study. Cardiac 31P-MRS was performed before surgery. Tissue from the right atrial appendage was obtained during surgery for high-resolution respirometry for the assessment of mitochondrial function. There was no correlation between the PCr/ATP ratio and ADP-stimulated respiration rates (octanoylcarnitine R2 < 0.005, p = 0.74; pyruvate R2 < 0.025, p = 0.41) nor with maximally uncoupled respiration (octanoylcarnitine R2 = 0.005, p = 0.71; pyruvate R2 = 0.040, p = 0.26). PCr/ATP ratio did correlate with indexed LV end systolic mass. As no direct correlation between cardiac energy status (PCr/ATP) and mitochondrial function in the heart was found, the study suggests that mitochondrial function might not the only determinant of cardiac energy status. Interpretation should be done in the right context in cardiac metabolic studies.

Objectives The objective of the study was to validate PCr/ATP ratios as an in vivo marker for cardiac mitochondrial function.Background Cardiac energy status, measured as PCr/ATP ratio with 31P-MRS in vivo, was shown to be a prognostic factor in heart failure and is lowered in cardiometabolic disease. As mitochondrial function is also hampered in these diseases and oxidative phosphorylation is the major contributor to ATP synthesis, the PCr/ATP ratio might be a reflection of cardiac mitochondrial function.Methods Thirty-eight patients scheduled for open heart surgery were enrolled in this study. Before surgery, cardiac 31P-MRS was performed. During surgery, tissue specimens from the right atrial appendage were obtained for the ex vivo assessment of mitochondrial function using high-resolution respirometry.Results The patient population included was heterogenous resulting in wide ranges of PCr/ATP ratios and ADP-stimulated respiration rates (PCr/ATP ranging from 0.533 to 1.717; ADP-stimulated respiration rates ranging from 28.5 to 94.6 pmol/mg/s). Correlation analysis however showed no relationship between PCr/ATP and ADP-stimulated respiration rates fueled by various substrates (octanoylcarnitine R2 < 0.005, p = 0.74; pyruvate R2 < 0.025, p = 0.41). Also, no correlations between PCr/ATP and maximally uncoupled respiration were found (octanoylcarnitine R2 = 0.005, p = 0.71; pyruvate R2 = 0.040, p = 0.26).Conclusions Our results do not support the use of cardiac energy status (PCr/ATP) as a surrogate marker of mitochondrial function in the heart. The dissociation of the two parameters in the present study suggests that mitochondrial function is not the only determinant of cardiac energy status.Condensed abstractThis study does not support the use of in vivo cardiac energy status (PCr/ATP ratio) as a surrogate marker of ex vivo mitochondrial function (maximal oxidative respiration). Although both PCr/ATP and mitochondrial function are reduced in cardiovascular disease, the dissociation of the two parameters in the present study shows that PCr/ATP is determined by more factors than only mitochondrial function. Hence, PCr/ATP is not a good marker for mitochondrial function, but it can be a valuable marker for cardiometabolic health in cardiometabolic studies.Trial registration: https://clinicaltrials.gov (NCT03049228).