Andrew Apps1, Justin Lau1,2, Jack Miller1,2, Mark Peterzan1, Andrew Lewis1, Michael Dodd3, Angus Lau4, Ferenc Mozes1, Oliver Rider1, Stefan Neubauer1, and Damian J Tyler1,2
1Oxford Centre for Magnetic Resonance Research, Oxford, United Kingdom, 2Department of Physiology, Anatomy and Genetics., University of Oxford, Oxford, United Kingdom, 3School of Life Sciences, Coventry University, Coventry, United Kingdom, 4Sunnybrook Research Institute, University of Toronto, Toronto, ON, Canada
Synopsis
Hyperpolarised 13C MRS offers
unparalleled opportunities for studying in-vivo, real time metabolism. In our
current study we demonstrate how the technique easily demonstrates early
pathological changes in PDH flux in the diabetic heart, and is complementary to
other spectroscopic and imaging techniques, in defining the metabolic and
structural changes characterising the disease.
Introduction
The development of type 2 diabetes
is associated with a panoply of myocardial structural and metabolic
aberrations. Such changes include impaired myocardial energetics (PCr/ATP), the
onset of diastolic dysfunction and increased myocardial fat content.1 Such changes often precede development of the overt systolic dysfunction characteristic
of diabetic cardiomyopathy. The transition from the fasted to fed state is
characterised by a shift in energy substrate utilisation towards glucose and
away from fatty acids, mediated in part by the activation of Pyruvate
Dehydrogenase (PDH). Flexibility of substrate usage is lost in diabetes, which
is characterised by blunted flux through PDH.2 We aimed to investigate the ability of human hyperpolarised 13C MRS
to characterise such changes in an early type 2 diabetic phenotype and to
correlate this to alterations in myocardial energetics, resting diastolic
function and myocardial lipid content. Method
Five people with type two diabetes (age 53±4years, HbA1c 6.8±0.7%, Left
Ventricular Ejection Fraction (LVEF) 58±5%) and
four controls (age 50±12, LVEF 59±3%) received 1H CINE imaging for functional
assessment, [1-13C]pyruvate hyperpolarized MRS, 31P MRS,
and 1H MRS 3,4 for assessment of PDH flux, myocardial energetics and myocardial lipid content (proton density fat fraction (PDFF)) respectively, and echocardiographic assessment of diastolic function in the
fasted state. Five participants (3 Control, 2 Diabetic) then went on to receive successful
repeat 13C imaging 45 minutes after a 70g oral glucose load
(Rapilose®). Hyperpolarized [1-13C]pyruvate (SpinLab, GE healthcare,
0.4ml/kg) was injected via a Medrad syringe, following which an ECG gated, 13C
slice selective spectroscopy sequence was initiated for four minutes (FA=100,
BW5kHz, minimum TR 500 ms). Results
60 seconds of hyperpolarized spectra
were summed, beginning from the first appearance of pyruvate within the LV.
Baseline cardiac, demographic, 13C, 31P, 1H,
and echocardiographic data are shown in table 1. H13CO3-/Pyr
for all successful injections are shown in figure 2, alongside the time course
of H13CO3- production for a control and diabetic
participant. Diabetes significantly reduced PDH flux (2-way ANOVA paired
datasets, df =1, p<0.05). In our fasted participants (controls vs diabetes)
trends toward impaired myocardial energetics (PCr/ATP 1.89+/-.14 vs 1.71+/-.36
p=.38), increased lipid content (PDFF (%) 1.5+/-.5 vs 3.0+/-1.9 p=.17), and
impaired diastolic function (E/e’ (sep) 5.1+/-1.4 vs 7.8+/-1.4) were seen in diabetes.
Across all participants fasting PDH flux was mildly correlated with PCr/ATP
(positively) and fat fraction (inversely, figure 3). Discussion
In a mildly insulin resistant
diabetic cohort, using a multi-nuclear spectroscopic approach, we have successfully
characterised multiple pathological metabolic alterations that may collectively
drive progression toward the diabetic cardiomyopathy phenotype.Conclusion
Using 13C MRS, for the
first time in human participants, we have demonstrated impaired cardiac PDH flux in diabetes, and
shown how the signal generated via this technique gives huge power over other
techniques (such as those used in this study) to detect pathological change.Acknowledgements
This work was supported by the British Heart Foundation under grant number HSR00620References
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