Introduction Obesity is associated with improved prognosis in heart failure, despite diminished myocardial energetic stores. It has been shown that reduced ATP transfer from the mitochondrion to the myofibril via creatine kinase is related to increased mortality. Given that the creatine kinase rate constant (k f CK) is elevated in obesity in the absence of cardiovascular disease, we hypothesised that the rate of ATP transfer would also be raised in obese heart failure.
Methods 43 individuals (14 normal weight (BMI <25 kg/m2); 29 obese (BMI >30 kg/m2)) with DCM (EF 25%–45%) underwent MR imaging (3 T Siemens) of visceral, hepatic and myocardial lipid, and cardiac structure and function. They also underwent Triple Repetition time Saturation Transfer (TRiST) 31P magnetic resonance spectroscopy, to calculate apical myocardial k f CK.
Results Obese DCM participants had greater BMI (37±5 kg/m2 compared to 23±3 kg/m2, p<0.001), and fat mass (46±13 kg compared to 17±8 kg, p<0.001). There were no significant differences in LV EDV (obese 227±58 ml, normal weight 210±48 ml, p=0.349), mass (obese 164±38 g, normal weight 145±42 g, p=0.165) or ejection fraction (obese 41%±6%, normal weight 37%±5%, p=0.119).
However, k f CK was significantly higher in the obese group compared to normal weight (0.17±0.08s-1 compared to 0.08±0.07s-1, p=0.002). k f CK was significantly correlated with visceral fat volume (r=0.473, p=0.008).
Conclusion Here we demonstrate that myocardial k f CK is higher in obese DCM, despite identical cardiac parameters to the control group. It has previously been shown that low k f CK is associated with heart failure events and mortality. Utilising multinuclear MRS to demonstrate the reverse in obesity, we propose this as a novel energetic basis underlying the obesity paradox.
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