Published in:
01-08-2007 | Original article
Myocardial pre-synaptic sympathetic function correlates with glucose uptake in the failing human heart
Published in: European Journal of Nuclear Medicine and Molecular Imaging | Issue 8/2007
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Purpose
We have previously shown that the myocardium of patients with heart failure (HF) is insulin resistant. Chronic β-adrenergic stimulation has been implicated in insulin resistance in cultured cardiomyocytes in vitro, where sustained noradrenaline stimulation inhibited insulin-modulated glucose uptake. As the failing heart is characterized by increased sympathetic drive, we hypothesized that there is a correlation between pre-synaptic sympathetic function and insulin sensitivity in the myocardium of patients with HF.
Methods
Eight patients (aged 67 ± 7 years) with coronary artery disease and left ventricular dysfunction (ejection fraction 44 ± 10%) underwent function and viability assessment with cardiovascular magnetic resonance. Myocardial glucose utilization (MGU) was measured using positron emission tomography (PET) with 18F-fluorodeoxyglucose (FDG). Pre-synaptic noradrenaline re-uptake was measured by calculating [11C]meta-hydroxy-ephedrine (HED) volume of distribution (V
d) with PET. Two groups of healthy volunteers served as controls for the FDG (n = 8, aged 52 ± 4 years, p < 0.01 vs patients) and HED (n = 8, aged 40 ± 6 years, p < 0.01 vs patients) data.
Results
MGU in patients was reduced in both normal remote (0.44 ± 0.14 μmol·min−1·g−1) and dysfunctional (0.49 ± 0.14 μmol·min−1·g−1) segments compared with controls (0.61 ± 0.7 μmol·min−1·g−1; p < 0.001 vs both). HED V
d was reduced in dysfunctional segments of patients (38.9 ± 21.2 ml·g−1) compared with normal segments (52.2 ± 19.6 ml·g−1) and compared with controls (62.7 ± 11.3 ml·g−1). In patients, regional MGU was correlated with HED V
d.
Conclusion
The results of this study provide novel evidence of a correlation between cardiac sympathetic function and insulin sensitivity, which may represent one of the mechanisms contributing to insulin resistance in failing human hearts.