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Related Experiment Videos

Pre- and post-synaptic sympathetic function in human hibernating myocardium.

Anna S John1, Marco Mongillo, Christophe Depre

  • 1National Heart and Lung Institute, Imperial College, Hammersmith Hospital, Du Cane Road, London, UK.

European Journal of Nuclear Medicine and Molecular Imaging
|July 31, 2007
PubMed
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Sympathetic neuroeffector function, including noradrenaline uptake-1 and beta-adrenoceptor density, is reduced in patients with hibernating myocardium and chronic left ventricular dysfunction. This generalized reduction may contribute to overall left ventricular remodeling.

Area of Science:

  • Cardiology
  • Nuclear Medicine
  • Neuroscience

Background:

  • Hibernating myocardium (HM) is associated with impaired pre-synaptic noradrenaline uptake-1 mechanisms in swine models.
  • Adrenergic neuroeffector abnormalities require investigation in human HM.

Purpose of the Study:

  • To assess pre- and post-synaptic sympathetic function in human HM.
  • To investigate adrenergic neuroeffector abnormalities in patients with chronic left ventricular dysfunction.

Main Methods:

  • Combined cardiovascular magnetic resonance (CMR) and positron emission tomography (PET) for in vivo functional measurements.
  • Measured myocardial noradrenaline uptake-1 (using [(11)C]meta-hydroxy-ephedrine; HED) and beta-adrenoceptor (beta-AR) density (using [(11)C]CGP-12177) with PET.
  • Compared PET data from 12 patients with coronary artery disease and chronic LV dysfunction to 18 healthy controls.

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Main Results:

  • Significantly reduced volume of distribution (V(d)) of HED in hibernating myocardium (HM) and infarcted myocardium compared to controls.
  • Lower V(d) of HED in normal myocardium of patients compared to controls (p=0.06).
  • Significantly lower myocardial beta-AR density in HM, infarcted, and normal segments of patients compared to healthy controls.

Conclusions:

  • Noradrenaline uptake-1 mechanism and beta-AR density are reduced in the myocardium of patients with chronic LV dysfunction and HM.
  • Increased sympathetic activity to the heart in these patients is a generalized phenomenon.
  • This generalized sympathetic alteration likely contributes to the remodeling of the whole left ventricle, rather than causing HM.