Atherosclerosis
Volume 192, Issue 2 , Pages 275-282, June 2007

Imaging of vulnerable atherosclerotic plaques with FDG-microPET: No FDG accumulation

  • Jacob Marsvin Laurberg

      Affiliations

    • Department of Cardiology and Institute of Clinical Medicine, Aarhus University Hospital (Skejby), Aarhus, Denmark
    • Corresponding Author InformationCorresponding author at: Department of Cardiology, Research Unit, Aarhus University Hospital (Skejby), Brendstrupgaardsvej, DK-8200 Aarhus N, Denmark. Tel.: +45 8949 6231; fax: +45 8949 6009.
  • ,
  • Aage Kristian Olsen

      Affiliations

    • The PET Centre, Aarhus University Hospital, Aarhus, Denmark
  • ,
  • Søren Baarsgaard Hansen

      Affiliations

    • The PET Centre, Aarhus University Hospital, Aarhus, Denmark
  • ,
  • Morten Bottcher

      Affiliations

    • Department of Cardiology and Institute of Clinical Medicine, Aarhus University Hospital (Skejby), Aarhus, Denmark
  • ,
  • Matthew Morrison

      Affiliations

    • GE Healthcare, The Grove Centre, Amersham, UK
  • ,
  • Sally-Ann Ricketts

      Affiliations

    • GE Healthcare, The Grove Centre, Amersham, UK
  • ,
  • Erling Falk

      Affiliations

    • Department of Cardiology and Institute of Clinical Medicine, Aarhus University Hospital (Skejby), Aarhus, Denmark

Received 25 January 2006; received in revised form 13 June 2006; accepted 11 July 2006. published online 21 August 2006.

Abstract 

Background

Non-invasive methods of evaluating atherosclerosis in humans and experimental animals are needed. Studies indicate that FDG-PET has a potential to detect vulnerable, inflamed atherosclerotic lesions.

Methods

Nine atherosclerotic apoE-deficient mice were PET scanned. Four to determine optimal timing for imaging, and five post mortem after 1h redistribution of FDG and again after sequential removal of the interscapular brown fat and the atherosclerotic aortic arch. Uptake in various tissues in fasting (n=13) and non-fasting (n=7) apoE-deficient mice, including atherosclerotic and non-atherosclerotic aorta, was measured. Finally, accelerated atherosclerosis was induced by carotid ligation (n=12), and FDG-uptake was measured.

Results

FDG accumulation initially thought to correspond to the atherosclerotic aortic arch was recorded. Removal of interscapular brown fat, but not atherosclerotic aortic arch, removed the signal. The aortic arch accumulated less FDG than the non-atherosclerotic thoracic aorta both in fasting (ratio 0.5, p=0.008) and non-fasting (ratio 0.33, p=0.02) conditions. Carotid atherosclerosis likewise failed to increase FDG-uptake compared to the non-ligated artery (ratio 1.03).

Conclusion

Spontaneously developed advanced atherosclerotic lesions in aorta were, paradoxically, associated with reduced FDG uptake, and accelerated carotid atherosclerosis also failed to increase FDG-uptake. The results seriously question the potential of FDG-PET for imagining of advanced, vulnerable atherosclerotic lesions.

Keywords: Cardiovascular diseases, FDG, PET, Imaging, Inflammation, Nuclear medicine, Tomography

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PII: S0021-9150(06)00415-1

doi:10.1016/j.atherosclerosis.2006.07.019

Atherosclerosis
Volume 192, Issue 2 , Pages 275-282, June 2007