SNM Annual Meeting Abstracts
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     




J Nucl Med. 2008; 49 (Supplement 1):183P
This Article
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Hacker, M.
Right arrow Articles by Bartenstein, P.
PubMed
Right arrow Articles by Hacker, M.
Right arrow Articles by Bartenstein, P.

Cardiovascular: Basic Science

Basic Science Posters

In vivo therapy monitoring by [99mTc]-sestamibi pinhole SPECT: G-CSF reduces infarct size after myocardial infarction in mice

Marcus Hacker1, Michael Groebner2, Sebastian Nowak1, Bruno Huber2, Rebecca Fischer2, Christoph Rischpler2, Wolfgang-Michael Franz2 and Peter Bartenstein1

1 Department of Nuclear Medicine; 2 Department of Cardiology, University of Munich, Munich, Germany

798

Objectives: Granulocyte-colony stimulating factor (G-CSF) was shown to improve cardiac function after myocardial infarction (MI). We non-invasively investigated G-CSF effects on perfusion after MI in mice using pinholeSPECT.

Methods: MI was induced by coronary artery ligation in wildtype mice (C57BL/6J). G-CSF (100 µg/kg; n=5) or saline (controls, n=4) was daily injected for 5 consecutive days. After injection of 370 MBq [99mTc]-sestamibi, left ventricular perfusion was determined using a triple-headed gamma camera, each detector head equipped with a 0.5 mm diameter pinhole collimator. Imaging was performed 6 (baseline) and 30 days after LAD-occlusion. Polar maps were normalized by mean of a standardized reference region of interest (ROI) in the septum. Best threshold value for identifying infarcted areas was determined after comparing perfusion defects with the histological infarct sizes. Defect size was indicated as percent of left ventricular myocardium. Primary endpoint was change of defect size from baseline to 30 days after MI.

Results: Mean infarct size was similar in controls(20.6% ± 0.9) and G-CSF group (19.2% ± 1.1) at baseline. 30 days after MI, a slight difference (p=0.05) was found between controls (20.2 ± 0.8) and G-CSF (16.5% ± 1.2) injected mice. However, change of defect size was significantly different between G-CSF (-2.6% ± 0.8) and control animals (-0.3% ± 0.1, p=0.02).

Conclusions: The preliminary results of the present study showed a significant reduction of left ventricular perfusion defect sizes in mice after LAD-occlusion when treated with G-CSF compared to mice without G-CSF-treatment, indicating positive effects on ventricular remodelling.





This Article
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Hacker, M.
Right arrow Articles by Bartenstein, P.
PubMed
Right arrow Articles by Hacker, M.
Right arrow Articles by Bartenstein, P.