OtherBASIC SCIENCE INVESTIGATIONS

A New 18F-Labeled Myocardial PET Tracer: Myocardial Uptake After Permanent and Transient Coronary Occlusion in Rats

Takahiro Higuchi, Stephan G. Nekolla, Marc M. Huisman, Sybille Reder, Thorsten Poethko, Ming Yu, Hans-Jurgen Wester, David S. Casebier, Simon P. Robinson, Rene M. Botnar and Markus Schwaiger
Journal of Nuclear Medicine October 2008, 49 (10) 1715-1722; DOI: https://doi.org/10.2967/jnumed.108.053967

Article Figures & Data

Figures

  • FIGURE 1. 
    FIGURE 1. 

    Schemas of experimental protocols of permanent and transient coronary occlusion and imaging: normal heart (A), permanent LCA occlusion (B), transient LCA occlusion (C), reinjection after permanent LCA occlusion (D), and reinjection after transient LCA occlusion (E). 18F-BMS = 18F-BMS-747158-02.

  • FIGURE 2. 
    FIGURE 2. 

    (A) Examples of 18F-BMS-747158-02 (18F-BMS) PET images of chest of healthy rat at 15, 45, and 115 min after tracer injection and 13N-ammonia PET image at 10 min in coronal view. Example of regions of interest for measurement of tracer activity is displayed in white box. (B and C) Ratio of 18F-BMS uptake between myocardium and surrounding organs (B) and absolute 18F-BMS activity of myocardium (%ID/cm3) (C). (D) Comparison of 18F-BMS uptake ratios at 15 min after injection and 13N-ammonia at 10 min.

  • FIGURE 3. 
    FIGURE 3. 

    Normal pattern of left ventricular 18F-BMS-747158-02 (18F-BMS) distribution at 15, 45, and 115 min after tracer injection as shown in mean polar maps (A) and as mean uptake values (% left ventricle maximum) with SD (B). Uptake was nearly homogeneous throughout left ventricle, with slightly lower uptake in apical segment.

  • FIGURE 4. 
    FIGURE 4. 

    Short-axis images of rat heart 1 wk after coronary occlusion using 18F-BMS-747158-02 (18F-BMS) PET and 13N-ammonia PET. Arrows indicate localization of myocardial infarction.

  • FIGURE 5. 
    FIGURE 5. 

    Representative short-axis images of rat hearts without coronary occlusion, permanent coronary occlusion, and transient coronary occlusion at different time points after tracer administration. Tracer redistribution is seen in induced defect after reperfusion (arrows).

  • FIGURE 6. 
    FIGURE 6. 

    Changes in myocardial 18F-BMS-747158-02 (18F-BMS) distribution after both permanent and transient coronary occlusion are shown in representative polar maps (A) and as defect area expressed as percentage of total left ventricular myocardium (B). Normalized counts of circumferential profiles after permanent occlusion (C) or transient occlusion (D) are also shown. Mean values are shown for tracer activity in induced defect and normally perfused myocardium after permanent (E) and transient occlusion (F). Tracer activity in defect increased over time after reperfusion in transient coronary occlusion.

  • FIGURE 7. 
    FIGURE 7. 

    Myocardial 18F-BMS-747158-02 (18F-BMS) distribution patterns before and after tracer reinjection in rats after permanent and transient coronary occlusion. Representative polar maps (A) and plots of defect area (B) are shown. Tracer uptake defects resolved after tracer reinjection in rats after transient coronary occlusion but not in permanent coronary occlusion.

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