A new ^18F-labeled myocardial PET tracer: Myocardial uptake after permanent and transient coronary occlusion in rats

Conventional myocardial perfusion PET tracers require onsite tracer production because of their short radioactive half-lives. To investigate the potential of a new ¹⁸F-labeled pyridazinone analog ( ¹⁸F-BMS-747158-02), we characterized this tracer in a rat model of permanent and transient coronary occlusion using small-animal PET. Methods: Myocardial ¹⁸F-BMS-747158-02 distribution in healthy rats (n = 7), rats with transient (3-min) left coronary artery occlusion (n = 11), and rats with permanent left coronary occlusion (n = 11) was analyzed with a dedicated small-animal PET scanner. Results: Normal hearts demonstrated intense and almost homogeneous tracer uptake throughout the left ventricle for more than 2 h. During permanent coronary occlusion, PET demonstrated perfusion defects, which remained unchanged (37.6% ± 8.8%, 37.4% ± 10.2%, and 36.2% ± 9.8% left ventricle at 15, 45, and 115 min, respectively, after tracer injection). After transient ischemia, the induced defect size decreased significantly after reperfusion (16.2% ± 9.3%, 6.0% ± 6.5%, and 1.4% ± 1.3% left ventricle). Tracer reinjection after transient ischemia resulted in normalization of the induced defect. Conclusion: Coronary occlusion yielded distinct myocardial ¹⁸F-BMS-747158-02 uptake defects in the area of ischemia, which demonstrated normalization of activity after reperfusion and reinjection. These promising kinetic parameters may allow for assessment of flow using exercise-rest protocols similar to those used in combination with exercise and rest perfusion SPECT.