Key result
Noninvasive molecular imaging with the novel 68Ga-mCXCL12 PET tracer successfully quantified cardiac CXCR4 upregulation in mice after acute myocardial infarction, peaking at day 3 post-MI.
Why the study?
CXCR4 and CXCL12 represent potential imaging and therapeutic targets after MI, and a novel murine-specific 68Ga-mCXCL12 PET tracer could enable serial in vivo quantification of cardiac CXCR4 expression.
Does the 68Ga-mCXCL12 PET tracer allow for in vivo quantification of cardiac CXCR4 expression in a mouse model of acute myocardial infarction?
Does the 68Ga-mCXCL12 PET tracer allow for in vivo quantification of cardiac CXCR4 expression in a mouse model of acute myocardial infarction?
Absolute Event Rate: 4.5% vs 1.4%
p-value: p=<0.001
Noninvasive molecular imaging of cardiac CXCR4 expression using a novel 68Ga-mCXCL12 tracer is feasible in a mouse model of acute myocardial infarction.
May enable serial CXCR4 PET in murine MI models; hypothesis-generating and should not yet change practice.
Background The chemokine receptor CXCR4 and its ligand CXCL12 have been shown to be a possible imaging and therapeutic target after myocardial infarction (MI). The murine-based and mouse-specific 68 Ga-mCXCL12 PET tracer could be suitable for serial in vivo quantification of cardiac CXCR4 expression in a murine model of MI. Methods and Results At days 1-6 after MI, mice were intravenously injected with 68 Ga-mCXCL12. Autoradiography was performed and the infarct-to-remote ratio ( I / R ) was determined. In vivo PET imaging with 68 Ga-mCXCL12 was conducted on days 1-6 after MI and the percentage of the injected dose (%ID/g) of the tracer uptake in the infarct area was calculated. 18 F-FDG-PET was performed for anatomical landmarking. Ex vivo autoradiography identified CXCR4 upregulation in the infarct region with an increasing I / R after 12 hours (1.4 ± 0.3), showing a significant increase until day 2 (4.5 ± 0.6), followed by a plateau phase (day 4) and decrease after 10 days (1.3 ± 1.0). In vivo PET imaging identified similar CXCR4 upregulation in the infarct region which peaked around day 3 post MI (9.7 ± 5.0 %ID/g) and then subsequently decreased by day 6 (2.8 ± 1.0 %ID/g). Conclusion Noninvasive molecular imaging of cardiac CXCR4 expression using a novel, murine-based, and specific 68 Ga-mCXCL12 tracer is feasible both ex vivo and in vivo.
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Zacherl et al. (2020) studied Acute myocardial infarction (mouse model). 68Ga-mCXCL12 PET tracer vs. Remote myocardium / Unblocked controls was evaluated on Infarct-to-remote ratio (I/R) of 68Ga-mCXCL12 uptake (p=<0.001). Noninvasive molecular imaging with the novel 68Ga-mCXCL12 PET tracer successfully quantified cardiac CXCR4 upregulation in mice after acute myocardial infarction, peaking at day 3 post-MI.
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