Multidimensional immunoimaging to characterize the inflammatory reaction after permanent and temporary coronary artery occlusion in mice

Abstract Background The immune response following acute myocardial infarction encompasses a delicate balance between inflammatory and reparative programs. Our knowledge of these complex mechanisms is mainly derived from studies using murine model permanent coronary artery occlusion. In this study we developed, validated implemented multiparametric imaging methods to investigate cardiac function the systemic in transient or occlusion mouse models. Methods models encompassed either (40 min) LAD C57BL/6 mice, non-infarcted mice were used as controls. Two seven days later, animals subjected immunoimaging bone marrow, spleen myocardium with late gadolinium enhancement MRI (LGE cMRI), 18F-fluorodeoxyglucose (18F-FDG) PET, 18F-Fluorothymidine (18F-FLT) 64Cu-CCR2 PET targeting monocytes, 89Zr-CD11b nanobody 19F-HDL-PERFECTA MRI, both myeloid cells. addition, same applied atherosclerosis-prone Apoe−/− inflammation plaque progression assessed by flow cytometry immunohistochemistry four weeks after infarction. Results Through LGE cMRI 18F-FDG observed that temporary resulted smaller infarct size, better viability compared Multiparametric CD11b+ cells Ly6Chi monocytes demonstrated had less cell influx ischemic myocardium. This finding was confirmed analysis zone. contrast, cause similar marrow multimodal subsequent numbers blood. Both aggravate atherosclerosis higher macrophage monocyte aortas larger size without Conclusions We developed employed multimodal, protocols characterize heart, two While superior ischemia reperfusion model, types accelerated atherosclerosis. Funding Acknowledgement Type funding sources: Other. Main source(s): NIH DFG