Perfusion defect size predicts engraftment but not early retention of intra-myocardially injected cardiosphere-derived cells after acute myocardial infarction |
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| Authors: | Lautamäki Riikka Terrovitis John Bonios Michael Yu Jianhua Tsui Benjamin M Abraham M Roselle Bengel Frank M |
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| Affiliation: | (1) Division of Nuclear Medicine, Department of Radiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA;(2) Division of Cardiology, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, MD, USA;(3) Division of Medical Imaging Physics, Department of Radiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA;(4) Department of Nuclear Medicine, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany; |
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| Abstract: | Therapeutic cell retention and engraftment are critical for myocardial regeneration. Underlying mechanisms, including the role of tissue perfusion, are not well understood. In Wistar Kyoto rats, syngeneic cardiosphere-derived cells (CDCs) were injected intramyocardially, after experimental myocardial infarction. CDCs were labeled with [18F]-FDG (n = 7), for quantification of 1-h retention, or with sodium-iodide-symporter gene (NIS; n = 8), for detection of 24-h engraftment by reporter imaging. Perfusion was imaged simultaneously. Infarct size was 37 ± 9 and 38 ± 9% of LV in FDG and NIS groups. Cell signal was located in the infarct border zone in all animals. No significant relationship was observed between infarct size and 1-h CDC retention (r = −0.65; P = 0.11). However, infarct size correlated significantly with 24-h engraftment (r = 0.75; P = 0.03). Residual perfusion at the injection site was not related to cell retention/engraftment. Larger infarcts are associated with improved CDC engraftment. This observation encourages further investigation of microenvironmental conditions after ischemic damage and their role in therapeutic cell survival. |
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