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Intramyocardial Implantation of Bone Marrow–Derived Stem Cells Enhances Perfusion in Chronic Myocardial Infarction: Dependency on Initial Perfusion Depth and Follow-up Assessed by Gated Pinhole SPECT

¹ School of Surgery, Faculty of Medicine-UHP, Nancy, France; ² UHP-INSERM U684, Nancy, France; ³ In Vivo Cellular and Molecular Imaging Center, University of Brussels, Brussels, Belgium; and ⁴ Department of Nuclear Medicine, CHU-Nancy, Nancy, France

Correspondence: For correspondence or reprints contact: Nguyen Tran, PhD, Laboratory of Surgery School, Faculty of Medicine, 9 Avenue de la Forêt de Haye, 54500 Vandoeuvre-lès-Nancy, France. E-mail: Nguyen.Tran{at}medecine.uhp-nancy.fr

Cell therapy–induced changes in the perfusion of areas of myocardial infarction (MI) remain unclear. This study investigated whether an original pinhole SPECT technique could be applied to a rat MI model to analyze local improvement in myocardial perfusion relating to engraftment sites of bone marrow–derived stem cells (BMSCs). Methods: Four-month-old MI rats were either untreated (n = 8) or treated (n = 10) by intramyocardial injection of ¹¹¹In-labeled BMSCs. Early distribution of ¹¹¹In-BMSCs within the MI target was evidenced by dual ¹¹¹In/^99mTc pinhole SPECT 48 h later. Myocardial perfusion was serially monitored by ^99mTc-sestamibi pinhole gated SPECT up to 3 mo after transplantation. Results: Forty-eight hours after transplantation, ¹¹¹In-BMSCs were observed in all treated rats and in 18 of their 32 underperfused MI segments (<70% sestamibi uptake before transplantation). During the subsequent 3-mo follow-up, the perfusion of MI segments worsened in untreated rats (absolute change in sestamibi uptake, –3% ± 3%; P < 0.05) but improved in treated rats (+4% ± 7%; P < 0.05). This perfusion improvement was unrelated to the initial detection of ¹¹¹In-BMSCs (+2% ± 6% in segments with ¹¹¹In-BMSCs vs. +5% ± 7% in those without; not statistically significant) but was strongly associated with less severe perfusion defects before transplantation (+6% ± 6% in segments with 60%–70% sestamibi uptake [n = 19] vs. –1% ± 6% in those with <60% uptake [n = 13]; P = 0.003). Conclusion: When BMSCs are injected within chronic MI, perfusion enhancement predominates in the MI areas showing a high enough residual perfusion before treatment but not in those of the initial cell engraftment, giving evidence of dependency on the perfusion and metabolic environment at implantation sites.

Key Words: myocardial infarction • rats • stem cell therapy • bone marrow mesenchymal stem cells • sestamibi • ¹¹¹In-oxine • pinhole SPECT

COPYRIGHT © 2007 by the Society of Nuclear Medicine, Inc.

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