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First published online March 14, 2008, 10.2967/jnumed.107.046706
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Journal of Nuclear Medicine Vol. 49 No. 4 557-563
© 2008 by Society of Nuclear Medicine

doi: 10.2967/jnumed.107.046706

Clinical Investigation

Effect of Progenitor Cells on Myocardial Perfusion and Metabolism in Patients After Recanalization of a Chronically Occluded Coronary Artery

Kai Kendziorra1, Henryk Barthel1, Sandra Erbs2, Frank Emmrich3, Rainer Hambrecht2,4, Gerhard Schuler2, Osama Sabri1 and Regine Kluge1

1 Department of Nuclear Medicine, University of Leipzig, Leipzig, Germany; 2 Heart Center Leipzig GmbH, University of Leipzig, Leipzig, Germany; 3 Institute of Clinical Immunology and Transfusion Medicine, University of Leipzig, Leipzig, Germany; and 4 Heart Center Bremen, Bremen, Germany

Correspondence: For correspondence or reprints contact: Kai Kendziorra, Department of Nuclear Medicine, University of Leipzig, Stephanstrasse 11, 04103 Leipzig, Germany. E-mail: kenk{at}medizin.uni-leipzig.de

Even after recanalization of a chronic total coronary occlusion, functional recovery is incomplete and parts of the myocardium remain hypoperfused. In this randomized, placebo-controlled, and double-blinded study, we investigated relative changes in myocardial perfusion and glucose metabolism induced by intracoronary administration of blood-derived circulating progenitor cells (CPCs), compared with the natural course in a control group after recanalization of total coronary occlusion. Methods: After recanalization of total coronary occlusion, 26 patients were randomly assigned to the CPC treatment or placebo group. Regional myocardial perfusion and glucose metabolism were assessed by 99mTc-tetrofosmin SPECT and 18F-FDG PET at baseline (after recanalization of total coronary occlusion) and 3 mo after the administration of 69 ± 14 x 106 CPCs or cell-free serum, respectively. Segments were classified as "normal," "perfusion–metabolism mismatch" (dysfunctional segments with a 99mTc-tetrofosmin–18F-FDG mismatch), or "scar." Results: In contrast to the placebo group, CPC administration resulted in a significant decrease in the number of segments with a perfusion–metabolism mismatch, from 3.0 ± 0.5 to 1.7 ± 0.6 segments (P < 0.05 vs. baseline). Of the normal segments at baseline, 2.7% in the CPC group and 30% in the placebo group revealed a perfusion–metabolism mismatch at follow-up after 3 mo (P < 0.05 vs. placebo). Conclusion: Intracoronary administration of CPCs significantly reduces the amount of myocardium with a perfusion–metabolism mismatch and prevents areas with normal perfusion and metabolism after recanalization of total coronary occlusion from becoming dysfunctional during the next 3 mo. These results show that PET and SPECT can be used to monitor the effect of progenitor cells on myocardial integrity. More important, they provide evidence supporting expansion of the use of progenitor cell treatment to chronic coronary artery disease.

Key Words: ischemic heart disease • perfusion–metabolism mismatch • progenitor cells • 18F-FDG PET

COPYRIGHT © 2008 by the Society of Nuclear Medicine, Inc.


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