Effect of progenitor cells on myocardial perfusion and metabolism in patients after recanalization of a chronically occluded coronary artery.
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 10(6) 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).


CONCLUSIONS
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.
Kendziorra
Kai
K
Department of Nuclear Medicine, University of Leipzig, Leipzig, Germany. kenk@medizin.uni-leipzig.de
Barthel
Henryk
H
Erbs
Sandra
S
Emmrich
Frank
F
Hambrecht
Rainer
R
Schuler
Gerhard
G
Sabri
Osama
O
Kluge
Regine
R
D003324:Coronary Artery Disease / Q000503:physiopathology / Q000628:therapy*; D003326:Coronary Circulation; D005947:Glucose / Q000378:metabolism; D006801:Humans; D009204:Myocardial Revascularization; D009206:Myocardium / Q000378:metabolism*; D009943:Organophosphorus Compounds; D015609:Organotechnetium Compounds; D033581:Stem Cell Transplantation; D013997:Time Factors
D009943:Organophosphorus Compounds; D015609:Organotechnetium Compounds; C078700:technetium tc-99m tetrofosmin; D005947:Glucose