Monitoring of bone marrow cell homing into the infarcted human myocardium

M Hofmann, KC Wollert, GP Meyer, A Menke… - Circulation, 2005 - Am Heart Assoc
M Hofmann, KC Wollert, GP Meyer, A Menke, L Arseniev, B Hertenstein, A Ganser
Circulation, 2005Am Heart Assoc
Background—Intracoronary transfer of autologous bone marrow cells (BMCs) promotes
recovery of left ventricular systolic function in patients with acute myocardial infarction.
Although the mechanisms of this effect remain to be established, homing of BMCs into the
infarcted myocardium is probably a critical early event. Methods and Results—We
determined BMC biodistribution after therapeutic application in patients with a first ST-
segment–elevation myocardial infarction who had undergone stenting of the infarct-related …
Background— Intracoronary transfer of autologous bone marrow cells (BMCs) promotes recovery of left ventricular systolic function in patients with acute myocardial infarction. Although the mechanisms of this effect remain to be established, homing of BMCs into the infarcted myocardium is probably a critical early event.
Methods and Results— We determined BMC biodistribution after therapeutic application in patients with a first ST-segment–elevation myocardial infarction who had undergone stenting of the infarct-related artery. Unselected BMCs were radiolabeled with 100 MBq 2-[18F]-fluoro-2-deoxy-d-glucose (18F-FDG) and infused into the infarct-related coronary artery (intracoronary; n=3 patients) or injected via an antecubital vein (intravenous; n=3 patients). In 3 additional patients, CD34-positive (CD34+) cells were immunomagnetically enriched from unselected BMCs, labeled with 18F-FDG, and infused intracoronarily. Cell transfer was performed 5 to 10 days after stenting. More than 99% of the infused total radioactivity was cell bound. Nucleated cell viability, comparable in all preparations, ranged from 92% to 96%. Fifty to 75 minutes after cell transfer, all patients underwent 3D PET imaging. After intracoronary transfer, 1.3% to 2.6% of 18F-FDG–labeled unselected BMCs were detected in the infarcted myocardium; the remaining activity was found primarily in liver and spleen. After intravenous transfer, only background activity was detected in the infarcted myocardium. After intracoronary transfer of 18F-FDG–labeled CD34-enriched cells, 14% to 39% of the total activity was detected in the infarcted myocardium. Unselected BMCs engrafted in the infarct center and border zone; homing of CD34-enriched cells was more pronounced in the border zone.
Conclusions— 18F-FDG labeling and 3D PET imaging can be used to monitor myocardial homing and biodistribution of BMCs after therapeutic application in patients.
Am Heart Assoc