title: Beneficial effect of autologous cell transplantation on infarcted heart function: comparison between bone marrow stromal cells and heart cells.
abstract: BACKGROUND
  Cell transplantation may restore function after myocardial infarction, but the optimal cell type remains controversial. We compared autologous bone marrow stromal cells (BMCs) with autologous heart cells (HCs) in a porcine myocardial infarction model.
  
  
  METHODS
  Yorkshire pigs underwent coil occlusion of the left anterior descending artery. Bone marrow stromal cells were obtained from sternal marrow and HCs were obtained by left ventricular biopsy, then cultured for 4 weeks. Four weeks after infarction, a 99mTc-sestamibi single-photon emission tomography (99mTc-MIBI SPECT) scan was performed and the pigs were then transplanted with BMCs (n = 7), HCs (n = 7), or culture medium (n = 14). Four weeks after transplantation, 99mTc-MIBI SPECT scanning was repeated to evaluate regional perfusion. Pressure-volume loops were constructed from micromanometer and conductance catheter data to evaluate left ventricular function. Hearts were evaluated histologically.
  
  
  RESULTS
  Bone marrow stromal cells and HCs engrafted within the infarct and assumed a myocyte morphology. SPECT MIBI scans showed increased perfusion in the infarct in cell-transplanted pigs, while perfusion decreased in the control pigs. Heart cell transplantation improved preload-recruitable stroke work and HC and BMC transplantation both shifted the end-systolic pressure-volume relation to the left. Both BMCs and HCs prevented thinning and expansion of the infarct region, and some BMCs differentiated into endothelial cells in newly formed blood vessels perfusing the infarct.
  
  
  CONCLUSIONS
  Both BMCs and HCs engrafted in the infarct region and improved let ventricular function by preventing infarct thinning. Bone marrow stromal cells demonstrated greater plasticity in vivo, and may offer a practical alternative to HC transplantation to restore function and perfusion after a myocardial infarction.
authors.affiliation: Division of Cardiovascular Surgery, Department of Clinical Biochemistry, Toronto General Hospital, University Health Network, Toronto, Ontario, Canada.
authors.forename: Terrence M
authors.initials: TM
authors.lastname: Yau
authors.forename: Shinji
authors.initials: S
authors.lastname: Tomita
authors.forename: Richard D
authors.initials: RD
authors.lastname: Weisel
authors.forename: Zhi-Qiang
authors.initials: ZQ
authors.lastname: Jia
authors.forename: Laura C
authors.initials: LC
authors.lastname: Tumiati
authors.forename: Donald A G
authors.initials: DA
authors.lastname: Mickle
authors.forename: Ren-Ke
authors.initials: RK
authors.lastname: Li
mesh_terms: D000818:Animals; D016026:Bone Marrow Transplantation; D017690:Cell Transplantation; D002478:Cells, Cultured; D004195:Disease Models, Animal; D005260:Female; D006321:Heart / Q000502:physiology*; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology / Q000601:surgery*; D009206:Myocardium / Q000166:cytology*; D017154:Stromal Cells / Q000637:transplantation; D013552:Swine; D017256:Technetium Tc 99m Sestamibi; D015899:Tomography, Emission-Computed, Single-Photon; D014182:Transplantation, Autologous; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D017256:Technetium Tc 99m Sestamibi