title: The impact of the capability of circulating progenitor cell to differentiate on myocardial salvage in patients with primary acute myocardial infarction.
abstract: BACKGROUND
  Circulating endothelial progenitor cells (EPCs) are known to be involved in vasculogenesis and mobilized after acute myocardial infarction (AMI). To test the hypothesis that the angiogenic function of EPCs affects post-myocardial infarction (MI) myocardial salvage, we evaluated the number and potential differentiation of EPCs and compared these data with clinical parameters 6 months after MI.
  
  
  RESULTS
  Consecutive 51 patients (age, 61+/-8 years, mean+/-SD) with primary AMI who were successfully treated with stenting were enrolled. EPC identified as CD45low, CD34+, CD133+, and VEGFR2+ was quantified by a flow cytometry. The potential of EPCs to differentiate into endothelial cells (EPC differentiation) was also confirmed by the upregulation of CD31 and VEGFR2 after 7 days of culture. According to the proportion of EPC fraction, patients were divided into 2 groups (cut-off value=median). Although no difference was seen in myocardial damage shown by mean peak CK leakage and mean area at risk between the differentiated group (n=26) and nondifferentiated group (n=25), the number of attached cell was greater in differentiated group than in the nondifferentiated group (P=0.023). Left ventricular function and ischemic damaged area were assessed by scintigraphic images of (123)I-BMIPP in the acute phase and (99m)Tc-tetrofosmin in the chronic phase. We found that a greater increase in myocardial salvage (P=0.0091), decrease in end-systolic volume (P=0.012), and recovery of ejection fraction (P=0.011) occurred in the group with differentiated EPCs than in the nondifferentiated group.
  
  
  CONCLUSIONS
  In patients with primary AMI, the capability of EPCs to differentiate influences the functional improvement and infarct size reduction, indicating that manipulation of EPCs could be a novel therapeutic target to salvage ischemic damage.
authors.affiliation: Nagoya University Graduate School of Medicine, Department of Cardiology, 65 Tsurumai, Showa, Nagoya 466-8550. Japan. numa2@med.nagoya-u.ac.jp
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Numaguchi
authors.forename: Takahito
authors.initials: T
authors.lastname: Sone
authors.forename: Kenji
authors.initials: K
authors.lastname: Okumura
authors.forename: Masakazu
authors.initials: M
authors.lastname: Ishii
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Morita
authors.forename: Ryuji
authors.initials: R
authors.lastname: Kubota
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Yokouchi
authors.forename: Hajime
authors.initials: H
authors.lastname: Imai
authors.forename: Mitsunori
authors.initials: M
authors.lastname: Harada
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Osanai
authors.forename: Takahisa
authors.initials: T
authors.lastname: Kondo
authors.forename: Toyoaki
authors.initials: T
authors.lastname: Murohara
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers; D002454:Cell Differentiation; D042783:Endothelial Cells / Q000166:cytology*; D004730:Endothelium, Vascular / Q000166:cytology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D045164:Mesenchymal Stem Cell Transplantation; D059630:Mesenchymal Stem Cells / Q000166:cytology*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology / Q000601:surgery* / Q000628:therapy; D009206:Myocardium / Q000473:pathology; D018919:Neovascularization, Physiologic; D015607:Stents; D013318:Stroke Volume; D015899:Tomography, Emission-Computed, Single-Photon; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D015415:Biomarkers