PMID- 17152990
OWN - NLM
STAT- MEDLINE
DCOM- 20070112
LR  - 20161124
IS  - 0031-7144 (Print)
IS  - 0031-7144 (Linking)
VI  - 61
IP  - 11
DP  - 2006 Nov
TI  - Treatment with granulocyte-colony stimulating factor in patients with acute 
      myocardial infarction. Evidence for a stimulation of neovascularization and 
      improvement of myocardial perfusion.
PG  - 957-61
AB  - BACKGROUND: Stem cell therapy has been suggested to be beneficial in patients 
      after acute myocardial infarction (AMI). Strategies of treatment are either a 
      local application of mononuclear bone marrow cells (BMCs) into the 
      infarct-related artery or a systemic therapy with the granulocyte-stimulating 
      factor (G-CSF) to mobilize BMCs. Nevertheless, the mechanisms responsible for 
      improvement of cardiac function and perfusion are speculative at present. This 
      study has been performed to investigate the effect of G-CSF on systemic levels of 
      vascular growth factors and chemokines responsible for neovascularization, that 
      might help to understand the positive effects of a G-CSF therapy after AMI. 
      METHODS AND RESULTS: Five patients in the treatment group and 5 patients in the 
      control group were enrolled in this study. The patients in the treatment group 
      received 10 microg/kg bodyweight/day of G-CSF subcutaneously for a mean treatment 
      duration of 6.6 +/- 1.1 days. In both groups, levels of vascular endothelial 
      growth factor (VEGF), basic fibroblast growth factor (bFGF) and monocyte 
      chemotactic protein-1 (MCP-1) were measured on day 2 to 3 and day 5 after AMI. 
      The regional wall perfusion and the ejection fraction (EF) were evaluated before 
      discharge and after 3 months with ECG-gated MIBI-SPECT and radionuclide 
      ventriculography, respectively. Significant higher levels of VEGF (p < 0.01), 
      bFGF (p < 0.05) and MCP-1 (p < 0.05) were found in the treatment group compared 
      to the control group. Levels of VEGF and bFGF remained on a plateau during the 
      G-CSF treatment and decreased significantly in the control group. The wall 
      perfusion improved significantly within the treatment group and between the 
      groups (p < 0.05), respectively. The EF improved significantly within the 
      treatment group (p < 0.05), but the change of the EF between the groups was not 
      significant. CONCLUSION: In patients with AMI, the treatment with G-CSF modulates 
      the formation of vascular growth factors that might improve neovascularization 
      and result in an improved myocardial perfusion and function.
FAU - Kuethe, F
AU  - Kuethe F
AD  - Friedhelm Kuthe, MD, Friedrich-Schiller-Universitat Jena, Klinik fur Innere 
      Medizin I, Erlanger Allee 101, D-07740 Jena, Germany.
FAU - Krack, A
AU  - Krack A
FAU - Fritzenwanger, M
AU  - Fritzenwanger M
FAU - Herzau, M
AU  - Herzau M
FAU - Opfermann, T
AU  - Opfermann T
FAU - Pachmann, K
AU  - Pachmann K
FAU - Sayer, H G
AU  - Sayer HG
FAU - Werner, G S
AU  - Werner GS
FAU - Gottschild, D
AU  - Gottschild D
FAU - Figulla, H R
AU  - Figulla HR
LA  - eng
PT  - Case Reports
PT  - Journal Article
PL  - Germany
TA  - Pharmazie
JT  - Die Pharmazie
JID - 9800766
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Radiopharmaceuticals)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 103107-01-3 (Fibroblast Growth Factor 2)
RN  - 143011-72-7 (Granulocyte Colony-Stimulating Factor)
RN  - 971Z4W1S09 (Technetium Tc 99m Sestamibi)
SB  - IM
MH  - Acute Disease
MH  - Aged
MH  - Chemokine CCL2/blood
MH  - Chemokines/biosynthesis
MH  - Coronary Circulation/*drug effects
MH  - Electrocardiography
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Fibroblast Growth Factor 2/blood
MH  - Granulocyte Colony-Stimulating Factor/*pharmacology
MH  - Humans
MH  - Intercellular Signaling Peptides and Proteins/metabolism
MH  - Male
MH  - Middle Aged
MH  - Myocardial Infarction/diagnostic imaging/*drug therapy/*pathology
MH  - Neovascularization, Physiologic/*drug effects
MH  - Prospective Studies
MH  - Radionuclide Ventriculography
MH  - Radiopharmaceuticals
MH  - Stroke Volume/physiology
MH  - Technetium Tc 99m Sestamibi
MH  - Tomography, Emission-Computed, Single-Photon
MH  - Vascular Endothelial Growth Factor A/blood
EDAT- 2006/12/13 09:00
MHDA- 2007/01/16 09:00
CRDT- 2006/12/13 09:00
PHST- 2006/12/13 09:00 [pubmed]
PHST- 2007/01/16 09:00 [medline]
PHST- 2006/12/13 09:00 [entrez]
PST - ppublish
SO  - Pharmazie. 2006 Nov;61(11):957-61.