title: Angiogenesis stimulation in explanted hearts from patients pre-treated with intravenous prostaglandin E(1).
abstract: BACKGROUND
  Prostaglandin E(1) (PGE(1)) is a potent vasodilator and induces angiogenesis in animal tissues. Previous clinical studies demonstrated that PGE(1) improves hemodynamic parameters in patients with heart failure listed for heart transplantation (HTX). Therefore, we designed a retrospective immunohistochemistry study to investigate various markers of angiogenesis using hearts explanted from PGE(1)-treated patients with idiopathic dilated cardiomyopathy (IDCM).
  
  
  RESULTS
  We investigated neovascularization in 18 hearts explanted from patients with IDCM: 9 patients received treatment with chronic infusions of PGE(1) for end-stage heart failure before HTX, whereas the remaining patients with IDCM did not receive PGE(1) and served as controls. We used immunoreactivity against CD34, von Willebrand factor (vWf), vascular endothelial growth factor (VEGF), and MIB-1 (Ki-67) to quantify angiogenesis, and used sirius red staining to determine the degree of fibrosis. Compared with the control group, PGE(1)-treated patients had significantly more CD34-, vWf- and MIB-1-positive cells in the sub-endocardium, myocardium and sub-epicardium (p < 0.01). The degree of fibrosis in the hearts of PGE(1)-treated patients was significantly lower than in control patients (p < 0.05), but we did not see any difference in the percentage of muscle mass. Finally, throughout the ventricles, we found significantly more VEGF-positive capillaries in the PGE(1) group (p < 0.0001).
  
  
  CONCLUSIONS
  The data suggest that PGE(1) could be a potent inducer of angiogenesis and the angiogenic factor VEGF, and could cause reduced fibrosis in the failing human heart.
authors: Department of Cardiology, University of Vienna, Vienna, Austria. heartreza@hotmail.com
authors: M R
authors: MR
authors: Mehrabi
authors: C
authors: C
authors: Ekmekcioglu
authors: B
authors: B
authors: Stanek
authors: T
authors: T
authors: Thalhammer
authors: F
authors: F
authors: Tamaddon
authors: R
authors: R
authors: Pacher
authors: G E
authors: GE
authors: Steiner
authors: T
authors: T
authors: Wild
authors: M
authors: M
authors: Grimm
authors: P G
authors: PG
authors: Spieckermann
authors: G
authors: G
authors: Mall
authors: H D
authors: HD
authors: Glogar
mesh_terms: D000527:Alprostadil / Q000494:pharmacology*; D018952:Antigens, CD34 / Q000187:drug effects / Q000378:metabolism; D034961:Antigens, Nuclear; D016228:Endothelial Growth Factors / Q000378:metabolism; D005260:Female; D005355:Fibrosis; D006352:Heart Ventricles / Q000187:drug effects; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000166:cytology; D018919:Neovascularization, Physiologic / Q000187:drug effects*; D009687:Nuclear Proteins / Q000187:drug effects / Q000378:metabolism; D012189:Retrospective Studies; D014665:Vasodilator Agents / Q000494:pharmacology*; D014841:von Willebrand Factor / Q000187:drug effects / Q000378:metabolism
chemical_list: D018952:Antigens, CD34; D034961:Antigens, Nuclear; D016228:Endothelial Growth Factors; D019394:Ki-67 Antigen; D009687:Nuclear Proteins; D014665:Vasodilator Agents; D014841:von Willebrand Factor; D000527:Alprostadil