PMID- 16530020
OWN - NLM
STAT- MEDLINE
DCOM- 20061211
LR  - 20121115
IS  - 1537-1891 (Print)
IS  - 1537-1891 (Linking)
VI  - 44
IP  - 5
DP  - 2006 May
TI  - Improvement of contractility accompanies angiogenesis rather than arteriogenesis 
      in chronic myocardial ischemia.
PG  - 326-32
AB  - INTRODUCTION: Growth factor therapy provides a therapeutic alternative for "no 
      option" patients with coronary disease. Fibroblast Growth Factor-2 (FGF-2) 
      predominantly stimulates angiogenesis, the growth of new capillaries, whereas 
      Monocyte Chemoattractant Protein-1 (MCP-1) is considered an arteriogenic agent. 
      We hypothesised a synergetic effect of FGF-2 and MCP-1 in ischemic myocardium. 
      METHODS: A severe coronary stenosis was created in pigs. After one week, chronic 
      ischemia was confirmed by angiography, echocardiography, reduced ejection 
      fraction, and increase of marker enzymes. FGF-2, MCP-1, both, or vector only were 
      then injected intramyocardially as plasmid DNA in the impaired area. Regional 
      contractility and number of capillaries and arterial vessels were evaluated after 
      three months. RESULTS: FGF-2, FGF-2+MCP-1, and vector, but not MCP-1 alone 
      improved regional contractility at rest, whereas only FGF-2 alone ameliorated 
      function under stress conditions. Angiogenesis in the ischemic area was 
      stimulated by FGF-2 compared to MCP-1. In contrast, MCP-1 induced arteriogenesis 
      relative to FGF-2. CONCLUSION: Differences for vessel growth and regional 
      function were apparent between FGF-2 and MCP-1. This contrast could allow the 
      speculation that development of a flow reserve in chronically ischemic myocardium 
      is linked to angiogenesis rather than to arteriogenesis. No additional benefits 
      were seen following combined therapy.
FAU - Heilmann, Claudia
AU  - Heilmann C
AD  - Department of Cardiovascular Surgery, University Hospital Freiburg, Hugstetter 
      Str. 55, 79106 Freiburg, Germany. heilmann@ch11.ukl.uni-freiburg.de
FAU - Kostic, Caterina
AU  - Kostic C
FAU - Giannone, Bodo
AU  - Giannone B
FAU - Grawitz, Andrea Busse
AU  - Grawitz AB
FAU - Armbruster, Werner
AU  - Armbruster W
FAU - Lutter, Georg
AU  - Lutter G
FAU - Beyersdorf, Friedhelm
AU  - Beyersdorf F
FAU - Gobel, Heike
AU  - Gobel H
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060309
PL  - United States
TA  - Vascul Pharmacol
JT  - Vascular pharmacology
JID - 101130615
RN  - 0 (Chemokine CCL2)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 103107-01-3 (Fibroblast Growth Factor 2)
SB  - IM
MH  - Animals
MH  - Capillaries/growth & development
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Chronic Disease
MH  - Coronary Stenosis/metabolism/physiopathology/*therapy
MH  - Coronary Vessels/growth & development
MH  - Disease Models, Animal
MH  - Fibroblast Growth Factor 2/*biosynthesis/genetics
MH  - *Genetic Therapy
MH  - Genetic Vectors
MH  - Intercellular Signaling Peptides and Proteins/*biosynthesis/genetics
MH  - *Myocardial Contraction
MH  - Myocardial Ischemia/metabolism/physiopathology/*therapy
MH  - Myocardium/metabolism
MH  - *Neovascularization, Physiologic
MH  - Swine
EDAT- 2006/03/15 09:00
MHDA- 2006/12/12 09:00
CRDT- 2006/03/15 09:00
PHST- 2005/10/25 00:00 [received]
PHST- 2006/01/11 00:00 [accepted]
PHST- 2006/03/15 09:00 [pubmed]
PHST- 2006/12/12 09:00 [medline]
PHST- 2006/03/15 09:00 [entrez]
AID - S1537-1891(06)00021-8 [pii]
AID - 10.1016/j.vph.2006.01.002 [doi]
PST - ppublish
SO  - Vascul Pharmacol. 2006 May;44(5):326-32. doi: 10.1016/j.vph.2006.01.002. Epub 
      2006 Mar 9.