Document Detail


Extracorporeal cardiac shock wave therapy markedly ameliorates ischemia-induced myocardial dysfunction in pigs in vivo.
MedLine Citation:
PMID:  15520304     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Prognosis of ischemic cardiomyopathy still remains poor because of the lack of effective treatments. To develop a noninvasive therapy for the disorder, we examined the in vitro and vivo effects of extracorporeal shock wave (SW) that could enhance angiogenesis. METHODS AND RESULTS: SW treatment applied to cultured human umbilical vein endothelial cells significantly upregulated mRNA expression of vascular endothelial growth factor and its receptor Flt-1 in vitro. A porcine model of chronic myocardial ischemia was made by placing an ameroid constrictor at the proximal segment of the left circumflex coronary artery, which gradually induced a total occlusion of the artery with sustained myocardial dysfunction but without myocardial infarction in 4 weeks. Thereafter, extracorporeal SW therapy to the ischemic myocardial region (200 shots/spot for 9 spots at 0.09 mJ/mm2) was performed (n=8), which induced a complete recovery of left ventricular ejection fraction (51+/-2% to 62+/-2%), wall thickening fraction (13+/-3% to 30+/-3%), and regional myocardial blood flow (1.0+/-0.2 to 1.4+/-0.3 mL x min(-1) x g(-1)) of the ischemic region in 4 weeks (all P<0.01). By contrast, animals that did not receive the therapy (n=8) had sustained myocardial dysfunction (left ventricular ejection fraction, 48+/-3% to 48+/-1%; wall thickening fraction, 13+/-2% to 9+/-2%) and regional myocardial blood flow (1.0+/-0.3 to 0.6+/-0.1 mL x min(-1) x g(-1)). Neither arrhythmias nor other complications were observed during or after the treatment. SW treatment of the ischemic myocardium significantly upregulated vascular endothelial growth factor expression in vivo. CONCLUSIONS: These results suggest that extracorporeal cardiac SW therapy is an effective and noninvasive therapeutic strategy for ischemic heart disease.
Authors:
Takahiro Nishida; Hiroaki Shimokawa; Keiji Oi; Hideki Tatewaki; Toyokazu Uwatoku; Kohtaro Abe; Yasuharu Matsumoto; Noriyoshi Kajihara; Masataka Eto; Takehisa Matsuda; Hisataka Yasui; Akira Takeshita; Kenji Sunagawa
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Publication Detail:
Type:  Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-11-01
Journal Detail:
Title:  Circulation     Volume:  110     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2004 Nov 
Date Detail:
Created Date:  2004-11-09     Completed Date:  2005-06-21     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3055-61     Citation Subset:  AIM; IM    
Affiliation:
Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cells, Cultured / metabolism
Collateral Circulation
Coronary Circulation
Endothelial Cells / metabolism*
Endothelium, Vascular / cytology
High-Energy Shock Waves / therapeutic use*
Humans
Models, Cardiovascular
Myocardial Ischemia / physiopathology,  therapy*
Neovascularization, Physiologic / physiology
Proteins / genetics,  metabolism
RNA, Messenger / biosynthesis,  genetics
Sus scrofa
Umbilical Veins / cytology
Up-Regulation
Vascular Endothelial Growth Factor A / biosynthesis,  genetics
Vascular Endothelial Growth Factor Receptor-1
Chemical
Reg. No./Substance:
0/Proteins; 0/RNA, Messenger; 0/Vascular Endothelial Growth Factor A; EC 2.7.10.1/FLT1 protein, human; EC 2.7.10.1/Vascular Endothelial Growth Factor Receptor-1

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