title: Extracorporeal cardiac shock wave therapy ameliorates myocardial fibrosis by decreasing the amount of fibrocytes after acute myocardial infarction in pigs.
abstract: OBJECTIVE
  Extracorporeal shock wave (SW) therapy ameliorates cardiac remodeling after acute myocardial infarction (AMI). However, it remains to be examined whether and how SW therapy ameliorates myocardial fibrosis after AMI. Fibrocytes are associated with myocardial fibrosis. Thus, we examined whether SW therapy ameliorates myocardial fibrosis and whether fibrocytes are associated after AMI in pigs.
  
  
  METHODS
  AMI was created by coronary embolism. Twenty-five pigs were divided into three groups: AMI+SW group (AMI with SW therapy, n=15), AMI group (without SW therapy, n=5), and sham+SW group (SW therapy without AMI, n=5). The collagen area fraction was examined by Masson's trichrome staining. The presence of fibrocytes was identified by immunofluorescence and confocal microscopy. The location of CXCL12 was examined by immunohistochemistry.
  
  
  RESULTS
  Compared with the AMI group, the AMI+SW group showed significantly ameliorated myocardial fibrosis in terms of collagen area fraction (27.21±8.13 vs. 10.13±4.96, P<0.05) and reduced fibrocytes (CD34/α-smooth muscle actin: 35.40±11.72 vs. 12.27±7.71, P<0.05; CXCR4/α-smooth muscle actin: 40.80±8.96 vs. 16.54±6.38, P<0.05). There were positive correlations between the collagen area fraction and the number of fibrocytes (r=0.936; P<0.05) and between the number of CXCR4 fibrocytes and the SDF-1/CXCL12 cells (r=0.802; P<0.05) in the three groups.
  
  
  CONCLUSIONS
  The results show that SW therapy ameliorates myocardial fibrosis after AMI in pigs, which is associated with the decreased amount of fibrocytes.
authors.affiliation: Department of Forensic Medicine, Kunming Medical University, Kunming Medical University, Kunming, Yunnan Province, China.
authors.forename: Pu-Ping
authors.initials: PP
authors.lastname: Lei
authors.forename: Si-Ming
authors.initials: SM
authors.lastname: Tao
authors.forename: Qun
authors.initials: Q
authors.lastname: Shuai
authors.forename: Yu-Xia
authors.initials: YX
authors.lastname: Bao
authors.forename: Shang-Wen
authors.initials: SW
authors.lastname: Wang
authors.forename: Yong-Qiang
authors.initials: YQ
authors.lastname: Qu
authors.forename: Dian-Hua
authors.initials: DH
authors.lastname: Wang
mesh_terms: D000818:Animals; D054377:Chemokine CXCL12 / Q000378:metabolism; D003094:Collagen / Q000378:metabolism; D004195:Disease Models, Animal; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology*; D005355:Fibrosis; D005455:Fluorescent Antibody Technique; D019220:High-Energy Shock Waves / Q000627:therapeutic use*; D007150:Immunohistochemistry; D018613:Microscopy, Confocal; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D034421:Sus scrofa; D020257:Ventricular Remodeling
chemical_list: D054377:Chemokine CXCL12; D003094:Collagen