title: Cardiac shock wave therapy ameliorates left ventricular remodeling after myocardial ischemia-reperfusion injury in pigs in vivo.
abstract: OBJECTIVE
  Left ventricular (LV) remodeling after acute myocardial infarction (AMI) is associated with a poor prognosis and an impaired quality of life. We have shown earlier that low-energy extracorporeal cardiac shock wave (SW) therapy improves chronic myocardial ischemia in pigs and humans and also ameliorates LV remodeling in a pig model of AMI induced by permanent coronary ligation. However, in the current clinical setting, most of the patients with AMI receive reperfusion therapy. Thus, in this study we examined whether our SW therapy also ameliorates LV remodeling after myocardial ischemia-reperfusion (I/R) injury in pigs in vivo.
  
  
  METHODS
  Pigs were subjected to a 90-min ischemia and reperfusion using a balloon catheter and were randomly assigned to two groups with or without SW therapy to the ischemic border zone (0.09 mJ/mm(2), 200 pulses/spot, 9 spots/animal, three times in the first week) (n = 15 each).
  
  
  RESULTS
  Four weeks after I/R, compared with the control group, the SW group showed significantly ameliorated LV remodeling in terms of LV enlargement (131 +/- 9 vs. 100 +/- 7 ml), reduced LV ejection fraction (28 +/- 2 vs. 36 +/- 3%), and elevated left ventricular end-diastolic pressure (11 +/- 2 vs. 4 +/- 1 mmHg) (all P <0.05, n = 8 each). The SW group also showed significantly increased regional myocardial blood flow (-0.06 +/- 0.11 vs. 0.36 +/- 0.13 ml/min/g, P < 0.05), capillary density (1.233 +/- 31 vs. 1.560 +/- 60/mm(2), P < 0.001), and endothelial nitric oxide synthase activity (0.24 +/- 0.03 vs. 0.41 +/- 0.05, P < 0.05) in the ischemic border zone compared with the control group (n = 7 each).
  
  
  CONCLUSIONS
  These results indicate that our SW therapy is also effective in ameliorating LV remodeling after myocardial I/R injury in pigs in vivo.
authors.affiliation: Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Aoba-ku, Sendai, Japan.
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Ito
authors.forename: Kenta
authors.initials: K
authors.lastname: Ito
authors.forename: Takashi
authors.initials: T
authors.lastname: Shiroto
authors.forename: Ryuji
authors.initials: R
authors.lastname: Tsuburaya
authors.forename: Gao Jun
authors.initials: GJ
authors.lastname: Yi
authors.forename: Morihiko
authors.initials: M
authors.lastname: Takeda
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Fukumoto
authors.forename: Satoshi
authors.initials: S
authors.lastname: Yasuda
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Shimokawa
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002196:Capillaries / Q000503:physiopathology; D006328:Cardiac Catheterization; D017023:Coronary Angiography; D003326:Coronary Circulation; D004195:Disease Models, Animal; D004452:Echocardiography; D019220:High-Energy Shock Waves / Q000627:therapeutic use*; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D009206:Myocardium / Q000201:enzymology / Q000473:pathology*; D018919:Neovascularization, Physiologic; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D013318:Stroke Volume; D034421:Sus scrofa; D013997:Time Factors; D016277:Ventricular Function, Left; D017725:Ventricular Pressure; D020257:Ventricular Remodeling
chemical_list: D052250:Nitric Oxide Synthase Type III