title: Vascularized atrial tissue patch cardiomyoplasty with omentopexy improves cardiac performance after myocardial infarction.
abstract: BACKGROUND
  The tissue-engineered cardiac patch can alleviate ventricular remodeling and improve functional recovery in experimental myocardial infarction. However, the size of the engineered patch is limited due to insufficient vascularization. This study evaluated the effects of autologous atrial tissue patch cardiomyoplasty and omentopexy in rats with myocardial infarction.
  
  
  METHODS
  Myocardial infarction was induced by left coronary artery ligation in Sprague-Dawley rats. Three weeks later, either a patch of left atrium (A group) or omentum (O group) or both (OA group) were placed over the infarct zone. The atrial tissue patch was harvested from the autologous left atrial appendage along its long axis. The rats in the Control group received rethoracotomy only. After 4 weeks, the survival of the transplanted atrial tissue patch, ventricular remodeling, and cardiac performance were examined.
  
  
  RESULTS
  After 4 weeks, surviving myocardium was only detected in the OA group, as indicated by immunolabeling of cardiac troponin-I. Compared with the Control group, only animals in the OA group showed improved heart function assessed by left ventricular ejection fraction (57.9% ± 5.8% vs 47.5% ± 4.5%, p < 0.05) and left ventricular fractional shortening (25.2% ± 3.6% vs 20.7% ± 2.0%, p < 0.05). The histologic analysis demonstrated increased scar thickness in the OA group. This was accompanied by increased angiogenesis of the border zone but decreased expression and activity of matrix metalloproteinase and endothelin-1 levels.
  
  
  CONCLUSIONS
  The omentopexy supported the survival of the autologous atrial tissue patch, which resulted in attenuated ventricular remodeling and restoration of heart function in rats with myocardial infarction. Our findings might represent a novel therapeutic strategy for heart failure.
authors.affiliation: Department of Surgery, Chinese Academy of Medical Sciences, Beijing, People's Republic of China.
authors.forename: Changwei
authors.initials: C
authors.lastname: Zhang
authors.forename: Jianfeng
authors.initials: J
authors.lastname: Hou
authors.forename: Shuai
authors.initials: S
authors.lastname: Zheng
authors.forename: Zhe
authors.initials: Z
authors.lastname: Zheng
authors.forename: Shengshou
authors.initials: S
authors.lastname: Hu
mesh_terms: D000818:Animals; D001158:Arteries / Q000637:transplantation*; D018421:Cardiomyoplasty / Q000379:methods*; D004195:Disease Models, Animal; D006352:Heart Ventricles / Q000503:physiopathology / Q000601:surgery; D008297:Male; D009203:Myocardial Infarction / Q000503:physiopathology / Q000601:surgery*; D018919:Neovascularization, Physiologic; D009852:Omentum / Q000637:transplantation*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000502:physiology*; D013318:Stroke Volume; D013524:Surgical Flaps / Q000098:blood supply*; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000502:physiology*