Repeated implantation of skeletal myoblast in a swine model of chronic myocardial infarction

Eur Heart J. 2010 Apr;31(8):1013-21. doi: 10.1093/eurheartj/ehp342. Epub 2009 Aug 22.

Abstract

Aims: Although transplantation of skeletal myoblast (SkM) in models of chronic myocardial infarction (MI) induces an improvement in cardiac function, the limited engraftment remains a major limitation. We analyse in a pre-clinical model whether the sequential transplantation of autologous SkM by percutaneous delivery was associated with increased cell engraftment and functional benefit.

Methods and results: Chronically infarcted Goettingen minipigs (n = 20) were divided in four groups that received either media control or one, two, or three doses of SkM (mean of 329.6 x 10(6) cells per dose) at intervals of 6 weeks and were followed for a total of 7 months. At the time of sacrifice, cardiac function was significantly better in animals treated with SkM in comparison with the control group. A significantly greater increase in the DeltaLVEF was detected in animals that received three doses vs. a single dose of SkM. A correlation between the total number of transplanted cells and the improvement in LVEF and DeltaLVEF was found (P < 0.05). Skeletal myoblast transplant was associated with an increase in tissue vasculogenesis and decreased fibrosis (collagen vascular fraction) and these effects were greater in animals receiving three doses of cells.

Conclusion: Repeated injection of SkM in a model of chronic MI is feasible and safe and induces a significant improvement in cardiac function.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arrhythmias, Cardiac / etiology
  • Cell Differentiation
  • Chronic Disease
  • Fibrosis
  • Graft Survival
  • Immunohistochemistry
  • Myoblasts, Skeletal / cytology
  • Myoblasts, Skeletal / transplantation*
  • Myocardial Infarction / therapy*
  • Myocardium / pathology
  • Neovascularization, Physiologic / physiology
  • Swine
  • Swine, Miniature
  • Ventricular Dysfunction, Left / etiology
  • Ventricular Remodeling / physiology