Ultrasound-mediated stimulation of microbubbles after acute myocardial infarction and reperfusion ameliorates left-ventricular remodelling in mice via improvement of borderzone vascularization

PLoS One. 2013;8(2):e56841. doi: 10.1371/journal.pone.0056841. Epub 2013 Feb 20.

Abstract

Aims: Post-infarction remodelling (PIR) determines left-ventricular (LV) function and prognosis after myocardial infarction. The aim of this study was to evaluate transthoracic ultrasound-mediated microbubble stimulation (UMS) as a novel gene- and cell-free therapeutic option after acute myocardial infarction and reperfusion (AMI/R) in mice.

Methods and results: For myocardial delivery of UMS, a novel therapeutic ultrasound-system (TIPS, Philips Medical) and commercially available microbubbles (BR1, Bracco Suisse SA) were utilized in a closed-chest mouse model. UMS was performed as myocardial post-conditioning (PC) on day four after 30 minutes of coronary occlusion and reperfusion. LV-morphology, as well as global and regional function were measured repeatedly with reconstructive 3-dimensional echocardiography applying an additional low-dose dobutamine protocol after two weeks. Scar size was quantified by means of histomorphometry. A total of 41 mice were investigated; 17 received PC with UMS. Mean ejection fraction (EF) prior UMS was similar in both groups 53%±10 (w/o UMS) and 53%±14 (UMS, p = 0.5), reflecting comparable myocardial mass at risk 17%±8 (w/o UMS), 16%±13 (UMS, p = 0.5). Two weeks after AMI/R, mice undergoing UMS demonstrated significantly better global LV-function (EF = 53%±7) as compared to the group without PC (EF = 39%±11, p<0.01). The fraction of akinetic myocardial mass was significantly lower among mice undergoing UMS after AMI/R [27%±10 (w/o UMS), 13%±8 (UMS), p<0.001)]. Our experiments showed a fast onset of transient, UMS-induced upregulation of vascular-endothelial and insulin-like growth factor (VEGF-a, IGF-1), as well as caveolin-3 (Cav-3). The mice undergoing PC with UMS after AMI/R showed a significantly lower scar size. In addition, the microvascular density was significantly higher in the borderzone of UMS-treated animals.

Conclusion: UMS following AMI/R ameliorates PIR in mice via up-regulation of VEGF-a, IGF-1 and Cav-3, and consecutive improvement of myocardial borderzone vascularization.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cardiomegaly
  • Caveolin 3 / genetics
  • Caveolin 3 / metabolism
  • Disease Models, Animal
  • Echocardiography
  • Female
  • Gene Expression Regulation
  • Insulin-Like Growth Factor I / genetics
  • Insulin-Like Growth Factor I / metabolism
  • Mice
  • Microbubbles / therapeutic use*
  • Myocardial Infarction / diagnosis
  • Myocardial Infarction / physiopathology*
  • Myocardial Infarction / therapy*
  • Myocardial Reperfusion Injury / diagnosis
  • Myocardial Reperfusion Injury / physiopathology*
  • Myocardial Reperfusion Injury / therapy*
  • Myocardium / metabolism
  • Myocardium / pathology
  • Neovascularization, Pathologic
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor A / metabolism
  • Ventricular Remodeling*

Substances

  • Caveolin 3
  • RNA, Messenger
  • Vascular Endothelial Growth Factor A
  • Insulin-Like Growth Factor I

Grants and funding

J.D. and A.G. were supported by BONFOR (Intramural research foundation of the University of Bonn). A.G. was supported by the German Heart Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.