Myocardial infarction and cardiac remodelling in mice

Exp Physiol. 2002 Sep;87(5):547-55. doi: 10.1113/eph8702385.


We established a mouse model of cardiac dysfunction due to myocardial infarction (MI). For this we ligated the left anterior descending coronary artery in male C57BL/6J mice and assessed healing and left ventricular (LV) remodelling at 1, 2 and 4 days and 1, 2 and 4 weeks after MI. Echocardiography was performed at 1 and 2 weeks and 1, 2, 4 and 6 months after MI. We found that neutrophil infiltration of the infarct border was noticeable at 1-2 days. Marked macrophage infiltration occurred at day 4, while lymphocyte infiltration was apparent at 7-14 days. Massive proliferation of fibroblasts and collagen accumulation began by day 7-14, and scar formation was completed by day 21. LV diastolic dimension increased markedly at 2 weeks and remained at the same level thereafter. LV shortening fraction decreased significantly at 2 weeks and then slowly decreased. In non-infarcted areas of the LV, myocyte cross-sectional area and interstitial collagen fraction increased progressively, reaching a maximum at 4 months. This study provides important qualitative and quantitative information about the natural history of cardiac remodelling after MI in mice.

MeSH terms

  • Animals
  • Blood Pressure
  • Body Weight
  • Cell Division
  • Collagen / metabolism
  • Fibroblasts / pathology
  • Heart Rate
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Myocardial Infarction / mortality
  • Myocardial Infarction / pathology
  • Myocardial Infarction / physiopathology*
  • Myocardium / metabolism
  • Myocardium / pathology
  • Myocytes, Cardiac / pathology
  • Neutrophils / pathology
  • Organ Size
  • Ventricular Dysfunction, Left / mortality
  • Ventricular Dysfunction, Left / pathology
  • Ventricular Dysfunction, Left / physiopathology
  • Ventricular Remodeling / physiology*


  • Collagen