Atherosclerosis and leukocyte-endothelial adhesive interactions are increased following acute myocardial infarction in apolipoprotein E deficient mice

Atherosclerosis. 2010 Oct;212(2):414-7. doi: 10.1016/j.atherosclerosis.2010.06.022. Epub 2010 Jun 18.


Objective: To determine the effect of myocardial infarction (MI) on progression of atherosclerosis in apolipoprotein E deficient (ApoE-/-) mice.

Methods and results: MI was induced following left anterior descending coronary artery (LAD) ligation in wild-type (WT) (n=9) and ApoE-/- (n=25) mice. Compared to sham-operated animals, MI mice demonstrated increased intravascular leukocyte rolling and firm adhesion by intravital microscopy, reflecting enhanced systemic leukocyte-endothelial interactions. To determine if MI was associated with accelerated atherogenesis, LAD ligation was performed in ApoE-/- mice. Six weeks following surgery, atherosclerosis was quantitated throughout the arterial tree by microdissection and Oil-Red-O staining. There was 1.6-fold greater atherosclerotic burden present in ApoE-/- MI mice compared to sham-operated mice.

Conclusions: Acute MI accelerates atherogenesis in mice. These results may be related to the increased risk of recurrent ischemic coronary events following MI in humans.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Apolipoproteins E / metabolism*
  • Atherosclerosis / metabolism*
  • Body Weight
  • Cell Adhesion
  • Cholesterol / metabolism
  • Echocardiography / methods
  • Endothelial Cells / cytology*
  • Leukocytes / cytology*
  • Male
  • Mice
  • Mice, Transgenic
  • Myocardial Infarction / metabolism*
  • Myocardial Infarction / pathology
  • Tumor Necrosis Factor-alpha / metabolism


  • Apolipoproteins E
  • Tumor Necrosis Factor-alpha
  • Cholesterol