Echocardiographic measurement of left ventricular function following myocardial infarction in adult postnatally overfed mice

Abstract

Perinatal environment, such as nutritional state, is of major importance for short- and long-term cardio-metabolic status. Postnatal overfeeding (PNOF) induced in rodents by litter size reduction at birth reproduces the effects of childhood overnutrition and was shown to affect the cardiovascular function and to predispose to cardiovascular pathologies. The aim of our work was to follow the evolution of cardiac function for 60 days after in vivo myocardial infarction in control and PNOF mice. C57BL/6 male mice were raised in litter adjusted to 9 or 3 pups for control and PNOF group respectively. After weaning, mice of both groups had free access to standard diet and water. At 4 months, they were either subjected to a permanent ligation of the left anterior descending artery (LAD) to induce myocardial infarction or a sham surgery. Echocardiographic measurements were acquired at baseline and 7, 28, 45 and 60 days after surgery for cardiac function evaluation. Sixty days after surgery, the left ventricle (LV) was harvested for bio-molecular analyzes and lungs were weighed. At basal state, no difference of cardiac function was observed between the 4 groups. In both control and PNOF mice subjected to LAD ligation, the ejection fraction (EF) was significantly decreased 7 days after surgery while the systolic/diastolic LV area was significantly increased, and they both remained stable until 60 days. An increase of cardiac troponin I level and LV mass were also observed 24 h and 60 days after surgery respectively. However, no differences neither in LV contractile function nor in infarct size were noticed between control and PNOF mice. As demonstrated by the decreased LV contractility and dilation, the two groups of mice subjected to myocardial infarction developed heart failure, however, no differences between the control and PNOF groups were observed. Further experiments will be done in order to assess the cardiac expression of genes and proteins involved in heart failure, including the b-myosin heavy chain or the atrial natriuretic peptide.