Left ventricular remodeling and chronic heart failure after myocardial infarction in mice

Abstract

Today, various kinds of knock out or transgenic murine models enabled us to extend our murine research. This study was designed to establish the murine model of LV remodeling and heart failure after myocardial infarction. We induced myocardial infarction in 197, 8 to 9 weeks old male C57BL/6 mice. 24 hours, 3 days, and 1,2, 4, 8, 12, and 20 weeks after operation, groups of 4 or 5 mice each underwent echocardiographic study and were then sacrificed. Total heart, wet and dry lung weights were measured. Interstitial collagen deposition level were histologically measured using a computerized morphometdc system. The infarction area involved 57% of the left ventricle (LV) on average, and the mortality rate within 24 hours after operation was 53%. 17 out of 65 mice died of cardiac rupture within 8 days of coronary occlusion. Left ventricular end-diastolic diameter (LVEDd) increased from 3.4_+0.14 mm to 7.1_+0.59 mm (p<0.O01). Total heart and lung weights increased from 101+10 mg to 237_+34 mg (p<0.001), and from 147_+9.1 mg to 419-+55 mg, respectively (p<0.001). The wet/dry lung weight ratio increased from 4.49_+0.87 to 9.29_+0.31 (p<0.001). Volume collagen fraction increased from 0.64_+0.27% to 9.38_+0.63%. (p<0.001) In this murine model, the increase of wet/dry lung weight ratio was consistent with the development of chronic heart failure. It represents a promising experimental tool to study the molecular and biochemical mechanisms of LV remodeling and heart failure.