Survival, haemodynamics and cardiac remodelling follow up in mice after myocardial infarction

• Published in: Clinical and experimental pharmacology & physiology Vol. 30; no. 1-2; pp. 25 - 31
• Main Authors: Pons, S, Fornes, P, Hagege, AA, Heudes, D, Giudicelli, J-F, Richer, C
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Pty 01.01.2003
• Subjects: Animals; cardiac function; Echocardiography; Follow-Up Studies; Hemodynamics - physiology; left ventricular morphology; Male; Mice; Mice, Inbred C57BL; mortality; mouse; myocardial infarction; Myocardial Infarction - diagnostic imaging; Myocardial Infarction - pathology; Myocardial Infarction - physiopathology; Myocardium - pathology; Survival Rate; Ventricular Remodeling - physiology
• ISSN: 0305-1870; 1440-1681
• DOI: 10.1046/j.1440-1681.2003.03784.x

Summary 1. In the present study, the time‐course, over a 1 year period, of postischaemic dilated cardiomyopathy and/or development of congestive heart failure was investigated in mice in terms of survival and cardiac functional and structural characteristics. 2. C57BL/6 mice with myocardial infarction (MI mice; coronary ligation n = 78) or sham‐operated animals (n = 45) were used and echocardiographic, haemodynamic and histomorphometric parameters were assessed at 3, 6 and 12 months post‐MI. 3. At 12 months, the survival rate was 70% in MI mice. Left ventricular dysfunction was evidenced by a strong decrease in ejection fraction (EF; −48 and −53% at 6 and 12 months, respectively; both P < 0.05) and an increase in left ventricular end‐diastolic pressure (+100% at both 6 and 12 months; both P < 0.05). There was no major worsening in cardiac function between 6 and 12 months, suggesting strong compensatory mechanisms. Cardiac remodelling was observed, characterized by strong left ventricular hypertrophy (+38 and +62% at 6 and 12 months, respectively; both P < 0.05) and dilatation (+53% at 6 months; P < 0.05), but collagen was not significantly increased. Significant correlations were found between EF (echocardiography) and dP/dtmax, between end‐diastolic volume (echocardiography) and left ventricular internal perimeter (histomorphometry) and between left ventricular mass (echocardiography) and weight. 4. In conclusion, despite a high survival rate, the MI mouse model displays most of the hallmarks of postischaemic dilated cardiomyopathy and/or congestive heart failure, thus affording the necessary background for the subsequent evaluation of gene manipulation and/or drug effects. In addition, two‐dimensional echocardiography appears to be a suitable tool for the long‐term follow up of cardiac function and remodelling in this model.