Left ventricular (LV) remodeling occurs in many patients after myocardial infarction (MI). LV remodeling is characterized by progressive ventricular dilatation and contractile dysfunction, consequently to cardiomyocyte hypertrophy and fibrosis. Despite reperfusion therapies, this pathophysiological process is the main cause of cardiac evolution toward heart failure. Moreover, the outcome of patients after MI is largely dependent on the initial cardiac injury. Thus, this is of major clinical interest to develop new pharmacological strategies to limit infarct size and prevent or reverse left ventricular remodeling. Such preclinical cardiovascular treatments are often tested in rodents. The rat model of myocardial infarction is commonly used. In this model, the permanent ligation of the left anterior descending coronary artery is performed (Bousquenaud et al., 2013a).

After being used to this surgical technique and experimented, the operator will need 20 min per rat from the anesthesia to the rat recovering.