Diabetes (DM) increases mortality after myocardial infarction (MI) by accelerating postischaemic cardiac remodeling (REM). Thyroid hormone (TH) is thought as potential regenerative therapy due to its ability to regulate cell growth, differentiation and response to stress. We have previously shown that it can prevent REM when given immediately after an acute experimental MI. Thus, we investigated whether long-term TH treatment can reverse post-ischemic myocardial remodeling in diabetic rat hearts.Methods
Type I diabetes was induced in male Wistar rats by streptozotocin injection (35mg/Kg i.p.). Thirty day diabetic and normal rats were subjected either to sham-operation (SHAM, n=9 and DM-SHAM, n=9) or to experimental myocardial infarction (AMI, n=8 and DM-AMI, n=9) by coronary artery ligation (CAL). TH treatment was initiated in a group of diabetic post-infarcted rats, 2 weeks after CAL (DM-AMI + TH, n=8). Echocardiography analysis was performed at 8 weeks after CAL. Left ventricular (LV) internal diameter at the diastolic phase (LVIDd), LV internal diameter at the systolic phase (LVIDs), systolic velocity of the posterior wall radial displacement (SVPW) and the ejection fraction (EF%) were measured.Methods
TH can diminish postischaemic remodeling in the diabetic heart probably due to its regenerative effect.