Diabetes (DM) increases mortality after myocardial infarction and deteriorates postischaemic cardiac remodelling (1,2,3). Thyroid hormone (TH) signalling has a regulatory role in metabolism, cardiac function, growth and ischaemic stress (4,5). This study investigated possible implication of TH signalling in these responses. Type 1 diabetes was induced in male Wistar rats with a single i.p. injection of freshly prepared streptozotocin (30 mg/kg body wt) in 50 mM cold citrate buffer (pH 4.5). Thirty days after induction, the rats were anaesthetized with an i.p. injection of ketamine (70 mg/kg) and midazolame (0.1 mg/kg), intubated and ventilated via a tracheal cannula using a constant-volume rodent ventilator (Harvard Apparatus, Inspira, 50 breaths/min, 1ml/100g tidal volume). Anaesthesia was maintained by inhalation of small doses of sevoflurane (1-2%). Coronary artery ligation was performed in order to induce acute myocardial infarction (AMI) in rats with type I diabetes (DM) and age-matched control non-diabetic rats (NDM-AMI) while sham-operated animals served as controls (SHAM). Two weeks after ligation, rats were sedated with ketamine hydrochloric acid (100 mg/kg) and heart function evaluated by echocardiography. The α1 and β1 thyroid hormone receptor (THR) in the heart and levels of T3 and T4 in the plasma were determined by Western blotting analysis and by ELISA measurement, respectively. The results have demonstrated that AMI can cause tissue hypothyroidism leading to significant (p<0.05; Student’s t-test) down-regulation of the TH receptors, THRα1 and THRβ1, in the diabetic myocardium without changes in T3, T4 in the serum compared to non-diabetic myocardium. Typically, T3 and T4 in NDM-AMI were 1.02±0.06 nM and 50.3±2.3 nM, respectively, compared to DM-AMI in which the values were 1.09±0.08 nM and 52.3±3.1nM, respectively. This response was associated with increased expression of β-MHC (myosin heavy chain) and distinct changes in cardiac function and geometry. EF% (ejection fraction) was significantly (p<0.05) decreased in DM-AMI as compared to NDM-AMI. Systolic and diastolic chamber dimensions were increased without concomitant elevation in wall thickness and thus, Wall tension index (WTI; the ratio of (left ventricular internal diameter) LVIDd/2*Posterior Wall thickness), an index of wall stress, was significantly (p<0.05) increased compared to control. The results have shown that diabetes can exacerbate postischaemic cardiac remodelling and tissue hypothyroidism may, at least in part, be involved in this response.