It has been previously shown that regulators of physiological growth such as 
thyroid hormone (TH) can favorably remodel the post ischaemic myocardium. Here, 
we further explored whether this effect can be preserved in the presence of 
co-morbidities such as diabetes which accelerates cardiac remodeling and 
increases mortality after myocardial infarction. Acute myocardial infarction 
(AMI) was induced by left coronary ligation in rats with type I diabetes (DM) 
induced by streptozotocin administration (STZ; 35 mg/kg; i.p.) while 
sham-operated animals served as controls (SHAM). AMI resulted in distinct 
changes in cardiac function and geometry; EF% was significantly decreased in 
DM-AMI [37.9 ± 2.0 vs. 74.5 ± 2.1 in DM-SHAM]. Systolic and diastolic chamber 
dimensions were increased without concomitant increase in wall thickness and 
thus, wall tension index [WTI, the ratio of (Left Ventricular Internal Diameter 
at diastole)/2*(Posterior Wall thickness)], an index of wall stress, was found 
to be significantly increased in DM-AMI; 2.27 ± 0.08 versus 1.70 ± 0.05. 
2D-Strain echocardiographic analysis showed reduced systolic radial strain in 
all segments, indicating increased loss of cardiac myocytes in the infarct 
related area and less compensatory hypertrophy in the viable segments. This 
response was accompanied by a marked decrease in the expression of TRα1 and TRβ1 
receptors in the diabetic myocardium without changes in circulating T3 and T4. 
Accordingly, the expression of TH target genes related to cardiac contractility 
was altered; β-MHC and PKCα were significantly increased. TH (L-T4 and L-T3) 
administration prevented these changes and resulted in increased EF%, normal 
wall stress and increased systolic radial strain in all myocardial segments. 
Acute myocardial infarction in diabetic rats results in TH receptor 
down-regulation with important physiological consequences. TH treatment prevents 
this response and improves cardiac hemodynamics.