Thyroid hormone (TH) is critical for tissue differentiation at early stages of 
development, induces physiological hypertrophy and regulates the expression of 
important contractile proteins such as myosin heavy chain (MHC) isoform and 
calcium cycling proteins. Furthermore, TH seems to control the response to 
stress by regulating important cardioprotective molecules such as heat shock 
proteins (HSPs). Thus, the present study investigated whether TH administration 
immediately after acute myocardial infarction can favourably remodel the 
post-infarcted myocardium. Acute myocardial infarction was induced in rats by 
coronary artery ligation (AMI, n=10), while SHAM-operated animals served as 
controls (SHAM, n = 8). TH was administered for 13 weeks (AMI-THYR, n = 9). 
Cardiac contractile function and left ventricular (LV) chamber remodelling was 
assessed by serial echocardiography and in Langendorff heart preparations. AMI 
significantly reduced LV ejection fraction (EF%); 30.0 (s.e.m, 2.3) Vs. 73.8 
(1.8) in SHAM, P < 0.05. In addition, +dp/dt and -dp/dt (in mmHg/s) were 4,051 
(343) and 2,333 (118) respectively for SHAM Vs. 2,102 (290) and 1,368 (181) for 
AMI, P < 0.05. With TH treatment, EF% was increased to 49.5 (2.7) in AMI-THYR, P 
< 0.05, while +dp/dt and -dp/dt (in mmHg/s) were 3,708 (231) and 2,035 (95) for 
AMI-THYR, P < 0.05 Vs. AMI. A marked elevation of the expression of beta-MHC and 
a reduced ratio of SERCA/Phospholamban were found in viable myocardium of AMI 
hearts, which was prevented by TH. Furthermore, heat shock protein 70 myocardial 
content was decreased in AMI hearts and was significantly increased after TH 
treatment. An ellipsoidal reshaping of LV chamber was observed with TH; cardiac 
sphericity index, (ratio of long/short axis, SI), was 1.98 (0.03) for SHAM, 1.52 
(0.05) for AMI and 1.72(0.02) for AMI-THYR, P < 0.05. In conclusion, long-term 
TH administration immediately after AMI results in sustained improvement of 
cardiac haemodynamics.