Thyroid hormone (TH) is critical in cardiac cell differentiation (regulating 
contractile proteins and cell geometry) and this effect could be potentially 
exploited therapeutically in reversing the process of de-differentiation which 
underlies postischemic cardiac remodeling. Acute myocardial infarction was 
induced in male Wistar rats by ligating left coronary artery (AMI, n=8), while 
sham operated animals served as control (SHAM, n=8). 13 weeks after AMI, TH was 
administered in a group of animals for 4 weeks (AMI-THYR, n=9). TH significantly 
increased beta-MHC and decreased alpha-MHC expression in the myocardium. This 
response was accompanied by changes in cardiac geometry: sphericity index, (SI, 
long to short axis ratio) was found to be 1.95 (SEM, 0.02) in SHAM, 1.51(0.03) 
in AMI and 1.64(0.03) in AMI-THYR, p<0.05. As a consequence, cardiac function 
was significantly improved: left ventricular ejection fraction (EF%) was 74.5% 
(SEM, 2.8) in SHAM vs 29.5% (2.1) in AMI, and 40.0% in AMI-THYR, p<0.05. 
Furthermore, +dp/dt and -dp/dt were 4250 (127) and 2278 (55) in SHAM vs 
2737(233) and 1508 (95) in AMI vs 3866 (310) and 2137(111) in AMI -THYR, 
respectively, p<0.05. TH treatment partially reverses cardiac dysfunction in 
rats with old myocardial infarction by favorably changing cardiac chamber 
geometry and expression of myosin isoforms. Thyroid hormone, unlike current 
treatments, appears to be a paradigm of therapeutic intervention which aims at 
restoring cardiac geometry and may prove new effective treatment for heart 
failure.