The present study investigated whether changes in thyroid hormone (TH) 
signalling can occur after acute myocardial infarction (AMI) with possible 
physiological consequences on myocardial performance. TH may regulate several 
genes encoding important structural and regulatory proteins particularly through 
the TR alpha 1 receptor which is predominant in the myocardium. AMI was induced 
in rats by ligating the left coronary artery while sham-operated animals served 
as controls. This resulted in impaired cardiac function in AMI animals after 2 
and 13 weeks accompanied by a shift in myosin isoforms expression towards a 
fetal phenotype in the non-infarcted area. Cardiac hypertrophy was evident in 
AMI hearts after 13 weeks but not at 2 weeks. This response was associated with 
a differential pattern of TH changes at 2 and 13 weeks; T(3) and T(4) levels in 
plasma were not changed at 2 weeks but T(3) was significantly lower and T(4) 
remained unchanged at 13 weeks. A twofold increase in TR alpha 1 expression was 
observed after 13 weeks in the non-infarcted area, P<0.05 versus sham operated, 
while TR alpha 1 expression remained unchanged at 2 weeks. A 2.2-fold decrease 
in TR beta 1 expression was found in the non-infarcted area at 13 weeks, P<0.05, 
while no change in TR beta 1 expression was seen at 2 weeks. Parallel studies 
with neonatal cardiomyocytes showed that phenylephrine (PE) administration 
resulted in 4.5-fold increase in the expression of TR alpha 1 and 1.6-fold 
decrease in TR beta 1 expression versus untreated, P<0.05. In conclusion, 
cardiac dysfunction which occurs at late stages after AMI is associated with 
increased expression of TR alpha 1 receptor and lower circulating 
tri-iodothyronine levels. Thus, apo-TR alpha 1 receptor state may prevail 
contributing to cardiac fetal phenotype. Furthermore, down-regulation of TR beta 
1 also contributes to fetal phenotypic changes. alpha1-adrenergic signalling is, 
at least in part, involved in this response.