This review evaluates the hypothesis that the cardiac effects of amiodarone can 
be explained-at least partly-by the induction of a local 'hypothyroid-like 
condition' in the heart. Evidence supporting the hypothesis comprises the 
observation that amiodarone exerts an inhibitory effect on the binding of T3 to 
thyroid hormone receptors (TR) alpha-1 and beta-1 in vitro, and on the 
expression of particular T3-dependent genes in vivo. In the heart, amiodarone 
decreases heart rate and alpha myosin heavy chain expression (mediated via TR 
alpha-1), and increases sarcoplasmic reticulum calcium-activated ATPase and beta 
myosin heavy chain expression (mediated via TR beta-1). Recent data show a 
significant similarity in expression profiles of 8,435 genes in the heart of 
hypothyroid and amiodarone-treated animals, although similarities do not always 
exist in transcripts of ion channel genes. Induction of a hypothyroid cardiac 
phenotype by amiodarone may be advantageous by decreasing energy demands and 
increasing energy availability.