Thyroid hormones play a wide range of important physiological activities in 
almost all organism. As changes in these hormones levels-observed in 
hypothyroidism and hyperthyroidism-promote serious derangements of the 
cardiovascular system, it is important to know their mechanisms of action. 
Although the classic genomic actions which are dependent on interaction with 
nuclear receptors to modulate cardiac myocytes genes expression, there is 
growing evidence about T(3) and T(4)-triggered nongenomic pathways, resulted 
from their binding to plasma membrane, cytoplasm, or mitocondrial receptors that 
leads to a rapidly regulation of cardiac functions. Interestingly both actions 
converge to amplify thyroid hormone effects on cardiovascular system. T(3) and 
T(4) nongenomic actions modify inotropic and chronotropic effects, cardiac 
action potential duration, cardiac growth, and myocyte shape by protein 
translation through protein kinases-dependent signaling cascades, which include 
PKA, PKC, PI3K, and MAPK, and changes on ion channels and pumps activity. In 
respect to the decreased systemic vascular resistance seen in hyperthyroidism, 
T(3) appears to activate NOS or ATP-sensitive K(+) channels. In addition, a 
novel biologically active T(4)-derived metabolite has been described, 
3-iodothyronamine, T(1)AM, which also acts through membrane receptors to mediate 
nongenomic cardiac effects. This metabolite influences the physiological 
manifestations of thyroid hormone actions by inducing opposite effects from 
those stimulated by T(3) and T(4), such as negative inotropic and chronotropic 
effects. Therefore, beyond genomic and nongenomic effects of thyroid hormones, 
it is crucial for there to be an equilibrium between T(3) or T(4) and T(1)AM 
levels for maintaining cardiac homeostasis.