Cardiac actions of thyroid hormone metabolites

Thyroid hormones (THs) have a major role in regulating cardiac function. Their classical mechanism of action is genomic. Recent findings have broadened our knowledge about the (patho)physiology of cardiac regulation by THs, to include non-genomic actions of THs and their metabolites (THM). This review provides an overview of classical and non-classical cardiac effects controlled by: i) iodothyronines (thyroxine, T4; 3,5,3’-triiodothyronine,T3; 3, 5-diiodothyronine, T2); ii) thyronamines (thyronamine, T0AM; 3-iodothyronamine, T1AM); and iii) iodothyroacetic acids (3, 5, 3′, 5’-tetraiodothyroacetic acid, tetrac; 3, 5, 3’-triiodothyroacetic acid, triac; 3-iodothyroacetic acid, TA1). Whereas iodothyronines enhance both diastolic and systolic function and heart rate, thyronamines were observed to have negative inotropic and chronotropic effects and might function as a brake with respect to THs, although their physiological role is unclear. Moreover, thyronamines showed a cardioprotective effect at physiological concentrations. The cardiac effects of iodothyroacetic acids seem to be limited and need to be elucidated.