The heart and vascular system represent major targets of the thyroid hormone action, and marked changes occur in cardiac electro-mechanical function of patients with hyper-hypothyroidism. Thyroid hormones exert their effects through both genomic (nuclear) and nongenomic (extranuclear) mechanisms. Understanding the cellular mechanisms of thyroid hormone action on the heart and cardiovascular system is the basis to explain the changes in cardiac output, cardiac contractility, blood pressure, vascular resistance, and rhythm abnormalities secondary to thyroid dysfunction. Not only overt, but also subclinical thyroid diseases have been associated with systolic and diastolic cardiac abnormalities, and with alterations of well known cardiovascular risk factors. Moreover, the early diagnosis and treatment of thyroid diseases restore to normal most of the cardiovascular changes. Nowadays, it is becoming increasingly evident that, like a vicious circle, acute and chronic cardiovascular diseases may influence thyroid hormone metabolism, which, in turn, can contribute to cardiovascular impairment progression.