Besides its metabolic and thermoregulatory tissue effects, thyroid hormones plays a fundamental role in the cardiovascular homeostasis, mediated by genomic and non-genomic effects. Consequently, thyroid hormones deficits, as well as excesses, are expected to result in profound changes in cardiac function regulation and cardiovascular hemodynamics. Hyperthyroidism induces a hyperdynamic cardiovascular state, which is associated with enhanced left ventricular systolic, diastolic function, and the chronotropic and inotropic properties of thyroid hormones. On the other hand; in a hypothyroid state, thyroid hormones deficiency results in lower heart rate and weakening of myocardial contraction and relaxation, with prolonged systolic and early diastolic times. Subclinical hypothyroidism is characterized by abnormal lipid metabolism and cardiac dysfunction; diastolic hypertension conferring an elevated risk of atherosclerosis, and ischemic heart disease. The risk of cardiovascular mortality and atrial fibrillation [but not other outcomes] in subclinical hyperthyroidism is higher among patients with very low levels of thyrotropin. Finally, medications such as amiodarone may induce hypothyroidism [mediated by the Wolff-Chaikoff] as well as hyperthyroidism [mediated by the Jod-Basedow effect]. In both instances, the underlying cause is the high concentration of iodine in this medication.