Thyroid hormones may exert cardiovascular actions by direct effects on the myocardium, by interacting with the sympathetic nervous system and through alterations of the peripheral circulation. Then, thyroid hormones increase myocardial contractility and relaxation, sensitise the myocardium to sympathetic nervous system and decrease arterial resistance. Hyperthyroidism results in an enhanced myocardial contractility, an increased cardiac output and a fall in systemic vascular resistance. Nevertheless "high output" cardiac decompensation may occur. Thyrotoxicosis may trigger arrythmia and disease seems to be associated with an increase in the frequency of mitral valve prolapse. Even in mild or subclinical hyperthyroidism complication may occur. Sympathetic blocking agents are the treatment of choice in addition to aetiologic treatment. Hypothyroidism is associated with bradycardia, a decreased cardiac output, increased vascular resistance and perhaps a decreased sensitivity of the sympathoadrenal system. An increase in cholesterolemia leads to an additional risk for the development of atherosclerosis. Main cardiovascular complications of hypothyroidism are angina pectoris, diastolic hypertension, atrio-ventricular blocks or pericarditis. Mild hypothyroidism might also be correlated with an increase in adverse effects.