Altered cardiac function in thyroid disease is well recognized and has been 
extensively investigated, vascular function has however been less well studied 
in those with thyroid dysfunction. Thyroid hormones, thyroxine (T(4)) and 
triiodothyronine (T(3)) are important regulators of cardiac function and 
cardiovascular hemodynamics. The cardiovascular system responds to minimal but 
persistent changes in circulating thyroid hormone levels producing changes in 
vascular reactivity and endothelial function. The detection of endothelial 
dysfunction and/or arterial stiffness allows early identification of individuals 
at risk as these occur in both patients with risk factors for coronary artery 
disease and in those with established disease. This may allow treatment to be 
targeted at high risk individuals with the aim of slowing the progression of 
vascular disease. The various methods used to assess arterial function are 
reviewed and the changes demonstrated in human and animal models of thyroid 
dysfunction.